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A    TEXT-BOOK   OF    Mf:DIClXE 


VOTi.   IT 


'^^Vvsxw.   S^©^^^ 


A    TEXT- BOOK    OF 
MEDICINE 


BY 

G.    DIEULAFOY 

PnOFF.SSOB   OF    CLINIC/VL   MEl)ICi;iE   AT   THE   l-ACULTji    UE    MEDECINE    DE    PARIS;    PHYSICIAN 
TO    THE   hGtEL  DIEU  ;   MEMBRE   DE   L'aCADEMIE    DE   MEDECINE 


SECOND   EDITrON 

Authorized  Trafts/,i/io)t  from  the  Sixteen.'^  Edition  of  ^^  Manuel  de 
Patholosrte  Interne  " 


V.  E.   COLLINS,   M.D.   Lond.,   M.R.C.S.,   L.R.G.P. 

AND 

J.  A.   LIEBMANN,   Ph.D.,   M.A.,   LL.D. 


IN  TWO  VOLUMES 
VOL.  II 


NEW  YORK 

D.    APPLETON  AND   COMPANY 

1912 


First  Edition  (translated  from  Fifteentli  French  Edition),  June,  1510. 

Eeprinted  :May,  1911. 

Reprinted  August,  1911, 

Preprinted  March,  1912. 

Second  Edition  (translated  from  Sixteenth  French  Edition),  August,  1912. 


PRINTED   IN   LONDON 
BY    BAILLIERE,    TINDALL   AND   COX. 


CONTENTS    OF   VOL.    H 

PAET    III— Continued 
DISEASES  OF  THE   URINARY   SYSTEM 

CnAPTKR  PAGE 

I.  DISEASES   OF  THE    KIDNEYS      ---....  1077 

I.   ANATOMY   AND   PHYSIOLOGY   OF  THE   KIDNEYS       ....  1077 

II.    CONGESTION  OF  THE   KIDNEYS — CARDIAC   KIDNEY               -                -                 -  1081 

lU.    ACDTE   NEPHRITIS                .......  1082 

IV.   APPENDICULAR      KIDNEY  —  TOXIC      NEPHRITIS  —  APPENDICULAR      ALBU- 
MINURIA      .-.....-  1090 

V.       BRICUT'S  DISEASE  — CHRONIC  NEPHRITIS — PARENCHYMATOUS  NEPHRITIS 

— INTERSTITIAL   NEPHRITIS — MIXED   NEPHRITIS         -                 -                 -  1098 
Vr.   DISCUSSION      ON      UNILATERAL      NEPHRITIS — SURGICAL      TREATMENT     OF 

NEPHRITIS-                 .......  1144 

VII.    CASES   OF  ALBUMINURIA   NOT  DUE  TO   BKIGHt's   DISEASE                -                -  1150 

VIII.   AMYLOID   KIDNEY                 .......  1152 

IX.   TUBERCULOSIS   OF  THE   KIDNEY    ......  1153 

X.   RENAL       SYPHILIS  —  SECONDARY       SYPHILITIC       NEPHRITIS  —  TERTIARY 

SYPHILIS   OF   THE   KIDN*EY   .--.-.  1165 

XI.    CYSTS   OF   THE    KIDNEY — ENLARGED   POLYCYSTIC    KIDNEY                .                 -  1180 

XII.   HYDATID   CYSTS   OF  THE    KIDNEYS               -                 -                .                 -                .  1184 

Xin.    CANCER   OF  THE    KIDNEY                 -                -                -                -                 -                -  1186 

XIV.   RENAL   CALCULI  ....-'.-.  1191 

XV.   PYELITIS — PYELONEPHRITIS             ..--..  1212 

XVI.   SUPPURATIVE  NEPHRITIS                  -                -                *                -                -                 -  1212 

XVn.    PRIMARY  ANT)    SECONT)ARY  PERINEPHRITIC   ABSCESS           -                 -                -  1214 

XVin.    HYDRONTIPHROSIS  -  -  •-  -  -  -  -1219 

XIX.    HiEMATUBIA — CHYLURIA-                  ......  1220 

SX.    HEMOGLOBINURIA                -...--.  1223 

XXI.   MOVABLE   KIDNEY — COEXISTENT  UNILATERAL   NEPHRITIS                 -                -  1228 

II.  DISEASES   OF   THE    SUPRARENAL   CAPSULES          .....  1233 

I.  Addison's  disease — defaced  type  of  addison's  disease      -            -  1233 

n.    insufficiency      of      the       suprarenal      CAPSULES  —  HAEMORRHAGE  — 

SUPRARENALlTiS       .......  1241 


PART  rv 

DISEASES  OF   THE  NERVOUS   SYSTEM 

DISEASES   OF  THE   SPINAL  CORD  ......      1243 

T.    PROGRESSIVE       LOCOMOTOR       AT^^Y  —  TABES       DORSALIS  —  DUCHENNE's 

DISEASE        ....-..-      1243 


vi  CONTENTS   OF   VOL.   II 

CHAPTEE                                                                                                                                                               ■  PAGE 

I.  DISEASES  OF  THE  SPINAL  CORD — continued : 

II.  Friedreich's    disease    and    hereditary    cerebellar     ataxy  — 

SPASMODIC   FAMILY   PARAPLEGIA       .....  1266 

III.  COMBINED    SCLEROSIS         .......  1269 

IV.  SYRINGOMYELIA   ........  1272 

V.   PROGRESSIVE   MUSCULAR   ATROPHY              .....  1276 

VI.    SECONDARY      AND      PRIMARY      LATERAL      SCLEROSIS — SPASMODIC     TABES 

DOKSALIS      ----.-..  1283 

VII.  AMYOTROPHIC   LATERAL    SCLEROSIS               .....  1285 
VIIL   INSULAR  SCLEROSIS            .......  1287 

IX.    ACUTE   MYELITIS   IN   GENERAL      ......  1291 

X.  INFANTILE     POLIOMYELITIS — ATROPHIC      SPINAL     PARALYSIS     OF     CHILD- 

HOOD             -                 -                  -                 -                  -                 -                 -                  -  1294 

Xt.   POLIOMYELITIS     IN     THE     ADULT — ACUTE      SPINAL     PARALYSIS     IN      THE 

ADULT           -                  -         .        - 1298 

.  XII.   ACUTE   DIFFUSE   MYELITIS                 ......  1302 

XIII.  CHRONIC   DIFFUSE   MYELITIS           ......  1.305 

XIV.  SYPHILITIC   MYELITIS          .......  1307 

XV.   AFFECTIONS   OF   THE    CAUDA   EQUINA   AND    OF   THIi    FILUM   TERMINALE      -  1311 

XVI.    HiEMATOMYELIA   -                  -                 -                  -                 -                  -                 -                 •  131i 

XVII.    COMPRESSION   OF   THE    SPINAL   CORD            .....  1317 

XVIII.    SPINAL  MENINGITIS             .......  1318 

II.  POLIOENCEPHALITIS — DISEASES    OF   THE   PONS   AND    BULB  -  -  .1821 

I.  GLOSSO-LABIO -LARYNGEAL       PARALYSIS  —  INFERIOR       CHRONIC       POLIO- 

ENCEPHALITIS           .......  1322 

II.  CHRONIC    SUPERIOR   POLIOENCEPHALITIS  .                -                 -                .                -  1327 

III.  SYPHILITIC   POLIOENCEPHALITIS    OF  THE   BULB   AND    PONS                 -                 -  1330 

IV.  ACUTE   AND    SUBACUTE   POLIOENCEPHALITIS             -                  -                 -                 -  1335 
V.   WEBER's   syndrome — BONNIER's   SYNDROME          -                 -                .                .  1336 

III.   DISEASES    OF   THE    CEREBELLUM                 ......  1339 

ABSCESS,   TUMOURS,   AND    SYPHILIS    OF   THE    CEREBELLUM                 -                  -  1339 

rV.   DISEASES    OF   THE   BRAIN"*            .......  1348 

I.    CEREBRAL   CONGESTION    -                  •                  -                 -                 -                 -                 -  1348 

II.  CEREBRAL  AN^SIMIA             -           .      -                 -                 -                 -                 -                 -  1349 

III.  CEREBRAL   HEMORRHAGE                ......  1349 

rV.   CEREBRAL    SOFTENING — EMBOLISM — ATHEROMA    ....  1364 

V,  APHASIA-                ..---.-•  1369 

VI.  ENCEPHALITIS — ABSCESS   OF  THE  BRAIN                  ....  1376 
Vn.    CHRONIC    ENCEPHALITIS     OF     CHILDHOOD— HiEMORRHAGE— SOFTEN^NG— 

PORENCEPHALIA — LOBAR   SCLEROSIS — LITTLe's   DISEASE        -                 -  1378 

VIII.  CEREBRAL   TUMOURS           ..-----  1384 
IX.   CEREBRAL     SYPHILIS— SYPHILITIC     ARTERITIS— GUMMATA    AND     SCLERO- 

GUMMATOUS   LESIONS— SYPHILITIC   GENERAL   PSEUDO-PARALYSIS        -  1389 

X.    GENERAL   PARALYSIS— CHRONIC   MENINGO-ENCEPHALITIS                   -                 -  1404 

XI.  SYPHILITIC    NECROSIS   AND   PERFORATION    OF  THE   VAULT   OF  THE    SKULL 

— DIAGNOSIS   FROM  TUBERCOLOSIS   AND   FROM   CANCER          -                 -  1410 

14-97 

XII.    CEREBRAL   LOCALIZATION                -                 -                 "                "                 '  ^^^' 

XIII.   DISCUSSION       ON      MEDICO-SURGICAL       ERRORS      REGARDING      CEREBRAL 
LOCALIZATION  ..-•••" 


1431 


CONTENTS    OF    VOL.    Li 


vu 


CHAFTKR  rAOE 

IV.  DISEASES   OK   TlIK    HUMS  —rout i)i iirrf  : 

XIV.   TUHKUCITLAU    MKNINCJITIfl                  ......  1 437 

XV.    NON-TUHERCIU.AK    MKNINCITIS        ......  I441 

XVI.   OEUEIUtO-SriNAL   MENINGITIS          --....  J  444 

XVII.   OHKONIC  MENIN(JIT1S— I'ACIIVMENINtilTIS— ll/i;.MATOMA  OKTIIE  DUKA  MATKI:  1463 

XVIll.    SYnilUTIC   PACIiyMENINGITIS   OF  THE   BASE   OF  THE    liKAIN          -  1464 

XIX.  MENINOKAL    IIJEMORRIIAUE               ......  1457 

XX.  IIYDUOCErilALOS                    .......  1469 

V.   NEURITIS              -......-.  1471 

rOI.YNKURITIS       -                 .                 .                 .                  .                 .                  .                 -  1471 

n.  NEUROSES            ----.....  1477 

I.    ESSENTIAL    El'lLErSY — SECONDARY    EPILEI'SV         ....  I477 

II.   PARTIAL   EPILEPSY — .TACKSONIAN    KIMLKPSY             ....  14g3 

III.  TRAUMATIC    EPILEPSY        ---....  1490 

IV.  HYSTERIA                  ----....  1492 
V.    HY^PNOTISM — LETHARGY — CATALEPSY — SOMXAMIU'LISM      -                  -                  -  1509 

VI.   PATIIOMIMIA           -                 -                  -                  -                  -                  -                  -                 -  lal;j 

VII.   NEURASTHENIA     -..--...  1515 

Vlir.   ASTASIA — ABASIA                 .......  1518 

TX.   CEREBRO-CARDIAC   NEUROPATHY — KRISHABER's   DISEASE                   -                -  1520 

X.   PARALY'SIS   AGITANS — PARKINSOn's   DISEASE          -                 -                 -                -  1521 

XI.  Sydenham's  chorea — st.  vitus's  dance          .            .            .            .  1523 

Xn.   CHOREA    gravis — CHOREIC   PSYCHOSES        .....  1530 

XIII.   TETANY   -                  ........  1535 

XrV.   OCCUPATION  NEUROSES    .......  1537 

VII.   NEURALGIA        .........  1538 

I.   MIGRAINE                 ........  1538 

II.    NEURALGIA   OF   THE   TRIFACIAL   NERVE — TIC    DOULOURECX             -                -  1540 

III.  SYPHILITIC   NEURALGIA   OF  THE   TRIFACIAL   NERVE             -                 -                 -  1545 

IV.  CERVICO-OCCIPITAL   AND    CEKVK'O-BRACIIIAL   NEURALGIA                  -                 -  1547 
V.   NEUR.SXGIA    OF   THE    PHRENIC    NERVE        -                  -                  -  .              -                 -  1548 

VI.   INTERCOSTAL   NEUR.U.GIA — ZONA                   .....  1549 

VII.   LUMBAR   NEURALGIA           --....-  1552 

VIU.    SCIATIC   NEUR.ALGIA — SCOLIOSIS    ---.--  1552 

IX.    SY'PHILITIC    SCIATICA — HOMOLOGOUS   SCOLIOSIS     ....  1555 

X.   PARiESTUETIC  MERALGIA — NEURITIS  OF  THE  EXTERNAL  CUTANB0U5  NERVE  1560 

XI.   RADICULITIS            -                 -                 -                 -                  -                  -                  -                  -  1561 

VIII.    PARALYSES          .....-.--  15G3 

I.   FACUL   PARALYSIS               ...--.-  1563 

n.   SYPHILITIC   FACIAL   PARALYSIS      -                -                -                .                ■                -  1571 

in.    PAR.^LY'SIS    OF   THE   MOTOR   NERVES   OF   THE   EYE                 -                 -                  -  1578 

IV.   OPHTHALMOPLEGIA              .......  158G 

V.   PARALYSIS   OF   THE   MUSCULAR-SPIRAL   NERVE      ...                -  1588 

VI.   RADICULAR  PARALYSIS — RADICULAR  P.Ul.VLYSIS  OF  THE  BRACHIAL  PLEXUS  1592 
\^I.   P.\RALYSIS   OF   THE   TRIGEJHNAL   NERVE  -                  -                 -                  - 

IX.   TROPHIC   AND   VASOMOTOR   TROUBLES     .  -  .  -  - 

1.   TROPHIC   TROUBLES    IN    GENERAL — DYSTROPHIES  • 
II.    FACIAL   TROPHONEUROSIS  ..... 

III.  SCLERODERSnA      -..---. 

IV.  LOCAL  ASPHYHIA — SYMMETRICAL   GANGRENE   OF   THE    EX  IlIEMITIES            -  1604 


1595 

1598 
1598 
1601 
1603 


viii  CONTENTS   OF   VOL.   II 


PAET   V 

GENERAL   AND  INFECTIOUS   DISEASES 

CHAPTER  PAGE 


I.    ERUPTIVE    FEVERS 
I.   VARIOLA 
n.   VACCINIA 

III.  VARICELLA 

IV.  SCARLATINA 
V.   MEASLES 

VI.  RUBELLA 
Vn.  MILIARY  FEVER 
Vni.  DENGUE  - 

II.  TYPHOID  DISEASES 

I.  TYPHOID  FEVER 
II.  TYPHUS  FEVER 


1607 

1607 

1615 

-     --  1621 

-  1624 
1645 

-  1658 

-  1659 

-  1662 

-     -     -     -     -  1665 
1665 

-  1730 

ni.   RELAPSING   FEVER              .......  1733 

III.  INFECTIOUS    DISEASES   PROPER   TO   MAN                  .....  1743 

I.    STREPTOCOCCAL   INFECTION   OF   THE    BLOOD              .                 -                  -                  -  1743 

II.  ERYSIPELAS    OF   THE   FACE               -                 -                  -                  ...                 .  1748 

III.  STAPHYLOCOCCAL   INFECTION   OF   THE    BLOOD          -                  -                  .                 .  1755 

IV.  MUMPS      -                 -                 -                 -                 -                  -                  -                  -                 .  1756 

V.  CHOLERA        ........  1761 

VI.  INFLUENZA      -       .       -       -       -       -       -       .  1771 

VII.  YELLOW  FEVER — VOMITO  NEGRO        .....  1777 

VIII.  PLAGUE  -       -       .       -       -       -       -       -       -  1781 

IX.  TETANUS  .......       .       -  1787 

X.  M.A.LARIA        .._.....  1796 

XI.   SLEEPING   SICKNESS            .......  1821 

XII.    LEPROSY  .........  1826 

IV.  INFECTIVE   DISEASES    COMMON   TO   MEN   AND   TO    ANIMALS              -                 -                 -  1834 

I.    RABIES     -...-.-..  1834 

n.    ANTHRAX                  ........  1837 

III.  GLANDERS — FARCY              .......  1842 

IV.  ACTINOMYCOSIS     .--.----  1845 
V.   SPOROTRICHOSIS    ..-.-.--  1850 

VI,  PSITTACOSIS          ........  1853 

PAET   VI 

DISEASES  OF   THE   SPLEEN 

HYDATID  CYSTS    OF  THE    SPLEEN — DIAGNOSIS   OF   ENLARGEMENTS    OF   THE    SPLEEN  1858 

PAET   VII 

PATHOLOGY   OF   THE   BLOOD 

I.   CLINICAL   EXAMINATION   OF   THE   BLOOD  -                -                .                -                .  1877 

n.  ASJEMix  .....'.--  1881 

III.    PROGRESSIVE    PERNICIOUS    ANiEMIA             .....  1882 


CONTENTS    OF    Vol..    II 


IX 


IV.    LKUCOCYTH^.MIA 

V.    rill.OltOSIS — CULORO-BIUOHTISM    - 
VL   PUKl'UKA — 8CUKVY — INFANTILK   StUllVY 


FAOK 

1885 
18'J4 
l'J07 


PART    VI  IT 
RHEUMATIC   AND   DYSTUOPIIKJ   DISEASES 

I.    UniCUMATISM       ..-----. 
1.    ACUTB    ARTICULAK    RHEUMATISM  .  .  .  . 

II.    CHRONIC   RJIKUMATISM      ..---- 

III.  PSEUDO-RHEUMATISM    DUE    TO    GONOKIUICEA,    TUKEK(  UI.OSIS,    ETC. 

IV.  GOUT         ...----- 
V.    DIABETES    MELMTUS  ..--.- 

VI.  DIABETES    IXSII'IDUS  ..---- 

VII.  RELATIONS    BETWEEN    INjrRV    AND    DIABETES 

VIII.  OBESITY     -------- 

IX.  DIFFUSE   SYMMETltlCAI,   LIl'OMATOSIS  -  .  -  - 

X.  ADIPOSIS   DOLOROSA  ...... 

XT.  MYXEDEMA  ..----- 

XII.  SCROKl'LA— LYMPH ATISM  .  .  .  .  . 


1916 

1916 
1!»25 
19.33 
1937 
1948 
1982 
1984 
1995 
1998 
2003 
2004 
2008 


PART   IX 
PARASITIC  INFECTIONS 


I.    TRICHINOSIS 
II.    FILABIASIS 


2012 

2014 


PART    X 

DISEASES   AFFECTING   THE   LOCOMOTOR   SYSTEM 

I.    RICKETS  -------. 

n.  OSTEOJIALACIA  ----- 
ni.    AGROMEGALY         .  .  -  .  . 

IV.   PAGEt's   DISEASE — PROGRESSIVE   OSTEITIS   DEFORMANS 

V.    THOMSEN'S    DISEASE  -  -  .  . 

VI.  PROGRESSIVE   MUSCULAR    DYSTROPHIES      - 

VII.  PSEUDO-HYPERTBOPHIC    MUSCULAR    PARALYSIS     - 
Vm.    PROGRESSIVE    ATROPHIC    MYOPATHY 


2018 

2021 
2022 
2027 
2035 
2037 
2039 
2042 


PART   XI 

VENEREAL   DISEASES 

1.  GONORRHCEA  .  .  .  .  . 

A.  COMPLICATIONS   OF   GONORRHCEA 

B.  GONOCOCCAL    INFECTION    OF   THE    BLOOD 


2045 

2048 
2052 


X  CONTENTS    OF   VOL.    II 

CHAPTEK  PAGE 

n,    SOFT   CHANCEE     ...---••  2064 

III.  HABD    OE    SYPHILITIC    CHANCRE    (TREPONEMA.    PALLIDUM)                   •                   -  2067 

IV.  FaLiIIi;A>'T    GAXGBENE    OE   THE    PENIS     -                 -                 -                 -                 •  2076 


PAET   XII 
THE   INTOXICATIONS 


I.    ALCOHOLISM 


II.    MEEGUKIAL   POISONING HYDKARGYRISM 

ni.    LEAD-POISONING  -  -  -  - 

IV.   PHOSPHOEOUS-POISONIKG - 
Y.    ARSENICAL-POISONING 

VI.   POISONING   BY   OPIUM,   MORPHIA,   AND    COCAINE 
IVII.   POISONING  BY   TOBACCO     - 
Vni.    CARBONIC   OXIDE   POISONING 
IX,   INTOXICATION   BY    CAEBON   BISULPHIDE      - 
5.    PELLAGRA  .  .  -  - 


APPENDIX   ON   THERAPEUTICS 


2086 
2090 
2094 
2102 
2104 
2106 
2109 
2110 
2111 
2113 


I.   TREATMENT      OF      SYPHILIS  —  MEECrEY  —  HECTINE  —  EHRLICU's      606 — 

■WASSEEMANN's   REACTION     ------  2116 

n.    ARSENICAL    TREATMENT — CACODYLATE    OF   SODA  -  -  -  2122 

m.    INJECTIONS   OF   ARTIFICIAL   SERU-M  -  -  -  ■  -  2123 

IV.   TREATMENT      WITH       SUPEEHEATED       AIR  —  GANGRENE  —  ARTHRITIS  — 

NEURALGIA — GANGRENE    OF   THE   LIMBS — GONOCOCCAL   ARTHRITIS    -  2125 

V.   VACCINES— ORIGINAL   IDEAS    OF   PASTEUR — WEIGHT'S    OPSONIC   METHOD     -  2130 


INDEX 


2135 


PAHT   III 

DISEASES   OF   THE    URINARY  SYSTEM 

CHAPTER  I 
DISEASES  OF  THE  KIDNEYS 

T.  ANATOMY  AND  PHYSIOLOGY  OF  THE  KIDNEYS. 

Anatomy. — The  kidneys  are  situated  on  either  side  of  the  spine,  on  a  level 
^vith  the  two  upper  lumbar  vertebra}.  They  have  an  average  length  of 
4  inches,  a  width  of  2i  inches,  and  a  thickness  of  1^  inches.  They  weigh 
about  10  ounces.  The  kidneys  have  a  thin,  transparent,  fibro-elastic 
envelope,  which  can  be  detached  in  the  normal  condition,  but  which  is 
often  adherent  in  diseased  states.  They  are  surrounded  by  a  fatty  layer, 
in  which  perinephritic  abscesses  arise. 

A  cut  section,  from  the  convex  edge  towards  the  hilum,  presents  different 
parts.  In  the  central  or  medullary  substance  ten,  twelve,  or  fifteen  striated 
bundles  are  seen.  These  are  the  pyramids  of  Malpighi;  the  summits  of 
which  converge  towards  the  hilum.  The  cortical  substance,  v/hich  is  more 
red  and  granular,  is  about  f  inch  thick  ;  it  is  not  only  peripheral,  as  its  name 
might  seem  to  indicate,  but  also  central,  because  it  dips  in  between  the 
pyramids  of  Malpighi,  and  fornas  prolongations  which  protrude  into  the 
hilum,  and  are  known  as  Bertin's  columns. 

We  find,  therefore,  at  the  hilum  two  kinds  of  alternating  projections  i 
some,  red  and  conoid,  are  formed  by  the  summit  of  the  pyramids  of  Malpighi, 
and  are  called  papillae  ;  the  others,  yellowish  and  rounded,  are  formed  by 
the  prolongation  of  Bertin's  columns.  They  exist  only  in  the  central  parts 
of  the  hilum,  and  disappear  towards  its  lateral  parts,  because  Bertin's 
columns  do  not  there  descend  so  low. 

Each  papilla  is  pierced  by  ten  to  thirty  orifices.  Each  orifice,  visible 
with  a  lens,  is  the  opening  of  an  excretory  canal,  and  each  of  these  very 
short  canals  is  the  end  of  smaller,  slightly  divergent  canals,  which  are  called 
Bellini's  tubes,  and  unite  to  form  the  pvramids  of  Malpighi.  The  tubes  of 
Bellini,  or  collecting  canals,  ascend,  whilst  branching  out,  as  far  as  the 
II.  1077  69 


1078  TEXT-BOOK  OF  MEDICINE 

cortical  substance,  where  they  form  straight  tubes,  called  medullary  rays, 
which  are  the  ends  of  the  uriniferous  canaliculi. 

The  canaliculus  has  a  very  complicated  path.  It  arises  from  the 
glomerulus  of  Malpighi  in  the  cortical  substance.  The  glomerulus  is  a 
small  vascular  system  of  a  spherical  shape,  formed  by  the  union  of  the 
winding  arterioles,  and  surrounded  by  a  membrane,  known  as  Bowman's 
capsule. 

This  system  is,  as  it  were,  suspended  from  the  interlobular  arteries.  The 
afierent  arteriole  traverses  Bowman's  capsule,  and  divides  into  looped 
branches.  These  branches  unite  to  form  the  efferent  arteriole  which  leaves 
the  capsule  lq  close  contact  with  the  afferent  vessel,  and  gives  rise  to  a 
network  of  capillaries  which  envelops  the  glomeruli,  the  tubuli  contorti, 
and  the  meduUary  rays.  Whereas  the  afferent  arteriole  is  provided  with  a 
layer  of  circular  muscle  fibres  as  far  as  its  entrance  into  the  capsule,  the 
efferent  arteriole,  which  is  smaller,  has  only  muscular  fibres  in  the  neigh- 
bourhood of  the  capsule,  and  soon  loses  them,  to  split  up  into  capillaries. 
This  arrangement  forms  a  kind  of  sphincter,  which  probably  serves  to 
regulate  the  blood-pressure  in  the  interior  of  the  glomerulus.  The  structure 
of  the  capillaries  in  the  glomerulus  consists  of  an  amorphous  wall,  lined 
internally  with  an  endothelium  disposed  in  the  form  of  a  protoplasmic 
membrane  with  nuclei  here  and  there  (Hortoles),  The  vascular  tuft  is  not 
free  in  Bowman's  capsule,  but  has  a  covering  which  certain  writers  look 
upon  as  a  flattened  epithelium.  It  appears  to  be  rather  a  membrane  of  a 
connective  nature,  emanating  from  the  connective  envelope  which  accom- 
panies the  afferent  arteriole  at  its  entry  into  Bowman's  capsule  (Comil, 
Renaut,  Hortoles).  This  protoplasmic  pellicule  is  interposed  between  the 
loops  of  the  vascular  tuft. 

Bowman's  capsule,  which  surrounds  this  smaU  vascular  apparatus,  may 
be  considered  as  the  origin  of  the  uriniferous  canaliculi,  and  is  continuous 
with  them  by  a  constricted  point,  called  the  neck  of  the  capsule,  which  is 
formed  by  a  structureless  membrane,  provided  with  flat  epithelium. 

Immediately  after  its  origin  the  canaliculus  becomes  broad  and  convo- 
luted, whence  the  name  of  tubuli  contorti.  The  tubuli  contorti  are  situated 
in  the  cortical  layer  of  the  kidney,  and  play  a  considerable  part  in  the 
phenomenon  of  urinary  secretion.  After  a  sinuous  path,  the  convoluted 
part  of  the  canaliculus  becomes  constricted,  plunges  into  the  central  sub- 
stance of  the  kidney  to  a  variable  depth,  and  is  known  as  Henle's  descending 
branch.  The  canaliculus  then  curves  (Henle's  loop),  increases  in  size,  and 
ascends  parallel  to  its  descending  branch  (Henle's  ascending  branch) ;  it 
thus  reaches  nearly  to  the  surface  of  the  kidney,  where,  under  the  name  of 
intercalary  tubule  and  junctional  tubule,  which  is  seated  in  the  most 
superficial  layers  of  the  cortical  layer  of  the  kidney,  it  enters  into  the 


DISEASES  OF  THE  KIDNEYS  1079 

prolongation  of  a  medullary  ray,  which  is  itsolf,  ai  we  have  said,  hiit  a 
continuation  of  a  collecting  tube  of  Hollini. 

The  structure  of  the  canaliculus  varies  much  in  each  ol  its  parts.  The 
convoluted  tubes  have  a  structureless  membrane  and  an  epithelium  described 
by  Heidenhain.  The  epithelial  cells  are  so  large  that  they  leave  only  a 
narrow  lumen ;  their  appearance  is  cloudy  and  granular,  and  a  portion  of 
their  protoplasm  is  transformed  into  fine  rods,  perpendicular  to  the  axis 
of  the  tube,  which  give  the  section  a  striated  appearance.  These  rods  occupy 
the  part  of  the  cell  next  to  the  basement  membrane,  whilst  the  protoplasm 
and  the  nucleus  are  on  the  side  of  the  hunen.  The  epitheliima  of  lienle's 
descending  branch  is  pavemented  and  analogous  to  that  of  the  bloodvessels. 
The  epithelium  of  Henle's  ascending  branch  is  analogous  to  that  of  the 
convoluted  tubes.  The  epithelium  of  the  intermediary  pieces  and  of  the 
first  collecting  tubes  is  somewhat  like  cylindrical  epithelium. 

In  order  to  understand  the  relations  of  the  uriniferous  canaliculi  with 
the  different  elements  which  enter  into  the  structure  of  the  kidney,  it  is 
useful  to  study  them  in  transverse  sections. 

1.  In  a  section  made  in  the  region  of  the  papillae  we  find  the  large  ex- 
cretory tubes  which  divide  in  this  region,  and  some  loops  of  Henle's  tubes. 

2.  In  a  section  made  a  little  higher,  in  the  portion  of  Malpighi's  pyramid 
called  the  limiting  zone,  we  meet  with  three  varieties  of  tubes  :  Bellini's 
collecting  tubes,  Henle's  thin  or  descending  branches,  and  Henle's  large  or 
ascending  branches.  The  vasa  recta  traverse  this  zone  in  order  to  reach 
the  cortical  substance. 

3.  Transverse  sections  of  the  cortical  substance,  starting  from  the 
surface  of  the  kidney  towards  the  centre,  show  the  following  details  :  (1)  In 
the  most  superficial  layer  we  find  the  capsule  of  the  kidney,  hollowed  out 
by  cavities  which  are  lymphatic  spaces.  (2)  In  a  somewhat  deeper  section 
we  see  the  sinuous  canals,  which  represent  the  intercalary  and  junctional 
tubides — that  is  to  say,  the  end  of  the  uriniferous  canaliculi  in  the  medullary 
prolongations  ;  we  also  see  tubuli  contorti.  (3)  In  a  still  deeper  section  we 
see  the  renal  lobule,  which  is  formed  of  the  following  elements  :  In  the  centre 
is  Ferrein's  pyramid,  which  is  composed  of  the  cortical  prolongation  of 
Bellini's  tube  (medullary  ray)  and  Henle's  ascending  branches.  Around 
Ferrein's  pyramid  is  the  labyrinth,  and  by  "  labyrinth  "  must  be  under- 
stood the  space  between  two  pyramids  with  the  contents  of  this  space, 
tubuli  contorti,  and  interlobular  arteries  with  their  glomeruli. 

It  is  important  to  understand  the  structure  of  the  renal  lobule,  because 
it  is  in  this  region  that  most  of  the  pathological  phenomena  of  chronic 
nephritis  take  place. 

The  glomeruli,  uriniferous  and  collecting  tubes  are  embedded  in  un- 
equally distributed  connective  tissue.     "  The  comm'Anication  of  this  con- 

69—2 


1080 


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neotive  tissue  witli  the  lymphatic  vessels  shows  that  here,  as  elsewhere,  it 
is  made  up  of  lymph  spaces,  limited  by  flat  cells,  and  in  connection  with 
the  lymphatic  vessels." 

Physiology. — We  know  to-day  that  the  role  of  the  kidney  consists  in 
excretion,  and  not  secretion.  It  does  not  make  the  elements  of  the  urine, 
but  finds  them  ready-made  in  the  blood,  and  selects  them,  rejecting  some 
and  allowing  others  to  pass.  An  exception  must,  however,  be  made  in 
favour  of  hippuric  acid,  which  exists  in  the  urine  of  herbivorous  animals, 
and  appears  to  be  made  by  the  kidney  (Koch). 

In  the  normal  condition,  the  urine  has  a  pale  yellow  colour,  an  acid 
reaction,  and  a  peculiar  odour.  Its  density  is  from  1018  to  1020,  and  the 
quantity  passed  by  an  adult  in  twenty-four  hours  varies  from  40  to  50  ounces. 

Urine  is  composed  of  the  following  elements  : 


Passed. 

Composition  of  the  Urine. 

Per  litre. 

Per  24  hours. 

Gr. 

Gr. 

Organic  elements 

26-27 

35-36 

Jlineral  elements 

3-3-10 

12-14 

Total  of  dissolved  matter 

34-37 

43-52 

^      /Men 

\  Women   . . 

18-24 

25-38 

10-20 

20-32 

Uric  acid 

0-30-040 

0-50-0-70 

Phosphoric  acid 

1-66 

2-50 

Sulphuric  acid  . . 

2-00 

3-00 

Chloride  of  sodium 

6-6-8-0 

10-12 

Lime  . . 

0-28-0 -30 

0-33-0 -45 

Urea,  which  represents  the  last  stage  in  the  oxidation  of  the  albuminoids, 
is  manufactured  in  the  interior  of  the  tissues,  and  especially  in  the  liver. 
I  shaU  not  review  the  numerous  theories  of  the  secretion  of  the  urine.  It 
is  not  certain  that  the  glomerulus  has  only  a  mechanical  role,  as  was  main- 
tained by  Ludwig  ;  the  glomerular  epithelium  seems  to  play  a  certain  part  in 
the  physiological  and  pathological  functions  of  the  glomerulus  (Heidenhain). 
It  is  through  the  glomerulus  that  the  aqueous  portion,  with  the  salts  of  the 
plasma,  transudes  (Bowman).  The  glomerulus  eliminates  the  sugar  in  diabetic 
patients  and  the  albumin  in  albuminuric  ones.  The  tubuli  contort!  and 
Henle's  ascending  branch,  which  are  furnished  with  a  special  epithelium  (Heid- 
enhain), represent  the  true  glandular  part  of  the  kidney,  and  have  as  their 
mission  the  making  of  urine,  by  selecting  and  excreting  its  principal  products. 

Chatin  and  Guinard  would  give  to  the  kidney,  by  analogy  with  other 
glands,  an  internal  secretion,  which  appears  indeed  to  exist. 


DISEASES  OF  THE  KIDNEYS  lusi 


IT.  CONGESTION  OF  THE  KIDNEYS— CARDIAC  KIDNEY. 

Congestion  of  the  kidneys  may  be  active  or  passive.  Active  congestion 
is  associated  with  iiiHaniniation  and  new  growths  of  the  kidneys,  and  will, 
consequently,  be  described  with  these  various  morbid  conditions.  Passive 
congestion  will  be  di.scussed  in  this  section. 

Whenever  the  blood-pressure  increases  in  the  area  of  the  efferent 
veins,  or  in  the  vena  cava  above  the  mouth  of  these  veins,  the  kidneys 
become  congested.  Tumours  of  the  abdomen,  aneurysms  of  the  abdominal 
aorta,  and  pregnancy,  may  create  a  mechanical  obstacle  to  the  blood-flow 
in  the  renal  veins.  Pleuro-pulmonary  affections  (pleurisy,  emphysema, 
phthisis)  may  also  form  an  obstacle  to  the  afflux  of  the  blood  from  the  vena 
cava  to  the  right  side  of  the  heart,  and  become  an  indirect  cause  of  renal 
congestion  ;  but  none  of  these  causes  can  compare  with  disea.ses  of  the 
heart.  As  the  result  of  ill-compensated  cardiac  lesions  and  in  consequence 
of  attacks  of  asystole,  the  kidneys  participate  in  the  chronic  congestion 
which  affects  all  the  \ascera,  and  the  cardiac  kidney  (Jaccoud),  which  is 
analogous  to  the  cardiac  liver,  results.  Post  mortem  the  kidneys  are 
congested  and  enlarged  ;  the  capsule  strips  readily ;  the  surface  of  the 
organ  is  red,  and  streaked  with  swollen  venae  stellatse  ;  the  capillaries  and 
the  veins  are  congested  with  blood.  On  section,  the  surface  is  of  a  deep 
red.  Small  glomerular  and  intratubular  haemorrhages  are  sometimes 
seen.  The  tissue  of  the  kidney  is  indurated,  and  histological  examination 
shows  that  the  intertubular  connective  tissue  of  Malpighi's  pyramid  is 
transformed  in  places  into  embryonic  tissue  forming  an  early  stage  of 
cirrhosis.  Fatty  granules  are  present  in  the  epithehum  of  the  tubuh  con- 
torti,  but  the  cells  do  not  perish.  In  short,  this  congested  condition  causes 
a  shght  degree  of  cirrhosis,  but  the  bloodvessels  are  hardly  ever  attacked  by 
endarteritis.  The  striated  epithelium  of  the  convoluted  tubes  preserves 
its  integrity,  and,  consequently,  the  cardiac  kidney  does  not  show  chronic 
nephritis,  and  is  not  the  starting-point  of  Bright's  disease. 

This  opinion  is  the  most  generally  accepted,  and  it  must  be  added  that 
it  is  correct.  Exceptions  must,  however,  be  noted,  and  Fauquez  has  col- 
lected cases  which  tend  to  prove  that  the  cardiac  kidney  may  end  in  the 
interstitial  and  parenchymatous  lesions  of  Bright's  kidney. 

The  cardiac  kidney  reveals  itself  during  Hfe  by  e\'ident  changes  in  the 
urine.  The  urine  becomes  scanty,  thick,  and  high-coloured.  Urates,  urea, 
and  uric  acid  are  found  in  abundance  ;  but  albumin,  when  it  exists,  is  in 
small  quantity.  Under  the  microscope  wliite  and  red  corpuscles,  epithehal 
cells,  and  sometimes  casts  of  various  kinds,  are  seen. 

The  insufficiency  of  urinary  depuration,  resulting  from  the  lesions 
just  described,  is  partially  responsible  for  the  symptoms  of  asystole  ;  but 


1082  TEXT-BOOK  OF  MEDICINE 

it  very  rarely  ends  in  true  uraemia.  Tlie  treatment  described  under  Mitral 
Diseases  causes  the  cardiac  kidney  to  resume  its  functions,  and  it  is,  indeed, 
througli  tlie  kidney  that  asystole  is  in  a  large  part  averted. 


III.  ACUTE  NEPHRITIS. 

Discussion. — ^The  history  of  acute  nephritis  is  still  somewhat  obscure ;  the  nature 
of  the  lesions,  the  aetiology  of  the  disease,  and  its  modes  of  termination,  have  been 
the  subject  of  such  contradictory  opinions  that  it  is  not  possible  at  the  present  time 
to  propose  a  classification  of  the  acute  toxi-infections  of  the  kidney.  Not  long  ago 
acute  nephritis  was  divided  into  catarrhal  and  parenchymatous.  Catarrhal  nephritis 
had  the  attributes  of  being  sUght  and  temporary,  of  limiting  its  process  to  the  excretory 
canals,  and  of  leaving  the  organ  unaffected ;  whereas  parenchymatous  nephritis,  which 
was  more  grave  and  more  persistent,  was  locaUzed  in  the  epithehum  of  the  secretory 
canals  (tubuh  contorti).  In  order  to  accentuate  this  distinction,  writers  Ukened 
catarrhal  nephritis  of  the  excretory  tubes  to  common  bronchitis,  and  parenchymatous 
nephritis  of  the  secretory  tubes  to  lobular  pneumonia,  or  capillary  bronchitis  (Lscorche). 
This  distinction,  however,  in  no  way  corresponds  to  the  true  lesions  of  acute  nephritis, 
in  which  the  entire  kidney  participates  more  or  less  in  the  morbid  process.  Another 
division  consisted  in  separating  acute  nephritis  into  epitheUal  and  interstitial,  the  one 
invading  the  epithelia  of  the  kidney,  and  the  other  the  connective  tissue ;  but  this 
division,  so  simple  in  appearance,  cannot  serve  as  a  basis  for  a  description  of  the  acute 
infections  of  the  kidney. 

The  acute  process  of  nephritis  was  for  a  long  time  considered  as  exclusively  vested 
in  the  epithehum,  whereas  the  interstitial  tissue  of  the  organ  seemed  to  lend  itself  only 
to  a  chronic  process  (Bartels).  It  was  soon  felt  that  it  was  wrong  to  reject  inter- 
stitial nephritis  from  the  varieties  of  acute  nephritis.  The  inflammatory  nature  of  the 
epithehal  nephritis  was  even  contested  (Klebs) ;  it  was  said  that  the  process  in  acute  epi- 
thehal  nephritis  was  not  irritative,  but  only  degenerative,  and  the  really  active  part  of 
the  inflammatory  process  was  vested  in  the  interstitial  tissue.  Nephritis  in  smallpox 
(Traube),  scarlatina  (Klebs),  diphtheria,  cholera  (Kelsch),  and  typhoid  fever  was  looked 
on  as  acute  and  interstitial,  and  at  this  time  acute  interstitial  nephritis  may  be  said  to 
have  comprised  almost  the  entire  history  of  acute  nephritis. 

Fresh  researches,  however,  assisted  by  experiments  and  favoured  by  perfected 
methods  of  preparation  (Comil),  have  enabled  us  to  state  the  facts  more  correctly.  It 
is  seen  that  what  had  been  described  as  an  interstitial  lesion  becomes  partially  reduced 
to  the  diapedesis  of  the  white  corpuscles,  and,  in  short,  the  preponderance  of  the  morbid 
process  remains  with  the  parenchyma.  The  lesions  of  acute  nephritis  are  parenchyma- 
tous lesions,  which  attack  the  various  parts  of  the  gland,  the  excretory  tube,  the  secre- 
tory tube,  and  the  glomerulus ;  with  these  lesions  there  are  associated  interstitial  and 
vascular  changes  that  are  more  or  less  pronounced  in  different  cases. 

Do  the  anatomical  forms  of  acute  nephritis  vary,  according  to  their  cause  ?  and  is 
the  nephritis  of  scarlet  fever,  for  example,  distinct  from  early  syphihtic  nephritis,  from 
typhoid  nephritis,  or  from  the  nephritis  which  appears  after  a  chill  ?  The  answer  is 
negative.  Whether  the  nephritis  be  primary  {a  frigore),  which  has  not  been  proved ; 
whether  it  be  of  an  experimental  nature  (injections  of  cantharides)  (Comil) ;  or  whether 
it  appear  during  the  course  of  scarlatina,  syphilis,  smallpox,  diphtheria,  or  pneumonia, 
it  may  be  said  that  the  acute  changes  in  the  kidney  do  not,  in  any  case,  assume  a  reaUy 
distinct  type.  These  changes  may  be  more  or  less  extensive,  more  or  less  intense, 
more  or  less  transient,  more  or  less  lasting,  more  or  less  degenerative,  may  end  more 
or  less  quickly  in  necrosis  of  the  epithehum,  and  may  be  more  marked  in  this  or  that 


DISEASES  OF  THE  KIDNEYS  1083 

part  of  the  organ  ;  but  thoy  have  no  particular  character,  and  the  topography  of  the 
lesions,  no  more  than  their  retiologj',  allows  us  to  divide  nephritis  into  distinct  kinds. 

I,  therefore,  unite  in  one  description  the  varieties  of  acute  nephritis,  which  were 
formerly  destrihod  as  catarrhal  nephritis,  acute  albuminous  nephritis,  acute  parenchy- 
matous nephritis,  and  epithelial  nephritis. 

In  spite  of  this  apparent  simplification,  the  anatomical  description  of  acute  nephritis 
remains  surroimded  with  difficulties,  because  the  lesions  show  notable  differences, 
according  to  the  cause,  the  duration,  and  the  intensity  of  the  inflammatory  process. 
As  a  matter  of  fact,  the  changes  are  sometimes  superficial  and  transitory,  and  at  other 
times  deep  and  lasting. 

In  mild  cases  of  acute  nephritis  the  lesion  is  rather  hyperaemic  than  infiammatory. 
and  we  might  bo  tempted  to  replace  the  word  "  nephritis  "  by  the  names  "  congestive 
cedema,"  ''  inflammatory  byperiemia,"  or  "  congestive  nephritis."  In  severe  cases  of 
acute  nephritis  the  leucocytic  infiltration  and  acute  degeneration  of  the  epithelia  pre- 
dominate, wliile  the  iiritative  lesions  of  the  connective  tissue  and  of  the  glomeruli  are 
but  slightly  marked.  Finally,  in  some  cases  the  diffuse  changes  attack  the  epithelia, 
the  bloodvessels,  and  the  connective  tissue. 

Furthermore,  the  division  of  acute  nephritis  into  congestive,  slight,  and  intense 
would  be  purely  artificial,  for  there  is  no  defined  hmit  between  these  forms,  and  we 
pass  from  one  to  the  other  by  insensible  gradations.  There  is  no  absolute  relation  to  be 
established  between  nephritis  and  its  cause,  for  the  same  cause — scarlatina,  for  instance 
— may  bring  about  congestive  nephritis,  slight  and  transitory  nephritis,  or  grave  and 
permanent  nephritis.  It  must  be  added,  however,  that  the  intense  forms  are  not 
common  in  the  course  of  most  infectious  diseases,  though  they  are  so  in  scarlatina, 
syphilis,  and  perhaps  also  as  the  result  of  a  chiU. 

In  a  fatal  case  of  acute  nephritis  both  kidneys  will  be  found  equally 
affected.  They  are  larger  than  normal.  The  enlargement  is  due  to  the 
vascular  congestion  and  to  the  sweUing  of  the  cortex.  The  capsule  is  easily 
detached  ;  the  surface  of  the  organ  is  smooth  and  mottled.  According  to 
circumstances,  the  kidneys  are  whitish,  greyish,  or  reddish.  In  severe 
inflammation  the  kidneys  may  weigh  more  than  twice  their  normal  weight. 
The  tissue  forms,  as  it  were,  a  hernia  through  the  incised  capsule.  On 
section,  the  medullary  substance  appears  normal,  while  the  cortical  substance 
is  congested,  thickened,  and  of  a  yellowish  colour,  streaked  by  red  stria - 
tions,  and  studded  with  red  points. 

Let  us  now  study  the  histology  of  the  lesion  in  each  part  of  the  organ. 

1.  The  collecting  tubes  which  possess  cyhndrical  epithehum  and  the 
straight  tubes  which  have  cubical  epithehum  present  the  lesions  of  catarrhal 
inflammation — swelhng,  multiphcation,  and  desquamation  of  the  ceUs. 
The  lumen  of  the  collecting  tubes  is  blocked  with  cells  and  casts.  These 
catarrhal  lesions  were  long  supposed  to  be  the  sole  lesion  in  shght 
nephritis,  but  we  know  now  that  sHght  nephritis,  formerly  called  catarrhal, 
also  presents  changes  in  the  glomeruH  and  the  convoluted  tubes. 

2.  The  lesions  in  the  glomeruH  are  constant.  The  capillaries  become 
dilated,  and  an  albuminous  exudate,  which  contains  white  and  .red  cor- 
puscles, passed  through  by  diapedesis,  and  in  some  cases  hyaline  baUs,  is 
poured  out  in  the  interior  of  the  capsule.    The  red  corpuscles  are  sometimes 


1084  TEXT-BOOK  OF  MEDICINE 

so  numerous  as  to  form  a  glomerular  hsemorrkage.  The  passage  of  the 
blood-serum  into  the  capsule  explains  the  presence  of  the  albumin  in  the 
urine.  T\Tien  the  intracapsular  exudate  is  very  profuse,  it  presses  the 
vascular  tuft  against  the  wall,  passes  under  pressure  into  the  convoluted 
tubes,  and  may  rupture  them.  These  congestive  lesions  are  accompamed 
by  others  of  an  inflammatory  nature.  In  the  perivascular  protoplasmic 
layer  abundant  multiphcation  of  nuclei  is  noticed  (Cornil),  and  the  hning 
cells  of  Bowman's  capsule  swell  up  and  desquamate.  According  to  the 
duration  of  the  inflammatory  process,  the  vascular  coils  of  the  agglutinated 
capillaries  may  undergo  a  connective  transformation,  the  capsule  grows 
thicker,  and  the  glomerulus  tends  to  become  fibrous.  The  neighbouring 
arterioles  of  the  glomeruh  show  peri- arteritis  and  endarteritis. 

3.  The  changes  in  the  striated  epithehum  of  the  convoluted  tubes  and 
of  Henle's  ascending  tubules  have  given  rise  to  much  discussion.  The 
canaliculi  are  dilated  and  opaque  ;  the  epithehum  is  cloudy,  granular,  and 
swollen.  The  epithehal  cells  are  more  or  less  swollen  or  broken  up.  The 
protoplasm  shows  cloudy  swelling ;  the  nucleus  does  not  stain  well  with 
carmine  or  heematoxyhn.  The  condition  is  necrobiosis  of  the  epithehum. 
These  lesions,  according  to  some  writers,  are  said  to  be  purely  degenerative, 
while  others  hold  that  the  sweUing  of  the  cells,  the  granular  condition,  the 
multiphcation  of  the  nuclei,  and  the  secretion  of  coagulable  substances, 
show  an  inflammatory  process. 

In  a  remarkable  article  on  the  condition  of  the  cells  of  the  kidney  in 
albuminuria,  Cornil  has  stated  that  the  epithehal  cells  of  the  convoluted 
tubes  showed  more  or  less  large  vacuoles,  containing  granules  and  baUs 
of  proteid  substance.  According  to  Cornil,  the  renal  cells  are  said,  then, 
to  secrete  in  the  protoplasm  "  balls  of  albuminous  substance  in  almost  the 
same  manner  as  the  mucous  or  goblet  ceUs  of  the  intestinal  mucosa  and  of 
the  glands  secrete  mucus." 

These  baUs  of  coagulable  albuminoid  substance  are  formed  of  mucin 
and  albumin.  Thev  may  be  granular  or  hyahne  and  transparent.  These 
coagulable  elements,  with  the  coagulated  serum,  the  red  and  white  cor- 
puscles,  the  fragments  of  cells,  and  the  fibrous  reticulum,  take  part  in  the 
formation  of  the  casts.  The  formation  of  the  casts  commences,  then,  in 
the  glomeruh,  and  continues  in  the  tubes.  The  casts  found  in  the  urine 
will  be  described  under  Bright' s  Disease. 

If  the  inflammatory  process  is  severe,  the  dilatation  of  the  tubules  is 
very  marked.  The  tubules  are  filled  with  granular  and  colloid  exudate, 
with  red  corpuscles,  which  have  come  from  the  glomeruh,  and  with  fat 
corpuscles.  The  striated  epithelium  is  infiltrated  in  places  with  fatty 
granules. 

4.  The  changes  in  the  coimective  tissue  are  but  httle  appreciable  at 


DISEASES  OF  THE  KIDNEYS  1085 

tlio  cominencemeiit  of  slight  nephritis.  (Edciiwi  of  the  intertiibular  tissue 
and  diapedesis  of  the  white  corpuscles  \vhi(;h  infiltrate  the  intertubular 
spaces  are  not  indicative  of  interstitial  inflammation,  properly  speakijig. 
This  very  marked  infiltration  (Wagner's  lymphoniatous  nephritis)  is  accom- 
panied by  the  glomerular  lesions  of  which  I  have  already  spoken,  and  later 
by  a  thickening  of  the  tubular  walls.  In  the  end  the  fibrous  element  be- 
comes apparent ;  the  vascular  lesions  become  accentuated,  and  we  have 
diffuse  subacute  ne])hritis.  Such  are  the  lesions  of  acute  nephritis.  Several 
writers  have  held  them  to  be  degenerative  from  the  outset  (Traube,  Klebs, 
Kelsch).  We  liold  to-day  that  the  lesions  are  both  degenerative  and  in- 
fianmiatory.  The  last  word  has,  I  admit,  not  yet  been  said  on  the  nature 
of  tlie  lesions  in  the  striated  epitheUum,  but  this  is  no  reason  for  classing 
the  fatty  condition  of  the  epithelium  amongst  the  number  of  purely  ischemic 
and  degenerative  changes,  when  it  may  be  the  result  of  an  inflammatory 
process.  "  The  change  in  the  cells  of  the  kidney,  which  writers  have  wrongly 
wished  to  distinguish  from  inflammation,  behaves  like  an  inflammatory 
process,  for,  independently  of  the  fibrino -albuminous  exudation  which  in- 
filtrates the  epithelial  elements,  the  latter  may  return  to  their  primary 
condition  or  undergo  granulo-fatty  degeneration "  (Lancereaux).  Fur- 
thermore, the  epitheUal  degeneration  is  associated  with  so  many  other 
inflammatory  manifestations  (glomeruhtis,  connective  irritation,  multi- 
plication of  the  nuclei)  that  the  nature  of  the  process,  taken  as  a  whole,  is 
manifestly  of  inflammatory  and  necrobiotic  origin. 

iEtiology. — The  causes  of  acute  nephritis  are  numerous  and  varied. 

1.  Infectious  Nephritis. — Toxi-infectious  diseases  occupy  the  first 
place  in  the  pathogenesis  of  acute  nephritis.  Scarlatina,  syphihs,  smallpox, 
measles,  pneumonia,  typhoid  fever,  diphtheria,  cholera,  influenza,  mumps, 
and  erysipelas,  predispose  to  acute  nephritis. 

The  pathogenesis  of  infectious  nephritis  has  been  variously  interpreted. 
It  has  been  asked  "  whether  a  profound  change  in  the  blood  would  not  be 
capable  of  changing  the  conditions  of  diffusibihty  of  the  albumin,"  by 
allowing  it  to  pass  through  the  kidney  (Jaccoud),  and  by  irritating  the 
epithehum.  The  current  view  of  this  question  is  as  follows  :  Microbes 
have  been  found  in  the  arterioles  of  the  kidneys  and  in  the  coils  of  the 
glomenili.  Such  are  the  microbes  of  anthrax,  pneumonia,  tuberculosis, 
typhoid  fever,  and  other  organisms,  streptococci  and  staphylococci,  which 
give  rise  to  secondary  infections.  Researches  have  since  been  made  as 
to  whether  these  microbes  have  of  themselves  a  pathogenic  action  on  the 
kidneys,  or  whether  the  pathogenic  action  be  due  to  the  toxines  which  they 
secrete. 

When  we  see  certain  microbes  traversing  the  kidneys  and  passing  into 
the  urine,  staphylococci,  pneumococci  (in  the  two  first  days  of  pneumonia), 


1086  TEXT-BOOK  OF  MEDICINE 

E  berth's  bacillus  (from  the  second  to  the  fourth  week  of  typhoid  fever), 
we  may  well  ask  whether  these  microbes  are  not  capable  of  modifying  the 
anatomical  condition  of  the  cells,  by  ischsemia,  congestion,  or  traumatism. 

On  the  other  hand,  however,  when  we  know  the  sHght  affinity  of  bacteria 
for  the  kidneys  and  the  feeble  tendency  of  the  kidneys  for  the  ehmination 
of  the  microbes  en  masse,  we  say  that  the  microbes  must  act  chiefly  on  the 
renal  epithehum  through  their  toxines.  Do  we  not  know,  too,  that  certain 
infectious  diseases,  such  as  diphtheria,  cholera,  or  tetanus,  cause  renal 
changes,  necrosis,  or  cellular  degeneration,  though  the  microbes  do  not 
enter  the  blood  ?  Have  we  not  seen  nephritis  supervene  in  consequence  of 
antitubercular  vaccinations  with  old  cultures,  and  after  subcutaneous 
injections  made  with  Koch's  tuberculin  ? 

Lesions  have  been  produced  in  the  kidney  by  injecting  cultures  of 
Eberth's  baciUus  (Chantemesse  and  Widal),  and  cultures  of  the  pneumo- 
coccus  (Roger  and  Gaume),  in  the  same  way  as  experimental  nephritis  has 
been  produced,  by  injections  of  toxines.  Charrin  observed  chronic  granular 
nephritis,  with  hypertrophy  of  the  left  ventricle,  in  rabbits  inoculated  with 
pyocyaneus  toxine.  In  a  monkey  inoculated  with  diphtheria  toxine 
Henriquez  and  HaDion  found  granular  nephritis,  with  hypertrophy  of  the 
left  ventricle. 

Claude  has  made  a  large  number  of  experiments  with  various  toxines 
(diphtheritic,  tetanic,  coH  -  baciEary,  streptococcic,  staphylococcic,  pyo- 
cyanic).  He  has  induced  acute  nephritis  (and  acute  hepatitis)  in  animals.  In 
the  case  of  intense  intoxication  we  find  inflammatory  and  degenerative 
changes  in  the  kidneys.  In  the  case  of  progressive  intoxication  we  find 
subacute  and  chronic  nephritis,  with  epithelial,  interstitial,  and  vascular 
lesions. 

These  facts  prove  that  the  tissues  of  the  kidney  are  afEected  by  the 
toxines,  just  as  they  are  by  the  mineral  poisons.  It  matters  httle  whether 
the  poison  acts  directly  on  the  epithelium  of  the  tubules ;  whether  it  acts 
on  the  arterioles,  causing  diapedesis  and  arterio- sclerosis ;  or  whether  the 
lesions  are  associated  or  independent,  degenerative  or  inflammatory.  We 
know  that  acute  nephritis  arises  in  the  infectious  diseases,  whether  the 
microbes  and  their  toxines  are  known  to  us  (pneumonia,  typhoid  fever, 
diphtheria,  tuberculosis,  cholera,  tetanus,  erysipelas,  puerperal  infection, 
influenza,  appendicitis),  or  whether  the  microbes  and  their  toxines  are  un- 
known to  us  (scarlatina,  measles,  smallpox). 

As  regards  prognosis,  it  is  important  to  note  that  these  various  infections 
do  not  attack  the  kidneys  with  the  same  violence  nor  with  the  same  tenacity. 
In  this  respect  nephritis  in  scarlet  fever  and  early  syphihtic  nephritis  are 
more  to  be  feared  than  nephritis  in  diphtheria,  typhoid  fever,  pneumonia, 
erysipelas,  etc.     Nevertheless,  W5  must  always  allow  for  shght  nephritis. 


DISEASES  OF  THE  KIDNEYS  1087 

because  the  damaged  kidneys  may,  at  a  given  moment,  under  the  influence 
of  some  fresh  infection  or  of  cold,  become  the  seat  of  fresh  lesions. 

2.  Nephritis  duk  to  Drugs. — We  must  not  confound  the  stoatogenous 
substances  (phosphorus,  arsenic)  which  cause  fatty  degeneration  of  the 
organ  with  the  irritating  substances  (cantharides,  blistering  fluids)  which 
cause  tnie  nephritis. 

Serotherapy. — Iiijections  of  antidiphtheritic  serum  are  said  to  cause 
renal  lesions  and  albuminuria.  My  view  from  the  clinical  standpoint  is  :  If 
injections  of  serum,  in  the  case  of  diphtheria,  be  administered  early,  they 
may  prevent  albuminuria ;  if  they  be  administered  when  albuminuria  is 
present,  they  have  no  retro-active  effect,  and  the  statement  that  they  have 
an  ill-effect  on  the  kidneys  has  not  been  proved,  in  my  opinion.  I  am, 
indeed,  disposed,  until  there  be  fresh  proof,  to  beHeve  the  contrary.  It  is, 
in  truth,  very  difficult,  when  albuminuria  is  found  in  a  case  of  diphtheria,  to 
assess  the  shares  of  the  serum,  of  the  diphtheritic  poison,  and  of  the  secondar\^ 
infections. 

3.  Auto-Intoxication. — The  ehmination  by  the  kidneys  of  an  excess 
of  tjn-'osin  and  of  other  extractives,  which,  for  divers  reasons  (diseases  of  the 
liver,  insufficiency  of  combustion,  slowness  of  nutrition,  cachexia),  have  a 
toxic  action  on  the  kidneys,  may  provoke  epithehal  lesions  in  the  kidneys 
and  albuminuria. 

4.  Pregnancy. — We  know  how  frequent  albuminuria  is  in  pregnant 
women.  It  may  be  due  to  congestion  from  compression  of  the  renal  veins, 
to  the  presence  of  special  waste  products  in  the  blood,  or  to  true  nephritis. 
There  is  also  a  variety  of  nephritis  which  may  be  looked  upon  as  one  of  the 
numerous  complications  of  pregnancy.  A  pregnant  woman  may  have 
simple  albuminuria,  or  albuminuria  associated  with  such  symptoms  of 
nephritis  as  oedema,  dyspnoea,  headache,  and  visual  troubles.  In  the 
presence  of  the  latter  symptoms  we  must  beware,  because  eclampsia  may 
come  on  during  labour.  Women  who  have  had  no  albuminuria  during 
pregnancy  have  it  during  labour.  This  distinction  is  very  important, 
because  albuminuria  which  appears  during  labour  is  transitory,  and  is  not 
the  precursor  of  eclampsia  (Tarnier). 

5.  Nephritis  a  Frigore. — Cold — and  by  this  word  we  must  understand 
cold  in  all  its  forms — seems  to  be  a  cause  of  acute  nephritis.  It  may  even 
be  said  that  the  so-caUed  nephritis  a  frigore  is  most  serious,  on  account  of 
the  intensity  and  the  possible  duration  of  its  lesions.  Cold,  however, 
'per  se  very  rarely  causes  acute  nephritis.  In  many  cases  it  acts  as  an 
exciting  cause  in  individuals  whose  Iddneys  are  predisposed  by  previous 
scarlatina,  by  some  infectious  disease,  by  syphilis,  etc.  In  some  cases, 
however,  the  most  minute  inquiry  fails  to  estabhsh  any  other  cause  but 
cold.     One  of  my  patients  was  taken  ill  with  acute  nephritis,  after  having 


1088  TEXT-BOOK  OF  MEDICINE 

been  exposed  all  day  to  an  ice-cold  rain.  Another  patient  was  taken  ill 
with  nephritis  after  going  out  one  very  cold  night  when  he  was  in  a  state  of 
perspiration. 

Symptoms. — Some  cases  of  nephritis  are  so  slight  that  they  escape 
aU  description.  Nephritis  in  diphtheria,  mumps,  pneumonia,  erysipelas,  or 
appendicitis,  generally  shows  no  other  appreciable  symptom  except  albu- 
minuria, so  that  many  fevers  and  diseases  were  said  to  cause  albuminuria 
without  appreciable  lesions  in  the  kidneys. 

The  nephritis  of  typhoid  fever  Ls  also  insidious  and  latent,  but  yet  it 
may  be  severe  and  formidable  (see  Typhoid  Fever).  '  The  nephritis  of 
scarlet  fever,  which  wiU  be  described  under  Scarlatina,  and  which  has 
many  symptoms  in  common  with  early  syphiKtic  nephritis  and  with  nephritis 
a  frigore,  is  of  the  utmost  importance. 

In  a  general  way,  the  course  of  acute  nephritis  is  as  follows  :  When  the 
nephritis  is  severe,  the  onset  is  violent.  The  patient  may  have  rigors,  fever, 
and  lumbar  pains ;  the  urine  is  scanty  and  brownish  or  hasmorrhagic. 
(Edema  appears  early.  The  anasarca  commences,  as  a  rule,  in  the  face, 
which  is  pale  and  swoUen,  and  in  a  few  days  invades  the  lower  limbs  and 
the  various  regions  rich  in  loose  cellular  tissue,  such  as  the  eyehds,  the 
scrotum,  the  prepuce,  and  the  labia  majora.  The  oedema  is  soft,  white, 
and  pits  readily. 

More  frequently  febrile  symptoms  are  wanting,  or,  at  least,  the  rigors 
and  the  fever  are  insignificant.  The  patient  has  no  pains  in  the  loins. 
CEdema  and  dyspnoea,  with  or  without  vomiting,  are  the  only  signs  of 
nephritis,  and  even  then  the  onset  of  the  disease  is  not  always  clear.  In 
some  cases  the  oedema  is  hmited  to  the  face  and  to  the  maUeoU,  while  one 
symptom,  such  as  dyspnoea,  headache,  or  vomiting,  assumes  an  especial 
importance  from  the  start  of  the  disease. 

In  acute  nephritis  the  amount  of  urine  passed  in  the  twenty-four  hours 
may  fall  below  30  ounces.  The  specific  gravity  may  be  normal  or  increased, 
and  the  urinary  deposit  contains  altered  epitheHal  cells,  red  corpuscles, 
leucocytes,  granular  and  hyahne  casts.  The  albumin  may  exceed  5  or 
6  grains  per  ounce.  The  urea  diminishes,  and  may  fall  to  a  drachm  instead 
of  an  ounce,  which  is  the  normal  quantity.  If  the  nephritis  be  very  acute, 
the  symptom- complex  of  acute  uraemia  may  appear  within  a  few  days  or 
a  few  weeks — i.e.,  dyspeptic  troubles  (nausea,  uncontrollable  vomiting), 
headache,  epistaxis,  dyspnoea,  visual  troubles  (amblyopia,  amaurosis), 
cutaneous  eruptions  and  itching,  nervous  symptoms  (convulsions,  dehrium, 
coma).  (Edema  of  the  lungs  or  of  the  glottis  and  effusions  in  the  pleura 
and  the  pericardium  may  appear.  When  the  nephritis  tends  towards  a 
favourable  ending,  the  symptoms  improve,  the  urine  increases,  the  albumin 
diminishes,  and  the  anasarca  gradually  disappears. 


DISEASES  OF  THE  KIDNEYS  1089 

Prognosis. — Acute  nephritis,  if  slight,  may  he  completely  cured  with 
proper  care  in  a  few  weeks.  In  other  cases  it  passes  into  a  subacute  state, 
and  the  symptoms  only  disappear  after  several  months.  Too  often,  how- 
ever, it  terminates  in  a  chronic  condition — Bright's  disease.  Under  some 
circumstances  the  disease  seems  to  be  cured,  and  the  patient  may  show 
hardly  a  trace  of  albumin  in  the  urine  ;  but  yet  one  or  two  years  later, 
under  the  influence  of  an  infectious  disease  or  of  a  chill,  the  symptoms  of 
nephritis  all  return,  as  if  there  were  a  recurrence  of  an  imperfectly  extinct 
process. 

The  prognosis  of  acute  nephritis  is  always  serious,  first,  because  certain 
cases  (nephritis  in  scarlatina,  syphihtic  nephritis,  nephritis  a  frigore)  may 
be  accompanied  by  fatal  uraemia  ;  and,  second,  because  many  cases  of 
acute  nephritis,  even  of  fairly  benign  appearance,  end  in  Bright's  disease. 
Moreover,  the  prognosis  of  acute  nephritis  does  not  depend  on  its  severity 
alone,  but  also  on  the  cause  which  has  given  rise  to  it.  The  slight  nephritis 
which  supervenes  during  the  course  of  the  infectious  diseases  recovers  after 
a  few  days  or  a  few  weeks,  and  is  not  nearly  as  serious  as  scarlatinal  or 
syphihtic  nephritis.  Etiology  alone  does  not  permit  us  to  say  that  the 
lesions  in  the  kidneys  are  slight  or  grave.  Nephritis  in  tA-phoid  fever  and 
in  influenza  is  usually  benign,  but  yet  it  may  sometimes  be  of  extreme 
gravity  (Renaut).  Scarlatinal  nephricis.  which  is  often  benign,  may  be 
very  severe,  or  may  become  the  origin  ot  Bright's  disease.  The  nephritis 
of  pregnancy  is  serious,  because  it  may  lead  to  eclampsia,  or  may  become 
chronic. 

Diagnosis. — The  diagnosis  of  acute  nephritis  demands  some  attention. 
In  many  infectious  diseases  nephritis  develops  insidiously,  and  the  urine 
must  be  carefully  examined  for  signs  of  renal  changes.  WTien  the  oedema 
is  transient  and  shght,  the  other  symptoms  may  be  so  marked  as  to  cause 
errors  in  diagnosis.  We  must  not  set  down  as  bronchitis  a  case  of  acute 
nephritis  in  which  the  chief  symptoms  are  violent  dyspncEa  and  scattered 
rales.  We  must  not  set  down  as  pleurisy  nephritis  in  which  the  chief 
sign  is  pleuritic  effusion.  It  is  sufficient  to  remember  the  possibihty  of 
these  errors  to  avoid  falUng  into  them.  Furthermore,  albuminuria  and 
oedema,  which  may  be  absent  in  some  cases  of  chronic  nephritis,  are  never 
wanting  in  acute  nephritis. 

Treatment. — The  treatment  of  acute  nephritis,  consisting  of  milk  diet, 
cupping  of  the  loins,  and  general  blood-letting  in  the  case  of  uraemic  symp- 
toms, difEers  httle  from  the  treatment  of  Bright's  disease,  which  is  given 
in  the  following  chapter. 

Blood-letting  is  indicated  when  we  find  s}Tnptoms  of  urjemia,  epilepti- 
form convulsions,  delirium,  or  coma.  In  this  case  10  to  20  ounces  of  blood 
must  be  withdrawn,  and  the  operation  repeated,  if  necessary.     This  measure 


1090  TEXT-BOOK  OF  MEDICINE 

is  most  valuable,  and  must  never  be  put  ofi.  Many  cases  of  acute  nephritis 
and  grave  ursemia  owe  tlieir  recovery  to  free  bleeding.  I  am  so  convinced 
of  its  efficacy  in  acute  nephritis,  that  I  would  even  advise  it  in  cases  of 
moderate  severity.  Blood-letting  has  not  only  an  immediate  action  on 
the  acute  symptoms  at  the  moment,  but  I  believe  that  it  diminishes  the 
risk  of  subsequent  chronic  mischief. 

Injections  of  serum  and  all  foods  containing  salt  must  be  proscribed. 

Milk  diet  is  of  the  utmost  importance.  It  must  be  continued  for  several 
weeks  even  after  the  supposed  cure  of  acute  nephritis,  and  it  is  one  of 
the  most  certain  means  of  avoiding  chronic  nephritis. 

IV.  APPENDICULAR  KIDNEY— TOXIC  NEPHRITIS— 
APPENDICULAR  ALBUMINURIA. 

I  have  repeatedly  mentioned  in  this  work  the  dire  results  of  the  appendi- 
cular toxines  on  the  system.  Under  Diseases  of  the  Liver  I  devoted  a 
special  section  to  toxic  appendicular  hepatitis.  I  shall  now,  under  Diseases 
of  the  Kidneys,  discuss  toxic  appendicular  nephritis. 

Reduced  to  its  simplest  terms,  toxic  appendicular  nephritis  reveals  itself 
by  a  single  sign — albuminuria.  In  nearly  all  severe  cases  of  appendicitis 
the  effect  on  the  kidneys  is  at  once  shown  by  albuminuria.  Since  my 
attention  was  drawn  to  this  im.portant  point,  I  have  found  albuminuria  in 
many  cases  of  appendicitis.  The  albumin  may  appear  on  the  first,  second, 
or  third  day,  and  is  sometimes  associated  with  shght  jaundice,  which  also 
indicates  toxic  poisoning.  We  may  find  only  a  small  quantity  of  albumin, 
but  at  other  times  we  may  find  10  to  15  grains,  or  even  more.  I  have 
several  times  followed  the  gradual  disappearance  of  the  albumin  after  re- 
moval of  the  appendix.     To  quote  examples  : 

I  was  asked,  at  the  Hotel-Dieu,  to  examine  a  patient  suffering  from  appendicitis 
which  had  been  allowed  to  "  grow  cold."  The  disease  was  of  three  weeks'  duration, 
and  had,  imfortunately,  been  left  to  the  vis  medicatrix  naturce.  After  an  apparent 
remission,  the  fever  and  vomiting  had  reappeared,  and  the  situation  was  critical.  I 
examined  the  patient,  and  concluded  that  the  appendicitis  had  set  up  peritoneal  infec- 
tion which  had  spread  to  the  subphrenic  region  (this  opinion  was  verified  at  the  opera- 
tion). Examination  of  the  urine  revealed  over  15  grains  of  albumin  ;  no  casts  in  the 
centrifugal  tube.  Mauclaire  operated,  and  the  condition  was  reheved.  At  the  same 
time,  the  albuminuria  gradually  diminished,  and  disappeared  in  a  month,  the  patient 
being  in  good  health.  Under  Appendicular  Hepatitis  I  referred  to  a  patient  in  my 
wards  with  gangrenous  appendicitis,  albuminuria,  and  jaundice  (toxic  appendicitis). 
He  was  operated  upon  on  the  morning  of  his  arrival.  The  improvement  was  slow  to 
show  itself,  but  in  a  few  days  the  albumin,  the  pigments,  and  the  jaundice  disappeared. 

Simple  albuminuria,  which  yields  after  resection  of  the  appendix,  is.  1 
repeat,  the  only  symptom  of  shght  appendicular  nephritis.  In  such  cases 
the  renal  lesion  is, neither  severe  nor  lasting,  and  yet  we  must  not  trust  tiiis 


DISEASES  OF  THE  KIDNEYS  1091 

apparent  benignity,  because  this  simple  albuminuria,  whether  it  be  associated 
or  not  with  jaundice,  is  at  times  the  first  warning  of  grave  troubles,  which 
may  end  in  death.     To  quote  examples  : 

I  was  askod  by  Marion  to  see  a  boy  wlio  had  been  adniittod  tlio  proviouH  ovuning 
into  the  Hotol-Diou.  The  disease  had  commenced  suddenly  throe  days  before.  He 
went  to  bod  in  his  usual  health,  but  woke  about  two  o'clock  in  the  morning  with  sUght 
umbiUcal  pains,  which  bccamo  more  severe.  Next  day,  in  spite  of  the  pains,  he  went 
to  work  again,  but  was  compelled  to  go  to  bed.  In  the  night  the  pains  in  the  belly 
became  acute,  but  there  was  neither  nausea  nor  vomiting.  Next  morning  (the  second 
day  of  tho  disease)  the  pains  were  very  severe,  and  his  doctor  sent  him  to  hospital  for 
appendicitis. 

On  the  third  day  of  the  disease  he  was  brought  to  the  Hotel-Dieu.  The  belly  was 
slightly  distended,  and  not  quite  as  painful  as  on  the  previous  days.  No  vomiting  ; 
mictui'ition  easy.  Pulse  96 ;  morning  temperature  101°  F. ;  evening  temperature  103°  F. 
An  ice-bag  was  applied  to  the  belly. 

I  saw  him  next  morning  at  ten  o'clock  (fourth  day  of  the  disease).  Pulse  was  88,  and 
the  temperature,  which  the  previous  evening  was  104°  P.,  had  fallen  to  99°  P.  In  spite 
of  this  apparent  improvement,  I  felt  that  we  were  face  to  face  with  a  treacherous  calm. 
The  face  was  earthy ;  the  features  were  drawn,  and  the  ala3  nasi  were  working.  He 
passed  gas  and  urine  ;  some  hiccough  ;  no  vomiting.  The  belly  was  neither  tympanitic 
nor  hoUow.  Palpation  showed  that  the  pain  was  most  acute  over  the  appendix. 
Hypersesthesia  and  muscular  resistance  were  present ;  no  dullness. 

We  had  to  deal  with  acute  appendicitis,  but  yet,  in  spite  of  the  bad  impression 
caused  by  his  facies,  peritonitis  was  not  the  prominent  feature  in  this  case.  These  forms 
are  suspicious  of  gangrene  of  the  appendix  and  of  poisoning,  which  may  be  severe.  I 
had  the  urine  analyzed,  and  the  analysis  confirmed  my  suspicions  as  to  the  toxic  nature 
of  the  case.  The  kidneys  and  the  Uver  were  afifected  by  the  toxines,  for  the  urine  con- 
tained a  fairly  large  proportion  of  albumin,  granular  casts,  leucocytes,  and  bile  pigment. 

The  prognosis  appeared  to  me  to  be  very  grave,  as  it  was  certain  that  his  system  was 
poisoned,  and  that  removal  of  the  appendicular  focus  would  perhaps  be  too  late. 

The  operation  was  performed  at  once  by  Predet.  Opening  the  peritoneal  cavity 
gave  exit  to  a  small  quantity  of  odourless  turbid  liquid.  No  adhesions  between  the 
intestinal  coUs,  and  but  Httle  exudate  ;  a  small  collection  of  foetid  pus  behind  the  csecum. 
The  appendix  was  situated  in  this  abscess,  and  was  sUghtly  adherent  to  the  posterior 
wall  of  the  caecum ;  it  was  detached  without  dilB&culty.  The  proximal  portion  of  the 
appendix  adjoining  the  caecum  appeared  healthy,  but  the  remainder  was  gangrenous  ; 
no  apparent  perforation.  The  wound  was  left  open.  Drainage  was  effected  by  means  of 
three  large  tubes  surrounded  with  gauze.  Next  night  (Tuesday)  he  was  restless ;  on 
Wednesday  repeated  vomiting  led  me  to  fear  hsematemesis,  which  is  so  common  in 
the  toxic  forms  of  appendicitis.  On  Thursday  his  face  still  kept  its  earthy  look ;  the 
pulse  was  rapid  ;  albuminuria  and  bile  pigments  still  present. 

On  Friday  he  was  worse,  being  quite  prostrate.  Extremities  bathed  with  cold  sweat ; 
m'ine  scanty ;  pulse  small  and  quick ;  respiration  accelerated ;  vomiting  painful  and 
frequent ;  the  stomach  was  quite  intolerant  of  food.  Analysis  of  the  'xrine  showed 
albumin  and  a  red-brown  pigment,  which  had  replaced  the  bile  pigment.  Next  night 
hsematemesis  supervened,  and  the  patient  succumbed,  after  a  series  of  black  vomits 
which  persisted  until  the  moment  of  death.  The  temperature  did  not  rise  beyond 
101°  F. 

Post-mortem  examination  :  Some  fibrinous  exudate  on  the  intestinal  coils  ;  no  puru- 
lent collection,  except  a  tablespoonful  of  hoijogeneous  pus  in  the  pelvis.  The  lungs 
were  of  a  violet  colour  and  congested  with  blood,  especially  at  their  bases ;  no  trace 
of  broncho-pneumonia.      Stomach  empty  ;  the  entire  mucous  membrane  of  the  great 

68—2 


1092  TEXT-BOOK  OF  MEDICINE 

curvature  was  covered  with  haemorrhagic  patches,  which  in  places  looked  like  purpura. 
The  small  bloodvessels  formed  a  distended  network.     No  ulceration. 

Heart  and  spleen  healthy.  The  hver  and  the  kidneys  were  of  normal  appearance, 
and  not  enlarged ;  had  we  been  satisfied  with  a  superficial  examination,  these  organs 
might  have  been  considered  healthy,  but  the  histological  examination  revealed  marked 
changes.  Letulle  imdertook  the  examination,  and,  in  view  of  the  importance  of  the 
subject,  I  give  his  report  in  extenso. 

Portions  of  the  kidneys  taken  twenty-five  hours  after  death  were  placed  for  twenty- 
four  hours  ia  formol  (1  per  cent.),  hardened  in  alcohol,  and  cut,  after  embedding  in 
collodion.  The  specimens  were  stained  with  hsemateine-eosin,  thionin,  and  Kern- 
schwarz's  polychrome  blue. 

1.  Under  a  low  power,  the  specimens  showed  necrosis,  affecting  many  of  the  con- 
voluted tubes  and  some  of  the  large  branches  of  Henle's  loops,  whilst  the  glomeruli  and 
the  straight  tubes,  as  well  as  the  pyramids,  had  evidently  escaped. 

2.  On  careful  study  of  the  topography  of  the  necrobiotic  zones,  the  integrity  of  many 
of  the  convoluted  tubes  in  the  cortical  tissue  was  evident.  The  contrast  between  the 
dead  tubes  in  the  parenchyma  and  the  living  ones  in  the  cortical  substance  was  most 
remarkable,  and  ehminated  the  hypothesis  of  a  post-mortem  lesion.  Furthermore,  the 
examination  of  the  lesions  with  the  high  power  confirmed  this  view. 

(1)  It  was  easy  to  see  that  all  the  epithelial  cells  in  the  section  of  a  convoluted  tube 
were  not  necrotic,  for  in  some  cells  the  nuclei  were  more  or  less  deeply  stained  a  lilac 
colour  by  the  haemateine. 

(2)  The  epithelial  ceUs  in  the  diseased  tubes  often  bulged  into  the  lumen.  They 
were  granular,  and  even  in  the  necrobiotic  regions  the  elements  were  on  the  way  to 
desquamation,  whether  their  nuclei  were  stained  or  not. 

(3)  The  cells  of  the  interstitial  tissue  and  the  capillaries  did  not  appear  to  be  much 
affected,  and  their  nuclei  were  stiU  present. 

The  giomeruh  were  engorged  with  blood ;  the  cavity  was  fiUed  with  rosy  scrum  in 
some  cases ;  the  endothehum  of  the  capsule  had  prohferated  at  many  spots  ;  the  inter- 
stitial ceUs  of  the  glomerular  loops  had  not  prohferated  ;  the  bloodvessels  of  the  cortical 
substance,  and  those  of  the  glomerular  portion  in  particular,  were  dilated,  but  there  was 
no  perivascular  diapedesis  ;  there  was  no  trace  of  serous  or  fibrinous  interstitial  exuda- 
tion. As  for  the  tissue  of  the  pyramids,  some  of  Henle's  loops  were  partially  necrotic. 
There  was  no  inflammation  in  the  collecting  tubes,  and  the  nuclei  of  the  epithehal  cells 
were  still  present. 

Fragments  stained  with  osmic  acid  showed  granulo -fatty  degeneration,  limited  to 
the  epithelial  cells  of  the  convoluted  tubes.  This  recent  lesion  was  characterized  by  the 
desquamation  of  the  renal  cells,  and  the  accumulation  of  fine  blackish  granules  in  the 
protoplasm.  These  granules  were  scattered  throughout  the  entire  cell,  and  were  not 
merely  accumulated  at  its  base.  Appropriate  technique  showed  that  in  some  of  the 
degenerated  epithehal  cells  the  nuclei  still  took  the  stain. 

After  staining  with  thionin,  the  necrotic  cells  showed  two  different  types,  which  did 
not  appear  to  be  two  stages  of  the  same  lesion,  and  which  never  coexisted  in  the  same 
portion  of  the  tubule. 

1.  The  first  type  was  a  fairly  good  example  of  coagulation  necrosis.  The  protoplasm 
of  the  cell  was  stained  a  greyish-blue  colour,  and  was  almost  homogeneous  and  trans- 
lucid.  The  protoplasm  was  cut  up  by  large  striations  with  iU-definod  edges,  and  the 
nucleus  no  longer  took  the  stain. 

2.  The  second  type  was  more  discrete,  and  characterized  by  granular  fragmentation 
of  all  the  epithehal  protoplasm  in  the  section  of  any  given  convoluted  tube.  The 
degeneration  had  led  to  the  disappearance  of  the  outhnes  of  the  cells.  The  granules  in 
the  dead  protoplasm  varied  in  size  ;  in  general,  they  were  fairly  large,  measuring  from 
2  to  5  ^.     They  stained  a  pale  violet  with  thionin,  and  were  rounded,  translucent,  and 


DISKASKS  (»K  Till':   KIDNKYS  lOO;i 

always  distinct  one  from  anotlRM-.  No  casts  were  prcHcnt  in  tho  liilns.  It  waH  diilicull 
to  say  whotlicr  all  tho  fatty  drops  stainoil  by  llio  OHinic  acid  coiiicidud  or  not  with  theso 
hyalino  masses.  It  was  to  bo  noted  that  at  many  points  tho  portion  of  tho  tubo  attacked 
by  the  degeuuration  corrospondod  with  the  origin  of  tlio  uriniforouB  tubo.     tSomo  of  the 


'C 


Fig.  55. — Section  of  Kidney. 
a,  Glomerulus  ;  h,  necrosed  tubules  ;  c,  healthy  tubules. 

atfoctcd  convoluted  tubides  reached  even  as  far  as  Bowman's  capsule.  In  the  de- 
generated cells  the  nuclei  were,  for  the  most  part,  refractory  to  the  stain ;  some  were 
stained  in  a  diffuse  manner,  or  showed  chromatolysis. 

In  short,  the  lesions,  as  a  whole,  proved  that  the  case  was  one  of  recent  superacute 
degenerative  nephritis,  the  cause  of  which,  through  escaping  microscopic  examination, 
appeared  to  be  some  toxic  substance  eliminated  by  the  secretory  apparatus  of  the  kidneys. 

The  liver  showed  granulo-fatty  degeneration  of  the  centro-lobular  cclla. 


^  1 


•■% 


Fig.  5t). — Section  of  Kidney. 

a,  Glomerulus  ;    g,  necrosed  cells  of  convoluted  tube  ;    b,   cells  undergoing  necrosis, 
iiuclbi  Btiii  present ;  c,  normal  convoluted  tube  ;  d,  healthy  connective  stroma. 

In  the  above  case,  then,  aijpendicitis  caused  infection  and  intoxication  of  the  patient. 
The  lesions  due  to  infection  caused  sMght  peritonitis  and  retrocsecal  abscess,  but  the 
lesiofki  due  to  the  appendicular  toxines  caused  during  life  symptoms  of  intoxication 
and  acute  changes  found  on  post-mortem  examinatior 

II-  70 


1094        ■  TEXT-BOOK  OF  MEDICINE 

The  patient,  therefore,  did  not  succumb  to  the  circumscribed  peritonitis, 
but  to  the  appendicular  poisoning,  which  proceeded  more  rapidly  than 
the  infection,  and  was  in  full  activity  on  the  fourth  day  of  the  disease. 
Peritonitis  is  not  the  aU-important  comphcation  in  appendicitis.  We  must 
takb  count  of  the  toxic  compHcations  which  sometimes  precede  the  infectious 
troubles,  and  are  the  more  to  be  feared  as  "  temporizing  "  surgery  is  power- 
less against  them.  When  we  see  these  cases  (and  they  are  numerous),  what 
are  we  to  think  of  the  short-sighted  teaching  which  only  takes  account  of 
the  peritonitis,  and  advises  an  interval  operation  ?  Such  teaching  fails  to 
recognize  that  the  toxines,  by  their  rapid  diffusion,  carry  off  the  patient 
whilst  the  interval  is  being  awaited. 

After  I  had  mentioned  this  question  at  the  Academic  de  Medecine,* 
Routier  told  of  the  following  case  : 

A  youth  was  admitted  at  the  Necker  Hospital  on  the  evening  of  July  6,  He  felt 
sick  two  days  before,  and  took  a  purge  to  relieve  his  "  indigestion."  The  pains  per- 
sisted. Next  morning  Dr.  Le  Guillant,  who  was  called  in,  at  once  diagnosed  appendi- 
citis, and  insisted  on  his  immediate  removal  to  the  Necker  Hospital.  Five  years  before 
Le  Guillant  had  attended  him  for  appendicitis.  He  advised  operation,  and  warned  the 
family  of  the  gravity  of  the  disease  and  of  its  probable  recurrence  ;  this  good  advice  was 
not  followed. 

On  admission  his  temperature  was  103°  F.  Routier  saw  him  next  morning.  Although 
the  temperature  had  fallen  to  100°  F.,  the  case  was  obviously  grave,  and  toxic  symp- 
toms accompanied  those  of  infection.  Pronounced  jaundice,  profuse  diarrhoea,  and  very 
quick  pulse  were  present.  The  belly  was  everywhere  painful,  with  muscular  resistance, 
especially  at  McBumey's  point. 

Routier  gave  a  very  grave  prognosis,  and  decided  on  immediate  operation ;  but  as  the 
parents  did  not  consent,  the  operation  was  postponed  tOl  the  next  day.  The  jaundice 
was  stiU  more  pronounced.  The  appendicitis  was  now  four  days  and  a  half  old.  The 
operation  disclosed  an  enormous  abscess  below  the  csecum,  and  a  large  collection  of  pus 
in  the  pelvis.  No  improvement  was  manifest  after  the  operation,  as  the  patient  was 
already  poisoned.  His  temperature  was  103°  F.,  the  pulse  120  ;  diarrhoea  and  jaundice 
persisted.     On  the  9th  extreme  restlessness  ;  on  the  10th  delirium  and  death. 

In  this  case,  as  in  the  preceding  one,  it  was  very  important  to  know  exactly  the 
lesions  present.  Histological  examination  of  the  kidneys  and  of  the  Hver  by  Nattan- 
Larrier  showed  similar  lesions  to  those  found  by  LetuUe  in  the  preceding  case.  In 
both  cases  the  acute  action  of  the  appendicular  toxines  was  evident.  I  give  the  histo- 
logical examination  in  extenso. 

The  kidneys  appeared  normal  to  the  naked  eye,  save  that  the  cortical  substance  was 
somewhat  pale.  Histological  examination  made  of  fragments  taken  a  few  hours  after 
death  showed  marked  lesions.  The  condition  was  one  of  superacute  degenerative 
nephritis  ;  the  lesions  were  locaUzed  to  the  convoluted  tubes  and  to  the  ascending  Hmb 
of  Henle's  loop.  It  was  a  systematized  lesion  of  the  whole  secretory  apparatus.  All 
the  convoluted  tubules  were  attacked  to  the  same  degree,  and  presented  the  same 
appearance.  The  cells  were  large  and  granular ;  the  nuclei  did  not  stain.  The  cell 
was  defined  at  its  base,  but  was  breaking  up  towards  the  lumen  of  the  tubule.  Cyto- 
logical  stains  showed  marked  reticulation,  in  the  meshes  of  which  large  rounded  granules 
were  present.     At  various  points,  and  especially  at  the  base  of  the  ceU,  there  were  masses 

*  Academie  de  Medecine,  seance  du  8  JuiUet,  1902. 


DISEASES  UF  THE  klDNEVS  1005 

of  fino  fatty  Ki'i'in'i"'*  i  ^^^  cells  were  undergoing  granulo-fatty  dogi-iuuiUioii.  Liio  ct^llu 
of  the  ascending  limb  of  Hcnlo's  loop  sliowcd  coagulutioa  noiirosiH.  The  nucloiiH  did  not 
Alain,  tuid  the  protophism,  studded  with  fat  globulon,  was  n-fractile,  atainod  well  with 
uosin,  and  took  a  pale  blue  with  polychrotno  blue.  The  shape  of  the  cell  wiis  chaugod. 
It  was  sUghtly  wiinkleil  at  its  base  ;  its  apex  was  irregular.  Desquamation,  however, 
was  absent  here,  as  in  the  convoluted  tubes.  These  cells  had  necrosed  in  siiu  ;  one 
section  showed  the  outline  of  a  few  cylindrical  cells.  The  colls  of  the  convoluted 
tubules  and  of  Henle's  loop  were  dead  as  far  as  their  functional  power  was  concerned. 
Whilst  wo  could  see  basal  striations  and  granules  which  were  stained  black  by  ircm  alum 
in  the  normally  secreting  coll,  none  of  the  figures  which  indicate  cellular  activity  could  bo 
detected.  The  most  higlily  differentiated  cells  of  the  kidneys  had  ceased  to  be  active. 
The  filtration  system  of  the  kidneys  was,  on  the  contrary,  practically  intact,  and  the 
glomeruli  wore  normal.  At  a  few  isolated  points,  shght  proliferation  of  the  endothchum 
of  Bowmann's  capsule  was  noticed,  and  osmic  acid  revealed  a  few  fatty  granules  in  the 
cells  of  the  straight  tubes.  These  lesions,  however,  were  of  minor  importance  compared 
wth  the  necrosis  and  acute  degeneration  in  the  convoluted  tubules  and  in  Henle's  ascend- 
ing limb — i.e.,  in  the  secretory  apparatus  of  the  kidneys.     Thalesion.'waa  the  more  clear 


/■• 


^^i.  Sim  ■»  ?'  »?>'" 


Fia.  57. — Section  of  Kidney. 

g,  Glomerulus  ;  a,  convoluted  tubes,  with  necrosed  cells  ;  b,  cells  in  process  of  necrosis, 
nuclei  still  present ;  c,  normal  convoluted  tube  ;  d,  connective  tissue. 

as  it  only  attacked  the  glandular  cell,  while  the  connective  tissue  and  the  bloodvessels 
were  normal.  No  diapedesis  of  leucocytes  ;  no  micro-organisms.  The  lesion  was  purely 
toxic,  and  its  locahzation  to  the  secretory  system  showed  that  it  was  due  to  the  ehmina- 
tion  of  toxic  material  by  the  cells  of  the  convoluted  tubes  and  of  Henle's  ascending  Umb. 
The  hver  was  very  much  congested  ;  the  condition  of  the  cells  was  remarkable,  and 
osmic  acid  showed  that  they  were  crammed  with  very  fine  fatty  granules.  The  nuclei, 
however,  took  the  stain  well,  but  ^-he  cells  showed  evident  granulo-fatty  degeneration. 

Lorrain  has  publislied  a  similar  case : 

A  man  who  had  had  two  previous  attacks  was  admitted  for  appendicitis.  On  his 
admission,  mduration  was  foimd  in  the  right  ihac  fossa ;  palpation  caused  acute  pain, 
and  the  skin  was  hvpersesthetic  ;  no  vomiting  and  no  fever.  Ice  and  opiiun  were  pre- 
scribed. A  few  days  later,  although  fever  was  absent,  the  belly  commenced  to  swell, 
tne  face  was  OraAvn,  and  the  pulse  was  bad.     Operation :  foetid  abscess  between  the 

70—2 


1096  TlilXT-BOOK  OF  MEDICINE 

small  intestine  and  the  csecum,  which  was  gangrenous.  A  fruitless  attempt  was  made 
to  find  the  appendix,  which  was  buried  in  the  adhesions.  He  succumbed,  and  at  the 
post-mortem  examination  the  gangrenous  appendix  was  discovered.  No  peritonitis ; 
no  collections  of  pus,  except  the  one  opened  at  the  operation.  Macroscopic  examination 
of  the  kidneys  showed  nothing  special,  but  histological  examination  revealed  the  follow- 
ing lesions :  The  epithelium  of  the  straight  tubes  was  normal,  and  the  nuclei  were  well 
stained.  The  convoluted  tubes  were  much  altered ;  here  and  there  a  few  epithehal 
cells,  with  a  weU-stained  nucleus,  were  seen,  but  in  general  the  nuclei  had  completely 
disappeared.  The  epithehal  cells  were  pale,  non-granular,  swollen,  and  had  a  tendency 
to  fill  up  the  lumen  of  the  tubules.  "  The  condition  was  one  of  coagulation  necrosis. 
The  lesions  afiected  aU  the  tubes  more  or  less,  but  some  few  tubes  seemed  to  have 
escaped  necrosis."  The  cells  of  the  liver  were  likewise  attacked,  and  contained  ochre 
pigment  m  abundance.  "  In  short,"  says  Lorrain,  "  the  clinical  course  and  the  lesions 
in  the  secretory  cells  of  the  kidneys  and  of  the  hver  showed  that  the  appendicitis  of  in- 
sidious course  and  necrosing  nature  caused  death,  not  by  infection,  but  by  profound 
intoxication  of  the  system." 

Description. — The  cases  above  quoted  give  the  necessary  details  for 
the  anatomical  and  choical  description  of  toxic  appendicular  nephritis. 
From  the  anatomical  point  of  view,  the  kidneys  at  first  sight  do  not  appear 
to  be  afEected.  They  are  neither  large  nor  pale,  and  do  not  resemble  the 
large  white  kidney.  On  histological  examination,  however,  the  situation  and 
the  nature  of  the  lesions  are  striking.  The  lesions  attack  almost  exclusively 
the  secretory  elements  of  the  organ,  and  in  severe  cases  the  cell  is  rapidly 
killed  by  the  appendicular  cytotoxine.     The  hver  cells  suffer  the  same  fate. 

From  the  chnical  point  of  view,  appendicular  nephritis  does  not  resemble 
the  other  known  forms  of  acute  nephritis.  It  is  not  comparable  with 
scarlatinal  or  early  syphiUtic  nephritis,  or  with  the  so-called  nephritis 
a  frigore.  SwelUng  of  the  face  and  of  the  eyehds,  acute  oedema,  dropsy, 
oedema  of  the  lungs,  and  serous  effusions  which  are  seen  in  other  kinds  of 
acute  nephritis,  are  not  present  in  appendicular  nephritis. 

As  oedema  of  the  eyehds  and  of  the  face  is  absent,  and  as  appendicular 
nephritis  does  not  show  itself,  as  a  rule,  by  any  visible  sign,  the  diagnosis 
is  by  no  means  evident,  and,  therefore,  this  variety  of  nephritis  has  passed 
unnoticed.  We  must  make  a  practice  of  examining  the  urine  in  every 
case  of  appendicitis. 

Albumin,  which  is  often  abundant  in  other  forms  of  acute  nephritis,  is 
generally  scanty  in  the  appendicular  form.  On  the  other  hand,  granular 
casts  may  be  found  in  the  urine  as  early  as  the  second  or  third  day,  and 
are  a  bad  sign.  Albumin  alone  does  not  make  the  prognosis  of  appendicitis 
absolutely  bad,  but  it  is  a  sign  of  poisoning,  and  a  danger-signal.  This 
danger  does  not  come  from  the  nephritis  alone  (which  may  end  in  urinary 
insufficiency  and  perhaps  ohguria) ;  it  arises  also  from  the  general  intoxica- 
tion of  the  system — that  is,  from  the  appendicsemia. 

Jaundice,  which  indicates  the  involvement  of  the  liver,  is  fairly  often 
associated  with  albuminuria.     These  two  signs  generally  appear  early  and 


DISEASES  OF  THE  KIDNEYS  1007 

together.  Tlieir  signification  may  not  be  fatal,  and  yet  no  one  can  sav 
whether  the  intoxication  will  confiae  itself  to  sli<j;hl,  nephritis  or  hepatitis, 
or  whether  it  will  end  in  more  extensive  lesions,  such  as  toxic  gastritis, 
vomito  negro,  renal  and  hepatic  insufficiency,  nervous  complicatioas,  general 
poisoning,  and  death. 

What  is  there  to  guide  us  in  the  prognosis  ?  The  fever  is  not  a  certain 
guide.  The  disease  may  end  fatally,  and  yet  the  temperature  may  remain 
normal.  In  my  first  case  the  temperature  oscillated  between  99°  and 
100°  F.,  although  the  fatal  complications  were  setting  in.  In  Lorrain's 
patient  the  temperature  was  about  99°  F.  for  some  days  before  death.  The 
pulse  itself  may  give  no  precise  information  as  regards  the  prognosis. 

The  history  of  appendicitis  is  always  deceptive,  and  the  poison  often 
accomphshes  its  work  without  giving  any  sign.  We  see,  then,  the  errors 
in  the  old  descriptions  of  appendicitis  as  a  purely  local  disease  in  which  the 
worst  complication  was  peritonitis.  Certain  pathological  classifications  on 
which  an  exact  prognosis  was  based  are  now  forgotten. 

The  cases  in  this  section  convey  a  great  lesson.  They  show  the  gravity 
of  toxic  appendicular  nephritis,  trace  the  series  of  toxic  comphcations 
(hepatitis,  gastritis),  and  prove  how  rapidly  the  appendicular  toxines  may 
act ;  they  furnish  fresh  arguments  in  favour  of  early  surgical  intervention, 
show  the  danger  of  delay,  and  condemn  the  teaching  which  advocates 
an  interval  operation. 

Some  day  the  advocates  of  delay  will  have  to  reply  to  these  arguments 
otherwise  than  by  words.  We  have  given  the  precise  facts  and  irrefutable 
proofs.  Let  them  do  the  same  in  support  of  their  teaching.  We  know  how 
many  patients  have  died  because  it  was  not  thought  advisable  to  operate 
before  the  appendicitis  had  become  quiescent,  and  we  can  show  the  toxic 
lesions  which  were  the  cause  of  death.  Why,  then,  should  we  not  operate 
on  patients  before  they  are  intoxicated  and  infected  ?  We  ask  for  an 
answer  based  on  facts  as  precise  as  our  own. 

I  do  not  wish  to  close  this  section  without  drawing  a  parallel  between 
the  appendicular  Uver  and  the  appendicular  kidney.  I  described  separately 
early  toxic  hepatitis,  which  is  non-suppurative,  and  infective  hepatitis, 
which  occurs  later,  and  occupies  a  prominent  place  in  the  history  of  the 
appendicular  liver.  This  purulent  hepatitis  is  readily  explained,  because 
the  infective  agents  are  carried  direct  from  the  appendix  to  the  Hver  by  the 
tributaries  of  the  portal  vein.  It  is  not  so  in  the  case  of  the  appendicular 
kidney,  which  can  only  become  infected  by  a  circuitous  path  ;  consequently, 
infective  nephritis  with  abscess  of  the  kidney  is  relatively  very  rare,  whilst 
toxic  nephritis,  especially  the  shght  form,  is  common. 

I  think  the  poisoning  of  the  kidneys  by  the  appendicular  toxine.s  may 
in  some  degree  account  for  the  origin  of  Bright's  disease. 


1098  TEXT-BOOK  OF  MEDICINE 

V.  BRIGHT'S  DISEASE— CHRONIC  NEPHRITIS— 
PARENCHYMATOUS  NEPHRITIS— INTERSTITIAL  NEPHRITIS- 
MIXED  NEPHRITIS. 

Diseussion. — In  1827  Ricliard  Bright  published  the  results  of  his  observations,  and 
taught  that  changes  are  found  in  the  kidneys  of  patients  who  die  after  passing  albumi- 
nous urine  and  suffering  from  persistent  dropsy.  Bright  certainly  made  use  of  the 
researches  of  Wells  and  Blackall,  but  no  one  had  previously  described  the  relation  be- 
tween the  symptom  and  the  lesion  of  the  disease  which  now  bears  his  name.  Bright's 
great  merit  consists,  then,  in  having  grasped  the  fact  that  albuminuria  and  persistent 
dropsy  are  dependent  upon  a  lesion  of  the  kidneys ;  but  he  took  care,  with  wise  reserve, 
not  to  state  the  nature  of  this  lesion,  because  many  years  of  anatomical  research  by  the 
EngHsh,  German,  and  French  schools  have  not  cleared  up  the  nature  of  these  lesions 
which  stiU  give  rise  to  contrary  opinions. 

All  observers  agree  that  post-mortem  examination  in  case  of  subacute  and  chronic 
nephritis  reveals  the  most  varied  changes  in  the  kidneys,  which  may  be  normal  or 
enlarged,  whitish  or  yellowish,  or,  again,  small  and  atrophied  (small  red  kidney).  The 
question,  then,  arises  whether  such  dissimilar  lesions  are  not  merely  successive  stages 
of  the  same  morbid  process,  which  begins  in  hypertrophy  and  ends  in  atrophy ;  or 
whether,  on  the  contrary,  they  represent  distinct  anatomical  forms. 

Bright,  not  wishing  to  specify  the  extent  and  nature  of  the  lesion,  abstained  from 
drawing  conclusions.  In  1840  Rayer,  in  a  work  which  Rosenstein  justly  calls  the 
"  Archives  of  Renal  Diseases,"  proclaimed  that  the  various  lesions  of  the  kidneys  are 
in  reality  only  successive  stages  of  one  inflammatory  process.  The  kidneys  are  enlarged 
and  congested  in  the  first  or  acute  stage.  In  the  subacute  and  chronic  stages  they 
become  ansemic  and  atrophied.  These  various  stages  were  divided  by  Rayer  into  six 
successive  degrees. 

In  1851  Frerichs,  who  followed  in  Rayer's  footsteps,  admitted  only  three  degrees 
in  chronic  nephritis ;  but  he,  Uke  Rayer,  maintained  the  unity  of  the  iaflanmiatory 
process,  which  commenced  with  congestion  of  the  organ  and  cloudy  swelling  of  its  cells 
(enlarged  kidney),  passed  on  to  fatty  degeneration  of  the  epithehum,  and  ended  in 
atrophy  of  the  organ  (small  kidney).  Whether  we  admit  six  periods  with  Rayer,  or 
three  with  Frerichs,  seven  with  Christison,  or  five  with  Martin  Solon,  it  is  none  the  less 
true  that  this  doctrine,  called  the  doctrine  of  the  imicists,  defended  by  Virchow  and  by 
Reinhardt,  recognizes  one  morbid  process,  which  causes  successive  hypertrophy  and 
atrophy  of  the  kidney.  The  contrary  doctrine  maintains  the  pluraUty  of  the  forms  of 
this  disease :  the  various  conditions  found  in  the  kidneys  post  mortem  are  not  succes- 
sive stages  of  one  morbid  process,  but  represent  absolutely  distinct  forms.  The  enlarged 
white  kidney  does  not  give  rise  to  the  small  contracted  kidney,  just  as  the  small  con- 
tracted kidney  never  commences  as  a  large  white  kidney.  In  the  small  contracted 
kidney  the  lesion  is  an  interstitial  nephritis,  and  has  nothing  in  common  with  the  en- 
larged kidney,  just  as  the  enlarged  kidney  which  represents  parenchymatous  nephritis 
has  nothing  to  do  with  the  small  kidney.  These  distinct  anatomical  processes  give  rise, 
it  is  true — to  some  similar  troubles,  so  the  adherents  of  this  theory  maintain — but  yet 
their  symptomatology  is  sufficiently  distinct  for  us  to  say,  from  the  clinical  as  well  as 
from  the  pathological  point  of  view,  that  one  patient  is  suffering  from  interstitial  neph- 
ritis, whereas  another  patient  has  parenchymatous  nephritis. 

According  to  some  writers,  these  two  forms,  the  small  and  the  enlarged  kidney, 
could  not  be  more  distinct.  The  anatomical  lesions  are  dissimilar — in  the  one,  vascular 
and  interstitial ;  in  the  other,  glandular.  The  symptoms,  course,  duration,  and  com- 
plications  are  said  to  form  a  very  different  ensemble  in  the  two  cases.  The  aetiology  is 
held  to  be  distinct ;  the  small  kidney  is  said  to  be  the  especial  appanage  of  gout. 


DISEASES  OF  THE  KIDNEYS  1091) 

phiinbisin,  and  old  ago,  wlieroaa  the  enlarged  kidney  is  said  to  bo  mot  with  "  almost 
exoliisivoly  in  tubercular  patients,  etc." 

Some  protests  wore  raised  against  this  forced  division  (Jaccuud).  I*  fought  against 
it  in  the  name  of  pathological  anatomy  and  of  clinical  medicine.  For  tho  sake  of  con- 
ciseness, I  shall  briefly  sum  up  in  a  few  lines  our  present  knowledge  of  the  question 
as  I  understand  it : 

Wo  know  that  in  chronic  nephritis  the  lesions  are  diffuse,  and  more  or  lesa  general 
in  tho  glandular,  vascular,  and  cormective  tissues.  We  need  not,  therefore,  absolutely 
retain  tho  old  division  into  paronch;yTnatou8  and  interstitial  nephritis.  It  is,  neverthe- 
less, true  that  the  lesions  may  be  unequally  distributed.  We  find  some  cases  of 
nephritis  in  which  the  interstitial  lesions  predominate,  and  others  in  wliich  the  parenchy- 
matous changes  are  most  marked ;  but  they  are  often  only  varieties,  and  the  nephritis, 
taken  as  a  whole,  is  still  diffuse. 

If  we  find  post  mortem  large  white  or  small  red  kidneys,  and  granular  or  cystic 
kidneys,  these  varieties  are  due  to  the  rapidity  or  to  the  slowness  of  the  process ;  to  the 
predominance  of  epitheUal,  vascular,  or  cormective  changes ;  to  the  nature  of  the 
toxines  or  of  the  poison  ;  to  the  virulence  or  the  attenuation  of  the  infective  agents  ; 
but  no  matter  what  is  the  nature  of  the  lesion,  as  soon  as  the  process  runs  a  progres- 
sive course,  the  final  result  is  the  same — viz.,  a  tendency  to  the  destruction  of  the 
organ,  to  the  abolition  of  its  functional  powers,  with  gradual  or  rapid  insufficiency  of 
urinary  depuration  and  uraemia. 

Numberless  discussions  have  been  held  as  to  whether  the  enlarged  kidney  may 
finally  become  small  and  sclerotic,  and  whether  the  contracted  kidneys  may  have  begun 
with  hypertrophy.  Divers  forms  may  here  present  themselves.  Certain  processes 
cause  hypertrophy  of  the  organ,  as  well  as  simultaneous  necrosis  of  its  essential  parts. 
In  this  case  the  hypertrophic  lesion  may  be  considered  as  the  final  stage  in  the  nephritis, 
since  it  has  caused  death.  On  the  other  hand,  when  we  find  the  kidneys  atrophied  to 
one-half  of  their  normal  size,  it  is  evident  that  the  kidney,  which  was  normal  at  the  onset 
of  the  disease,  has  atrophied  by  this  amount.  Many  discussions  have  also  been  held  to 
determine  the  varieties  of  nephritis  for  which  the  name  of  Bright's  disease  should  be 
reserved.  The  reply  seems  very  simple  to  me.  Every  case  of  chronic  nephritis  comes 
under  Bright's  disease  ;  "  Bright's  disease  "  and  "  chronic  nephritis  "  are  synonymous 
terms.  In  making  use  of  the  term  "  Bright's  disease,"  we  do  homage  to  an  illustrious 
man  who  was  the  first  to  estabUsh  clearly  the  course  of  the  disease  which  is  at  present 
occupying  our  attention  ;  and,  furthermore,  this  term  does  not  prejudge  the  nature  of  the 
lesions  :  it  is,  therefore,  well  adapted  to  new  discoveries. 

During  the  coirrse  of  this  article  the  word  "  Brightism  "  will  frequently  be  used  as 
synonymous  with  Bright's  disease.  When  I  coined  the  word  "  Brightism  "  I  apphed 
it  more  especially  to  the  mild  forms  of  this  disease.  When  I  say  that  a  patient  is  suffer- 
ing from  Brightism,  I  wish  it  to  be  imderstood  that  his  urinary  depuration  is  insufficient, 
but  that  so  far  rmld  symptoms  only  are  present ;  he  does  not  yet  show  the  grave  symp- 
toms of  ursemia. 

In  order  to  facihtate  the  anatomical  description,  I  shall  describe  separately  chronic 
nephritis  with  enlarged  kidneys  and  chronic  nephritis  with  small  kidneys ;  we  shaU 
see  later  the  intermediary  varieties  which  represent  the  most  common  form  of  Bright's 
disease. 

Parenchymatous  Nephritis. 

Cliromc  nephritis  with  enlarged  kidneys  is  generally  rapid  in  its  course ; 
indeed,  the  name  of  "  subacute  nephritis  "  might  be  more  suitable.     "  The 

♦  Dieulafoy,  Gaz.  Hebdom.,  1877,  Nos.  12  and  14. 


1100  TEXT-BOOK  OF  MEDICINE 

size  of  the  kidneys  is  explained  by  the  severe  inflammation,  the  intra- 
tubular  and  interstitial  exudates,  and  the  intense  glomeruUtis.  The  differ- 
ence in  colour  depends  on  the  degree  of  congestion,  on  the  amount  of 
exudate  in  the  tubes  and  on  the  more  or  less  profound  change  in  the  epithehal 
cells  of  the  tubuh  contorti "  (Brault).  These  enlarged  kidneys,  which  are 
generally  smooth,  may  be  whitish  or  haemorrhagic.  On  section,  they  cut 
readily,  are  rich  in  juice,  yellowish  at  certain  points,  and  sometimes  studded 
with  small  haemorrhages.  The  "  large  white  kidney  "  (Wilks),  therefore, 
represents  only  one  form  of  the  large  kidney  in  Bright's  disease.  Scarlatina, 
syphihs  and  malaria,  may  give  rise  to  the  enlarged  kidney,  by  reason  of  the 
severe  and  rapid  course  of  the  lesions. 

Pathological  Anatomy. — The  large  kidney  may  weigh  three  times  the 
normal  amount.  The  capsule  strips  readily,  and  we  find  neither  nodules 
nor  cysts,  as  in  the  granular  kidney.  The  cortical  substance  is  two  or  three 
times  its  ordinary  size. 

Under  the  microscope  the  glomeruli  and  the  tubuh  contorti  are  two 
or  three  times  as  large  as  normal.  The  epithehal  cells  show  cloudy  swelling, 
and  the  lumen  is  narrowed.  The  cells  rapidly  undergo  granulo-fatty  de- 
generation and  we  find  every  variety  and  degree  of  swoUen  and  "  granular 
cells  "  (Cornil).  In  the  convoluted  tubules,  and  especially  ia  the  straight 
tubules,  we  find  granular  detritus,  granular  or  hyahne  casts,  white  and  red 
corpuscles.  It  is  especially  in  the  interior  of  the  straight  tubules  that  the 
products  of  the  exudate  from  the  Malpighian  glomeruH  (corpuscles  and 
plasma),  and  from  the  epithehal  cells  of  the  convoluted  tubes,  become 
coagulated  and  transformed  into  hyaline  casts  (Cornil). 

The  stroma  is  enlarged,  through  the  diapedesis  of  the  white  corpuscles 
and  through  the  intertubular  oedema.  Many  glomeruh  are  anaemic  and 
shrunken.  We  may  find  abundant  multiphcation  of  the  nuclei  in  Bow- 
man's capsule  and  in  the  glomerulus.  The  cells  desquamate  and  compress 
the  vascular  tuft  inside  the  capsule. 

Referring  to  the  large  white  kidney,  we  might  recall  the  discussion  which 
was  held  and  the  doubts  which  arose  as  to  the  inflammatory  process  in 
so-caUed  parenchjnuatous  nephritis.  According  to  many  writers,  parenchy- 
matous nephritis  is  really  the  result  of  an  inflammatory  process,  the  epi- 
thehnm  being  the  chief  seat  of  the  inflammation  (Rosenstein,  Lancereaux, 
Corml  and  Ranvier,  Lecorche).  Other  writers,  on  the  contrary  (Johnson, 
Klebs,  Kelsch),  hold  that  the  epithehum  is  not  the  seat  of  an  inflammatory 
process,  because  no  trace  of  new  proliferation  is  found,  either  in  the  epi- 
thehum or  in  the  connective  tissue  of  the  diseased  kidney.  The  swelhng 
of  the  cells  and  the  granulo-fatty  degeneration  are  said  to  be  a  primary 
degenerative  process  rather  than  an  inflammatory  lesion.  This  explains  the 
name,  enlarged  fatty  kidney,  given  to  the  large  white  kidney  in  England. 


DTSEASE^i  OF  T(li:  KTDXF.YS  1101 

Brault,  who  buius  up  the  (juestion  in  an  important  work  on  nephritic, 
will  not  admit  the  hypothesis  of  a  purely  degenerative  process.  In  the  first 
place,  savs  lie,  the  presence  of  fat  in  the  cells  does  not  prove  that  the  process 
is  degenerative,  because  fat  is  always  found  in  inflammations  of  long  dura- 
tion. The  process  is  really  inflammatory,  judging  from  the  fihriiiou.s 
e.Kudate  in  the  tubules,  and  also  from  the  glomerulitis  which  is  always 
present.  Bowman's  capsule  is  often  thickened.  The  cells  lining  the 
capsule  encroach  upon  the  cavity  of  the  glomenilus.  The  loops  of  the 
glomerulus  are  obUterated ;  the  afferent  and  efferent  arteries  near  the 
glomerulus  sometimes  show  endarteritis  obhterans. 

The  preceding  description  is  especially  apphcable  to  the  large  whit« 
kidney.  In  other  cases,  however,  subacute  nephritis  has  a  congestive  or 
irritative  tendency,  and  the  enlarged  kidney  presents  a  different  aspect. 
Its  cortical  substance  is  reddish  or  yellowish  ;  the  glomeruh  and  the  capillaries 
of  the  cortical  substance  are  distended  with  blood ;  haemorrhage  occurs  in 
the  interior  of  the  glomerulus  ;  and  the  convoluted  tubule  is  filled  with  red 
corpuscles. 

Such  is  the  anatomical  description  of  the  enlarged  kidney.  The 
name  "  subacute "  nephritis  would  be  more  suitable  than  chronic 
nephritis.  Clinically  they  present  some  peculiarities,  which  I  shall  now 
mention. 

Chief  Symptoms. — The  s}Taptom3  comprise  oedema  of  the  face  and  legs, 
anasarca,  serous  effusions,  especially  into  the  pleura,  and  oedema  of  the 
lungs.  Headache,  dyspnoea,  vomiting,  epistaxis,  and  visual  troubles  ■  are 
frequently  present.  The  urine,  which  is  scanty,  high-coloured,  and  at  times 
bloody,  contains  abundant  albumin  and  casts. 

The  symptoms  of  Brightism — viz.,  pollakiuria,  dead  fingers,  cramps  in 
the  calves,  cryaesthesia,  etc. — are  less  frequent  than  in  other  forms  of 
chronic  nephritis. 

The  heari;  shows  httle  or  no  hypertrophy.  The  gallop  rhythm  is  rare. 
The  arteries  are  not  sclerotic,  and  the  pulse  is  soft,  contrasting  with  the  hard 
pulse  found  in  cases  of  nephritis  with  high  arterial  tension. 

Symptoms  of  uraemia — viz.,  delirium,  convulsions,  and  coma — are  more 
rare  than  in  the  other  varieties  of  chronic  nephritis.  Pneumonia,  pericar- 
ditis, erysipelas,  and  gangrene,  occur  as  secondary  infections. 

Subacute  nephritis  with  enlarged  kidneys  terminates  in  various  ways. 
The  lesions  are  sometimes  so  severe,  the  epithehal  necrosis  is  so  rapid,  that 
the  enlarged  kidney  represents  the  final  stage,  and  the  patient  succumbs 
in  a  few  months.  In  some  cases  the  lesions  are  not  so  profound,  and  the 
nephritis  may  be  cured.  The  kidney,  however,  is  transformed  into  an  organ 
of  minoris  resistenticB.  Finally,  in  other  cases  nephritis  which  has  com- 
menced with  symptoms  of  an  enlarged  kidney  makes  slow  progress,  and 


1102  TEXT-BOOK  OF  MEDICINE 

causes  a  diminution  in  the  size  of  the  organ  with  the  symptoms  of  an 
eminently  chronic  nephritis.  In  this  case  the  transformation  of  an  enlarged 
kidney  into  a  smaller  one  may  be  admitted. 

Interstitial  Nephritis. 

After  having  described  nephritis  with  enlarged  kidneys,  I  shall  now  give 
the  description  of  the  opposite  type — viz.,  chronic  nephritis  with  contracted 
kidneys. 

Pathological  Anatomy. — When  toxic  or  infectious  agents  (lead,  gout, 
alcohol,  secondary  infections)  act  in  small  and  repeated  doses,  or  when  the 
morbid  process  (arterio-sclerosis,  senihty)  is  very  slow,  it  is  only  after  many 
years  that  the  lesion  ends  in  atrophy  of  the  kidneys.  In  some  cases  the 
kidneys  are  reduced  to  one-third  of  their  normal  weight.  The  colour  may 
be  greyish,  yellowish,  or  reddish,  according  to  the  number  of  vessels  which 
persist  and  the  condition  of  the  cells.  Some  have  an  intense  red  colour 
(the  old  "  smaU  red  kidney  "),  which  depends  on  subcapsular  ecchymoses 
and  a  hsemorrhagic  motthng  visible  to  the  naked  eye. 

The  kidney  is  sometimes  nodular.  The  perirenal  fat  is  generally  much 
increased.  The  capsule  is  thickened  and  adherent,  so  that  it  is  impossible 
to  detach  it  without  removing  some  portions  of  the  kidney  substance.  The 
surface  of  the  organ  varies  in  colour,  and  is  studded  with  prominent  granula- 
tions of  the  size  of  a  miUet-seed.  These  granulations,  which  are  also  found 
deep  in  the  cortex,  are  formed  by  the  healthy  tubules,  which  are  embedded 
in  the  fibrous  tissue.  They  must  not  be  confounded  with  the  flat  patches 
in  the  large  fatty  kidney  which  are  incorrectly  called  granulations. 

On  section,  the  kidney  tissue  is  resistant.  The  atrophy  principally 
affects  the  cortex,  which  may  be  only  1  miUimetre  in  thickness.  In  some 
cases,  indeed,  the  capsule  touches  the  base  of  the  pyramids.  "  The  region 
of  the  glomeruh  and  of  the  convoluted  tubules  disappears,  as  if  there  had 
been  absorption  of  these  parts  "  (Brault).  Bertin's  columns,  which  are  a 
prolongation  of  the  cortical  substance,  do  not  show  such  marked  atrophy 
as  the  cortex. 

With  the  naked  eye  httle  cysts  are  seen.  They  are  generally  formed  at 
the  expense  of  the  convoluted  tubules,  which  are  strangled  by  the  fibrous 
tissue,  and  dilate  above  the  strangulation,  or  are  at  times  fused  with  enlarged 
tubules.  These  cysts  may  become  independent.  They  are  often  filled 
with  refracting  colloid  masses.  Some  are  as  large  as  a  pea,  and  project 
from  the  surface  of  the  kidney.  Other  cysts  may  result  from  enlargement 
of  Bowman's  capsule ;  others,  again,  of  an  ovoid  form,  or  disposed  Hke 
a  chaplet,  arise  from  the  strangulation  and  enlargement  of  the  straight 
tubules  in  the  medullary  substance.  The  atrophy  is  much  less  pronounced 
in  the  pyramids  than  in  the  cortex.     The  calyces  and  the  pelvis  are  some- 


DISEASES  OF  THE  KIDNEYS  1103 

times  very  dilated.  Subcortical  nodules  of  adenoma  are  found  (Tabourin). 
Small  concretions  of  uric  acid  and  urate  of  soda  are  common,  especially  in 
the  medullary  substance  and  in  the  interior  of  the  tubules.  They  will  be 
referred  to  under  Gout. 

A  section  of  the  cortex,  made  j)arallol  to  the  surface  of  the  organ,  and 
stained  with  picrocarniine,  shows  considerable  invasion  by  fibrous  tissue. 
In  some  places  the  renal  lobule  has  disappeared,  and  the  glomeruli  are 
represented  by  little  spheres  of  a  pale  rose  colour.  Islands  and  bands  of 
fibrous  tissue  are  found  round  the  tubes,  the  gloraeruh,  and  the  vessels. 

Tlie  glomeruli  show  enoi-mous  thickening  of  their  capsule,  which  is  itself 
surrounded  by  a  thick  fibrous  zone.  Between  the  capsule  and  the  vascular 
tuft  flattened  cells  and  fibrous  bundles  are  found.  The  glomerular  tuft  is 
atrophied  and  fibrous,  the  arterioles  are  in  part  obliterated,  and  the  afferent 
and  efferent  arteries  are  affected  with  endoperiarteritis.  Of  certain 
glomeruU  there  is  only  a  trace  left.  Every  element  has  disappeared  from 
their  interior,  and  they  blend  with  the  surrounding  connective  tissue. 
Hyaline  degeneration,  which  has  a  lardaceous  appearance,  is  frequently  seen. 
The  membrana  propria  of  the  tubuh  contorti  is  sclerotic,  and  some  of  the 
oanalicuh  are  much  reduced  in  cahbre.  The  changes  seen  in  nephritis  with 
enlarged  kidney  may  be  met  with  here  (Cornil).  When  the  epithehum  of 
the  convoluted  tubules  has  disappeared,  it  is  replaced  by  cubical  cells, 
which  at  times  fill  the  lumen  of  the  tubule  (Kelsch).  Many  tubules  are  filled 
with  granular  or  waxy  casts,  while  others  have  almost  disappeared,  and 
are  only  indicated  by  an  islet  of  round  cells. 

Theories. — There  are  many  theories  to  explain  the  anatomical  process  in 
the  small  granular  kidney,  according  as  the  lesion  is  held  to  begin  in  the  connec- 
tive tissue,  the  arteries,  the  glandular  tissue,  or  these  different  parts  together. 
According  to  the  first  theory,  the  process  is  said  to  commence  in  the 
interstitial  connective  tissue.  In  1850  Traube,  following  Beer,  ascribed  the 
principal  role  in  nephritis  to  the  connective  tissue  of  the  Iddneys,  and 
stated  that  Bright's  disease  was  the  result  of  an  interstitial  inflammatory 
process  ;  that  the  changes  in  the  glandular  epithelium  of  the  kidneys  were 
consequent  on  the  slow  alteration  in  the  connective  tissue ;  and  that  the 
sclerotic  process,  following  its  natural  course,  ended  in  atrophy  of  the  kidney. 
According  to  the  second  theory,  the  lesions  of  the  small  contracted 
kidney  were  said  to  be  a  local  form  of  general  arterio-sclerosis.  Arterio- 
sclerosis had  been  described  by  Sutton  and  Grull  under  the  name  of  arterio- 
capillary  fibrosis,  but  their  description  (1872)  had  been  preceded  by  Lan- 
cereaux's  work.  The  walls  of  the  small  vessels  undergo  a  transformation, 
which  is  not  due  to  hyaline  degeneration,  as  Sutton  supposed,  but  rather 
resembles  the  lesions  of  arteritis.  These  changes  in  the  small  vessels  are 
sometmies  associated  with  atheroma  of  the  larger  arteries. 


1104  TEXT-BOOK  OF  MEDICINE 

<Te)ieral  arterio-sclerosis  is  said  to  be  the  primary  trouble,  and  to  cause 
arterio-sclerosis  of  tbe  kidneys,  fibrous  hypertrophy  of  the  heart,  cirrhosis 
of  the  hver,  and  the  multiple  haemorrhages  (cerebral  or  retinal),  which  are 
so  common  in  this  form  of  Bright's  disease. 

This  theory  of  general  arterio-sclerosis,  which  has  been  confirmed  by  many 
post-mortem  examinations,  does  not  explain  all  the  cases  of  nephritis  in  which 
the  arteries  are  chiefly  afiected — e.g.,  Brault  speaks  of  a  young  man  who  suc- 
cumbed to  sclerotic  nephritis.  The  lesion  was  entirely  confined  to  the  kidneys 
and  to  the  heart,  arterio-sclerosis  and  atheroma  being  elsewhere  absent. 

The  third  theory  holds  that  the  small  contracted  kidney  is  the  result  of 
epithehal  cirrhosis.  Charcot,  relying  on  experiments  (ligature  of  the 
ureter)  and  on  the  renal  changes  produced  by  the  elimination  of  lead,  held 
that  interstitial  nephritis  belonged  to  the  class  of  visceral  cirrhoses.  "  The 
epithelial  change,  which  is  due  to  irritation,  and  is  a  primary  and  necessary 
fact,  reveals  itself  anatomically  by  the  return  of  the  cells  to  the  embryonic 
state ;  the  ■  interstitial  lesion,  the  consequent  fact,  also  reveals  itself — in 
the  initial  phases,  at  least — by  the  production  of  embryonic  tissue.  .  .  ." 
This  theory  of  epithehal  cirrhosis  and  the  return  of  the  cells  to  the  embryonic 
condition  is  no  longer  held  (Letulle). 

These  theories  seek  to  explain  the  production  of  the  smaU  kidney.  It 
would  be  wrong  to  admit  or  to  reject  them  systematically.  It  is  probable 
that  several  of  these  processes  are  predominant  or  concomitant,  according 
to  circumstances.  As  Brault  has  said,  the  expressions  "  glandular," 
"  arterial,"  and  "  interstitial "  nephritis  are  inexact ;  and  I  am  of  the  same 
opinion.  One  process  is  not  necessarily  subordinate  to  the  other.  They 
go  on  together  as  the  result  of  the  same  cause.  "  This  cause  creates  the 
reaction  of  the  fibrous  tissue,  which  increases  by  prohferation,  whilst  the 
epithehum  of  the  tubules  is  destroyed.  A  slow  irritation  determines  the 
wear  and  tear  of  the  epithehum,  which  gradually  disappears,  while  the  con- 
nective tissue  develops  and  becomes  indurated.  "  The  well-known  ana- 
tomical picture  of  general  arterio-sclerosis  is  not  affected  by  the  preceding 
considerations,  but  the  interpretation  of  them  varies.  Instead  of  sub- 
ordinating the  lesions  of  the  kidneys  to  general  arterio-sclerosis,  it  is  more 
rational  to  subordinate  the  lesions  both  of  the  kidneys  and  of  other  organs 
to  one  prime  cause  (gout,  lead,  old  age,  heredity,  etc.).  "  Besides,"  says 
Brault,  "  the  importance  of  the  arterial  lesions  in  their  relation  to  the  con- 
tracted kidney  has  been  much  exaggerated." 

Symptoms. — Nephritis  with  atrophied  kidneys  has  a  very  slow  course, 
and  lasts  several  years.  Gldema  is  rare,  and  dropsy  of  the  serous  mem- 
branes is  exceptional.  On  the  other  hand,  the  minor  sjnnptoms  of  Brightism, 
such  as  dyspnoea,  headache,  epistaxis,  and  ocular  troubles  (haemorrhage  of 
the  retina),  are  frequent. 


DISIvASKS  OK  Tin;   KIDNKYS  llOr, 

Cardiiu:  trouhles  are  almost  constant,  and  oxannnation  of  the  heart 
geiiorally  nu-eals  liypertrophy  and  a  gallop  rhythm  (I'otain). 

Dyspnoea  is  frequent.  It  may  occur  in  the  form  of  severe  attacks  like 
those  of  asthma  ;  at  other  times  it  shows  the  Chevne-Stokes  rhythm. 

The  pulse  is  hard,  and  the  arterial  tension  is  high.  The  secretion  of 
urine  is  increased.  The  urine  is  pale.  Albumin  may  be  present  in  small 
amount,  or  may  be  absent.  The  urea  remains  at  its  normal  amount,  and  the 
other  substances  are  very  slightly  diminished.    The  urine  contains  some  casts. 

Death  frequently  follows,  with  symptoms  of  ursemia,  such  as  delirium, 
convulsions,  and  coma.  Cerebral  hasmorrhage,  hseraiplegia,  and  apoplexy 
are  frequent  complications,  due  to  the  rupture  of  the  cerebral  arterioles,  on 
which  miliary  aneurysms  are  present. 

Mixed  Nephritis. 

We  find  between  the  two  extreme  types  already  described  a  host  of 
intermediate  types,  which  constitute  the  most  frequent  form  of  Bright's 
disease. 

Pathological  Anatomy. — In  these  intermediate  types,  which  are  subject 
to  relapse,  the  kidneys  may  be  normal  or  enlarged,  but  are  generally  on 
the  road  to  atrophy.  The  kidney  may  be  nodidar,  granular,  fibrous,  or 
cystic,  and  of  a  whitish- yellow,  or  reddish  colour  in  these  intermediate 
t}^es  of  chronic  nephritis.  Compensatory  hypertrophy  is  sometimes  met 
with  (Chauf?ard,  Grasset).  The  capsule  is  adherent.  The  cortical  sub* 
stance  is  atropliied,  and  the  glandular  tissue  is  more  or  less  degenerated. 

The  histological  changes  described  in  the  previous  section  affect  to  a 
variable  extent  the  vascular,  glandular,  or  connective  tissues.  I  would, 
therefore,  merely  remark  that  the  association  or  the  alternation  of  these 
lesions  leads  to  the  most  varied  intermediate  types.  The  mischief  may 
commence  as  a  subacute  nephritis,  with  enlarged  kidneys  and  parenchy- 
matous changes,  while  the  fibrous  and  vascular  lesions  later  gain  the  upper 
hand.  In  some  cases  we  find  at  first  vascular  and  connective  tissue 
changes,  and  it  is  only  later  that  the  parenchymatous  lesions  modify  the 
nature  of  the  case.  These  cases  are  generally  of  the  intermediate  type  from 
the  start,  but  in  some  circumstances  they  are  only  the  sequel  of  the  forms 
described  in  the  preceding  sections.*  These  differences  depend  on  the 
nature  and  the  severit}^  of  the  causes  of  the  nephritis.  We  shall  return  to 
this  question  under  ^Etiologv. 

*  RajTiaud  has  quoted  a  case  wliich  proves  the  identity  and  the  succession  of  these 
lesions.  At  the  post-mortem  examination  of  a  woman  who  had  died  of  Bright's  disease 
at  the  age  of  forty-eight  years,  he  found  one  of  the  kidneys  enlarged  and  white  and  tbe 
other  kidney  granular  and  atrophied.  The  histological  examination  showed  that  the 
sclerosis  was  commencing  to  invade  the  enlarged  kidney  (Bartel's  "  Annotations  of 
Lepine,"  p.  673). 


1106  TEXT-BOOK  OF  MEDICINE 

Lesions  of  the  Heart — Hypertrophy.— While  the  heart  may  be  hyper- 
trophied  in  any  form  of  chronic  nephritis,  enlargement  is  absent  or  not  so 
marked  in  subacute  nephritis  with  enlarged  kidneys.  The  hypertrophy 
is  most  pronounced  in  nephritis  with  small  kidneys.  These  lesions  had  not 
escaped  Bright' s  notice.  He  thought  them  secondary  to  the  lesion  in  the 
kidneys,  and  he  sought  for  the  mechanism.  Later,  Traube  described  these 
lesions,  but  he  was  wrong  in  beHeving  that  they  were  only  present  in  inter- 
stitial nephritis,  and  he  simply  took  note  of  the  hypertrophy.  We  know  to-day 
that  cardiac  lesions  may  exist  in  all  forms  of  chronic  nephritis,  and  we  also 
know  that  the  lesions  do  not  always  show  themselves  by  hypertrophy  of  the 
heart.  I  would  lay  great  stress  on  this  point,  as  it  is  too  often  said  that 
the  heart  is  always  enlarged.  The  heart  may  be  smaller  than  normal,  and 
may  at  first  sight  appear  to  be  healthy,  but  yet  histological  examination 
shows  advanced  arterio-sclerotic  lesions.  I  have  recently  seen  a  case  of 
this  kind. 

The  renal  heart,  as  it  is  still  called,  is  generally  large.  It  may  be  enor- 
mous, but  in  some  cases  its  size  is  not  increased,  although  its  intimate 
lesions  are  very  pronounced.  The  hypertrophy  chiefly  afiects  the  left 
ventricle,  and  appears  apart  from  any  valvular  change,  thus  differing  greatly 
from  the  hypertrophy  present  in  lesions  of  the  mitral  and  aortic  orifices. 
Nevertheless,  the  heart  in  Bright' s  disease  may  present  both  its  own  proper 
lesions  and  also  chronic  endocarditis  of  the  aortic  and  mitral  orifices.  The 
right  ventricle,  the  other  parts  of  the  heart,  or  even  the  entire  organ,  may 
participate  in  the  hypertrophy,  and  dilatation  is  common. 

Histological  examination  reveals  two  forms  of  lesions — the  one  affecting 
the  vessels  and  the  interstitial  tissue,  the  other  affecting  the  muscle  fibre. 
In  a  section  of  the  muscuh  papillares  much  fibrous  tissue  is  sometimes  visible 
with  the  naked  eye.  Under  the  microscope  we  see  patches  of  fibrous  tissue, 
forming  a  kind  of  network  with  other  bands  from  the  arterioles  which  are 
attacked  by  peri-arteritis.  The  arterial  lesions  are  probably  the  starting- 
point  of  this  fibrous  invasion,  wherein  the  muscular  tissue  has  in  part  dis- 
appeared. In  other  parts  of  the  heart  we  find  hypertrophy  of  the  muscular 
tissue,  which  chiefly  leads  to  the  enlargement  of  the  heart.  The  hyper- 
trophy of  the  muscle,  on  the  one  hand,  and  the  arterio-sclerosis  on  the  other, 
may  be  combined  in  various  ways.  As  a  result  the  heart  may  be  enlarged 
or  normal,  while  the  size  of  the  organ  gives  no  information  as  to  the  real 
nature  of  the  intimate  lesions.  Very  marked  hypertrophy  may  coexist 
with  very  moderate  arterio-sclerosis,  and,  reciprocally,  the  arterio-sclerosis 
may  be  advanced,  while  the  heart  is  not  hypertrophied. 

The  pathogenesis  of  the  renal  heart  has  given  rise  to  numerous  discus- 
sions. Two  theories  exist :  the  one  supposes  that  the  hypertrophy  of  the 
heart  is  secondary  to  the  renal  mischief;  the  other  holds  that  the  cardiac 


DISEASES  0\f  TIIK  KIDNKYS  1107 

and  renal  lesions  are  independent  of  one  another,  and  arise  fi(Mii  a  eomiaon 
eause.  In  the  first  hypothesis  we  have  to  show  how  the  renal  Icsitjn  pro- 
duces the  cardiac  hypertrophy.  We  may  see  in  this  chain  of  morbid  events 
the  result  of  high  arterial  tension  (Potain).  Is  this  high  arterial  teasioii 
due,  as  Bright  believed,  to  the  incomplete  elimination  of  the  waste  pro- 
ducts of  the  urine  ?  The  answer  is  negative,  because  insufficient  elimination 
does  not  raise  the  intravascular  pressure  (Potain) ;  and,  furthermore,  this 
explanation  would  not  agree  with  the  fact  that  hypertrophy  is  more  common 
and  more  marked  in  interstitial  nephritis,  where  the  excretion  of  the  solid 
matter  in  the  urine  is  but  slightly  modified  (Senator).  Are  the  high  arterial 
tension  and  the  hypertrophy  of  the  heart  due  to  the  contraction  or  the 
obUteration  of  the  renal  arterioles  in  the  atrophied  kidneys  (Traube)  ? 
This  is  not  probable,  because  experiment  has  shown  that  the  renal  arteries 
may  be  ligatured  without  appreciable  increase  in  the  arterial  pressure  ;  and, 
on  the  other  hand,  clinical  cases  testify  to  advanced  cardiac  hypertrophy, 
while  the  kidneys  are  not  atrophied. 

According  to  the  second  hypothesis,  the  kidneys  and  the  heart  suffer 
simultaneously  from  the  action  of  one  cause.  According  to  Gull  and  Sutton, 
this  cause  is  the  sclerotic  thickening  (arterio-capillary  fibrosis)  of  the  arterioles 
and  capillaries.  This  change  is  said  to  have  a  twofold  action,  being  the 
origin  of  sclerosis  in  the  kidneys,  the  heart,  and  other  organs,  and,  on  the 
other  hand,  placing  in  the  general  circulation  an  obstacle  which,  by  raising 
the  arterial  tension,  is  said  to  cause  the  cardiac  hypertrophy.  Buhl  tries 
to  prove  that  the  hypertrophy  is  the  result  of  myocarditis,  which  is  both 
interstitial  and  parenchymatous,  and  of  degenerative  lesions  of  the  heart. 
He  adds  that  the  inflammations  of  the  heart  and  of  the  kidneys  are  con- 
temporaneous and  independent.  Debove  and  Letulle  also  think  that  the 
cardiac  hypertrophy  depends  upon  interstitial  myocarditis  with  sclerotic 
lesions,  but  in  their  opinion  the  nephritis  and  the  myocarditis  are  secondary 
to  general  arterial  fibrosis. 

The  hypothesis  which  subordinates  the  hypertrophy  of  the  heart  to  the 
lesion  of  the  kidneys  and  of  the  vessels  is  discussed  and  in  part  admitted 
by  Potain.  "  In  a  fair  number  of  cases  it  is  clear  that  the  nephritis  is 
primary,  and  the  hypertrophy  of  the  heart  is  secondary."  The  hypertrophy, 
adds  Potain,  might  be  the  result  of  exaggerated  tonicity  of  the  small  vessels — 
a  tonicity  of  which  the  kidneys  would  be,  by  reflex  action,  the  point  of  de- 
parture. Charcot  also  holds  that  the  hypertrophy  of  the  heart  is  consequent 
upon  the  lesion  of  the  kidneys.  It  might,  indeed,  precede  the  renal 
sclerosis  if  it  be  admitted  that  this  sclerosis  is  itself  preceded  by  some 
functional  trouble,  the  effect  of  which  is  to  Hmit  the  secretory  energy  of  the 
kidneys. 

•  In   some   ingenious   experiments    Strauss   Hgatured    one    ureter    in    a 


1108  TEXT-BOOK  0¥  MEDICINE 

gmnea-pig.  He  killed  the  animal  some  montlis  later,  and  found  the  following 
lesions  : 

Fibrous  atrophy  of  the  kidney  on  the  side  of  operation ;  kidney  hyper- 
trophied  on  the  opposite  side  ;  hypertrophy  of  heart,  chiefly  of  the  left 
ventricle  ;  myocardium  and  arterioles  healthy.  These  experiments  prove 
that  the  hypertrophy  of  the  heart  may  follow  on  the  renal  lesion,  and 
that  we  need  not  expect  a  special  change  in  the  myocardium  or  general 
arterio-sclerosis. 

In  my  opinion  we  must  divide  the  question.  The  lesions  of  the  heart  in 
Bright's  disease  are  of  two  kinds — muscular  and  arterio-sclerotic.  The 
muscular  fibres  in  the  vicinity  of  the  sclerotic  tissue  disappear,  but  at  other 
points  they  develop,  causing  the  hypertrophy  just  mentioned.  This  hj^er- 
trophyis  not  due  to  the  sclerotic  lesions,  but  to  the  increased  arterial  tension, 
which  depends  upon  the  more  or  less  general  arterio-sclerosis  and  the  con- 
traction of  the  small  vessels  which  is  so  common  in  Bright's  disease.  The 
fibrosis  of  the  heart  results  from  the  cardiac  arterio-sclerosis,  which  is 
merely  a  local  feature  of  a  generahzed  process.  It  is  certain  that  the  mus- 
cular lesions  and  the  arterio-sclerosis  of  the  heart  may  be  anterior,  parallel, 
or  posterior  to  the  development  of  the  lesions  in  the  kidneys. 

etiology. — In  a  general  way  the  infectious  diseases  (scarlatina,  syphilis, 
pneumonia,  influenza,  typhoid  fever,  mumps,  erysipelas,  diphtheria,  malaria, 
etc.)  and  puerperal  conditions  which  give  rise  to  acute  nephritis  may  con- 
tribute to  the  aetiology  of  chronic  nephritis.  If  the  reader  will  refer  to  the 
section  on  Acute  Nephritis,  he  wiU  find  the  action  of  the  microbes  and  of  the 
toxines  discussed.  In  these  various  cases,  which  form  the  first  category, 
chronic  nephritis  may  be  only  the  end  of  acute  or  subacute  nephritis.  As  a 
matter  of  fact,  acute  nephritis  (when  it  is  not  fatal)  may  end  in  various 
ways  :  some  cases  recover,  others  apparently  do  so,  but  the  fije  smoulders 
under  the  ashes.  Some  shght  symptoms  prove  that  the  process  is  not  yet 
extinct,  untU  the  nephritis  ends  in  the  chronic  stage.  Others,  again,  pass 
insensibly  from  the  acute  to  the  subacute  stage,  and  end  in  chronic  nephritis. 

In  the  second  category  I  place  cases  which  are  chronic  from  the  outset. 
Gout  and  plumbism  hold  the  first  place  in  this  category.  I  also  include 
arterio-sclerosis;  but  here  we  must  remember  that  partial  or  general  arterio- 
sclerosis depends  on  a  primary  cause — viz.,  gout,  syphilis,  alcohohsm,  in- 
fectious diseases,  advancing  age,  or  heredity.  Heredity  plays  a  considerable 
part  in  the  pathogenesis  of  nephritis,  as  in  all  chronic  diseases ;  and  by 
heredity  I  mean  aU  the  hereditary  factors  which  make  the  organ  more 
vuhierable  or  which  favour  auto -intoxication. 

We  may  include  in  the  third  category  cases  of  nephritis  of  dyscrasic 
origin.  The  idea  of  Bright's  disease  as  a  primary  dyscrasia  with  secondary 
renal  changes  is  very  old,  seeing  that  Bright  himself  stated  it.     We  may  place 


DISEASKS  OF  TlIK  KIDNKYS  1  Hj'j 

nephritis  by  auto-intoxication  in  tiie  group  of  dyscrasic  causes,  the  renal 
lesion  being  due  to  the  elimination  of  excess  of  tyrosin  and  of  other  poisonous 
extractives,  due  to  insuflicient  oxidation  (diseases  of  the  hver),  too  rapid 
combustion  (fevers),  impaired  nutrition,  or  chlorosis. 

In  short,  a  person  may  become  a  sufferer  from  Bright's  disease  in  many 
ways.  In  the  first  place,  an  attack  of  acute  nephritis  does  not  recover,  but 
passes  into  the  subacute  or  chronic  stage.  In  such  a  case  the  course  of 
events  is  clear.  In  the  second  place,  the  invasion  of  the  renal  mischief 
is  slow  and  insidious,  the  minor  or  major  s\Tnptoms  of  urinary  insufhciency 
being  present.  This  condition  obtains  in  gouty  persons  and  in  people 
suffering  from  gravel,  lead-poisoning,  or  arterio-sclerosis.  In  them  Bright's 
disease  makes  slow  progress,  and  acute  attacks  are  wanting.  The  renal 
atrophy  is  of  slow  development. 

In  the  third  place,  the  course  of  events  is  as  follows  :  An  individual 
has  previously  suffered  from  some  infectious  disease.  This  disease  (scarla- 
tina, diphtheria,  mumps)  has  affected  the  kidneys,  and  may  have  caused 
but  slight  and  transient  nephritis.  Although  the  trouble  may  have  been 
slight,  the  kidneys  are  none  the  less  affected,  and  the  results  may  long 
remain.  Another  person  has  also  been  attacked  by  some  infectious  disease 
(pneumonia,  typhoid  fever,  influenza,  syphilis,  malaria),  which  has  caused 
only  sUght  nephritis.  Although  the  lesion  appears  trifling,  the  kidneys 
are  none  the  less  damaged,  and  here,  as  in  the  preceding  case,  the  effect  may 
remain.  These  persons  whose  kidneys  have  been  infected  by  scarlatina, 
typhoid  fever,  influenza,  pneumonia  or  syphilis  are  liable  to  acute  relapses 
of  nephritis,  or  to  more  gradual  mischief,  which  ends  in  Bright's  disease. 
In  one  subject  the  renal  lesions  may  progress  slowly ;  the  symptoms  may 
remain  confined  to  what  I  have  called  "  the  minor  troubles  of  Brightism," 
and  do  not  end  in  uraemia.  Let  them,  however,  take  cold  or  become 
pregnant,  or  let  any  other  cause  supervene  which  severely  affects  the 
kidneys,  and  acute  mischief,  with  all  its  consequences,  will  appear. 

These  persons  are  most  Uable  to  Bright's  disease  if  they  are  also  in- 
temperate, or  if  their  hver,  through  auto-intoxication,  transmits  to  the 
urine  unchanged  waste  products.  They  may  also  suffer  from  gout,  and 
their  kidneys  may  be  damaged  by  ehmination  of  uric  acid ;  or,  again,  they 
may  show  early  arterio-sclerosis,  or  may  be  suffering  from  heredity.  It  is 
then  evident  that  they  are  in  the  best  possible  condition  to  faU  victims  to 
Bright's  disease. 

If  a  young  girl  suffering  from  the  condition  which  I  have  caUed  "  chloro- 
Brightism"  marry  too  early,  and  become  pregnant  on  one  or  more  occasions, 
she  is  more  hkely  to  show  nephritis  gra\ddarum  and  eclampsia. 

These  examples  prove  that  very  different  routes  may  lead  to  chronic 
nephritis.     Recovery  depends  on  the  nature  and  the  severity  of  the  cause. 

II.  •  71 


1110  TEXT-BOOK  OF  MEDICINE 

The  disease  may  remain  stationary  or  may  be  split  up  into  latent  and  acute 
periods.  It  may  not  go  beyond  "  Brigbtism,"  but  too  often  it  ends  in 
renal  insufficiency  and  fatal  uraemia.  The  onset  of  ursemia  may  occur  with 
large  granular  or  cystic  kidneys,  but  it  chiefly  depends  on  the  severity, 
quality,  and  combination  of  the  toxi-infectious  agents,  and  also  on  the  con- 
dition of  the  other  organs. 

Description  of  Bright's  Disease. — Some  years  ago,  at  a  period  when 
the  different  forms  of  Bright's  disease  had  been  artificially  separated,  it 
was  customary  to  describe  parenchymatous  and  interstitial  nephritis  as  two 
distinct  diseases,  and  some  writers  went  so  far  as  to  ask  for  which  form 
the  name  of  Bright's  disease  ought  to  be  reserved.  I  do  not  hold  this 
view  of  Bright's  disease.  Typical  cases  of  atrophic  interstitial  nephritis 
and  of  parenchymatous  nephritis  with  enlarged  kidneys  merit,  both  ana- 
tomically and  clinically,  the  description  given  above.  The  chief  interest 
of  the  question,  however,  must  not  be  centred  in  them.  I  shall,  therefore, 
describe  the  most  common  clinical  form  of  Bright's  disease  which  corre- 
sponds to  the  intermediate  types  of  chronic  nephritis.  We  may  find 
glandular  lesions  compHcated  by  interstitial  and  vascular  changes,  or  inter- 
stitial and  vascular  changes  comphcated  by  glandular  lesions.  In  our 
description  we  shall  follow  the  onset,  the  nature,  and  the  variations  of  the 
symptoms  and  comphcations  which  constitute  Bright's  disease. 

Onset. — In  some  cases  Bright's  disease  follows  an  attack  of  acute  ne- 
phritis. It  is,  however,  more  often  chronic  from  the  outset.  I  have  often 
verified  the  fact  that  a  case  of  Bright's  disease  regarded  as  one  of  rapid 
course  was  really  a  case  of  slow  evolution,  in  which  an  acute  stage 
had  supervened.  An  individual  who  has  always  considered  his  health 
to  be  good  asks  for  advice  concerning  trouble  which  has  affected  him  for 
the  past  few  weeks.  He  has  had  headache  and  vomiting  or  dyspnoea. 
(Edema  of  the  face  and  of  the  legs  has  appeared.  The  urine  contains  albumin 
and  casts.  At  first  sight  the  case  looks  hke  acute  nephritis  of  recent  date. 
On  minute  inquiry,  however,  if  we  look  for  the  symptoms  preceding  this 
acute  episode,  we  shall  find  that  some  six  months  or  more  ago  the  patient 
has  had  headaches,  which  he  calls  migraine.  He  has  often  suffered  from 
frequent  micturition,  dead  fijigers,  palpitation  of  the  heart,  cramp  in  the 
calves,  and  puffiness  of  the  eyehds.  When  he  blows  his  nose  in  the  morning, 
blood  is  found  on  the  handkerchief.  On  various  •  occasions  he  has  had 
buzzing  in  the  ears,  defective  hearing,  itching,  cryeesthesia,  electric  shocks, 
etc.  By  grouping  these  symptoms,  which  have  been  practically  unnoticed, 
we  can  reconstruct  the  disease  which  has  been  slowly  maturing,  until  the 
marked  symptoms  make  their  appearance. 

In  its  most  common  form,  then,  Bright's  disease  has  an  insidious  onset. 
During  a  period,  which  may  be  of  long  duration,  the  symptoms  are  appar- 


OrSKASKS  OF  THE  KIDNKYS  IIU 

ently  trifling,  and  as  their  origin  is  not  discovered,  numerous  errors  in  diag- 
nosis result.  Headache,  frequent  micturition,  slight  epistaxis,  palpitation, 
cramps  in  the  calves  of  the  legs,  breathlessness,  pains  in  the  loins,  tingUng 
in-  the  ears,  defective  hearing,  vertigo,  visual  troubles,  itching,  dead  fingers, 
cryaesthesia,  and  digestive  troubles,  may  be  temporary  or  permanent,  and 
isolated  or  associated.  They  may  appear  and  then  disappear  for  a  long  time 
before  oedema  and  other  urgent  symptoms  of  Bright' s  disease  make  their 
appearance.  During  this  chronic  state,  which  is  intermediate,  as  it  were, 
between  health  and  disease,  acute  attacks  supervene,  and  are  characterized 
by  asthma-hke  dyspnoea ;  by  headaches,  which  resemble  those  of  syphilis ; 
by  acute  palpitation,  such  as  occurs  in  diseases  of  the  heart  and  of  the  aorta ; 
by  digestive  troubles,  such  as  we  find  in  ulcer  of  the  stomach ;  and  by  oedema 
of  the  face  and  the  Hmbs,  which  gives  a  useful  clue  to  the  diagnosis.  These 
acute  attacks  are  wrongly  taken  for  the  onset  of  the  disease. 

Minor  Symptoms  of  Brightism. — Under  this  name  I  would  include  the 
apparently  shght  symptoms  which  may  mark  the  onset  or  may  be  present  at 
any  stage  of  Bright' s  disease. 

1.  PoLLAKiURiA,  POLYURIA. — Amongst  the  urinary  troubles  pecuhar  to 
Bright's  disease  we  find  excessive  frequency  of  micturition.  In  chronic 
nephritis  the  patient  may  urinate  six  times  in  the  night,  or  ten  times  in 
the  twenty-four  hours.  The  desire  may  be  imperative,  and  the  quantity 
at  each  evacuation  is  small.  The  extreme  frequency  of  micturition  is  not 
always  due  to  excess  of  urine  (polyuria),  because  the  quantity  is  often 
below  the  average. 

There  are  two  distinct  and  independent  urinary  troubles  in  Bright's 
disease  :  the  one,  polyuria,  is  a  trouble  of  secretion,  and  concerns  the 
kidneys ;  the  other,  pollakiuria,  is  a  trouble  of  excretion,  and  concerns  the 
bladder.  It  is  indeed  remarkable  that  in  many  cases  the  pollakiuria 
precedes  the  polyuria. 

Although  these  troubles  are  dissociated  by  most  contemporary  writers, 
they  were  formerly  united  under  the  term  "  polyuria."  This  is  incorrect, 
since  polyuria  deals  only  with  the  secretory  trouble.  The  confusion  arose 
from  the  fact  that  we  had  only  one  word  for  two  symptoms.  The  frequency 
of  micturition  constitutes  an  independent  symptom  of  importance.  It 
was,  therefore,  necessary  to  give  it  a  distinctive  name,  and  I  have  proposed 
the  term  "  pollakiuria."  Polyuria  will,  then,  be  used  to  indicate  abundance 
of  the  secretion,  and  pollakiuria  will  be  reserved  for  frequency  of  mic- 
turition. 

Pollakiuria  may  appear  early  or  late.  In  the  former  case  it  is  an  early 
symptom  of  Bright's  disease.  It  appears  alone  as  a  precursory, symptom, 
but  more  often  it  is  associated  with  the  other  symptoms  of  Brightism. 
Pollakiuria  appears  late  in  certain  cases.     At  times,  especially  in  women, 

71—2 


1112  TEXT-BOOK  OF  MEDICINE 

it  is  painful.  Two  patients  in  my  wards  showed  this  pecuharity.  They 
suffered  from  excessive  poUalduiia.  The  quantity  of  urine  at  each  mictu- 
rition only  amounted  to  a  spoonful  at  most,  and  the  pain  supervened,  not 
at  the  moment  of  emission,  but  as  soon  as  micturition  ended.  The  pain  was 
acute,  and  had  aU  the  characteristics  of  spasm  of  the  neck  of  the  bladder. 
It  usually  lasted  for  some  minutes,  and  reappeared  after  each  micturition 

Pollakiuria  is  no  doubt  due  to  exaggerated  excitabihty  of  the  vesical 
mucosa  or  muscle,  which  has  been  found  hypertrophied.  When  the  muscles 
of  the  body  of  the  bladder  are  alone  at  fault,  the  poUakiuria  shows  itseK 
by  more  or  less  frequent  and  imperative  desire  to  micturate.  When  the 
sphincter  is  affected,  the  emission  of  urine  is  often  followed  by  painful 
spasm.  I  cannot  explain  what  cause  acts  thus  on  the  excretory  apparatus 
in  a  disease  where  the  secretory  apparatus  seems  alone  to  be  affected.  Is 
it  due  to  some  change  in  the  composition  of  the  urine  ?  I  do  not  think 
so,  because  poUalduria  is  often  present,  while  examination  of  the  urine 
reveals  nothing  abnormal.  Are  we  to  invoke  a  reflex  action  which  starts 
in  the  kidneys  and  ends  in  the  bladder  ?  It  is  possible,  but  proof  is 
lacking. 

Polyuria,  or  excessive  secretion  of  urine,  is  chiefly  seen  in  interstitial 
nephritis,  and  from  the  first  the  patient  may  pass  several  pints  of  urine 
daily.  In  parenchymatous  nephritis  the  quantity  of  urine  is  notably 
diminished,  and  may  not  be  more  than  30  to  40  ounces.  Variations,  how- 
ever, are  frequent,  and  the  quantity  may  be  normal  or  increased. 

2.  Dead  Fingers. — This  symptom  of  Bright's  disease  has  never  been 
noted  by  other  writers.  The  sensation  is  similar  to  that  experienced  when 
the  hands  are  exposed  to.  great  cold.  The  patients  complain  of  tinghng, 
pains,  and  cramps  in  the  fingers.  In  some  cases  the  tips  of  the  fingers  grow 
bloodless,  pale,  and  numb.  This  condition  lasts  for  some  time,  and  returns 
in  fits.  This  symptom  affects  the  fingers  and  rarely  the  toes.  It  is  present 
sometimes  in  one  finger,  sometimes  in  another,  or  in  several  fingers.  It  may 
be  symmetrical.  It  is  not  common  for  all  the  fingers  to  be  affected.  This 
symptom  is  seen  in  all  stages  of  Bright's  disease.  I  have  seen  it  as  an  initial 
symptom  when  the  other  symptoms  were  absent  or  shght.  The  trouble 
which  I  have  just  described  sometimes  invades  the  whole  hand  or  the  forearm. 
This  is  the  symptom  of  the  dead  arm.  Asphyxia  of  the  hmbs,  which  has 
been  seen  (very  rarely,  it  is  true)  in  the  course  of  Bright's  disease,  might 
be  reconciled  with  these  facts. 

3.  Auditory  Troubles. — Until  I  first  called  attention  to  the  auditory 
troubles  of  Bright's  disease,  this  symptom  had,  I  beheve,  remained  un- 
noticed.*   From  subsequent  observation  I  now  consider  the  auditory  much 

*  Dieulat'03',  France  Med.,  1877,  No.  16.  Gaz.  Hebd.,  1873,  No.  4.  Domergue, 
"Troubles  Nulritifs  dans  la  Maladie  de  Bright,"  These  de  Paris,  1881,  No.  13. 


DISEASES  OK  Till':  KIDXEVS  111:? 

more  fio(|ucnt  tliaii  the  ocular  troubles.  They  are  of  variou.s  ]dn<h.  They 
often  take  the  form  of  tinkling  or  huzziug  in  one  or  both  ears,  accoinpanied 
or  followed  by  defective  hearing.  As  a  nilc,  the  half -deafness  is  transient, 
and  subject  to  recurrences.  It  is  limited  to  one  ear.  The  deafness  is  rarely 
complete.  These  auditory  troubles  may  be  painless  or  be  accompanied  by 
pains  in  the  ears  and  the  face.  They  are  due  to  various  causes.  We  .sotne- 
times  find  on  examination  of  the  ear  sclerosis  of  the  membrane,  catarrh 
of  the  drum,  abnormal  vascularity  of  the  malleus,  and  haemorrhage  into  the 
mucosa  of  the  t}Tnpanum.  In  other  cases  the  lesions  are  not  appreciable, 
and  the  auditory  troubles  are  said  to  result  from  oedema  of  the  auditory 
nerve. 

Bonnier,  struck  with  the  frequency  of  auditory  troubles  in  B right's 
disease,  has  shown  that  the  ill-defined  syndrome  called  Meniere's  vertigo  is 
often  only  a  symptom  of  Bright' s  disease.  Vertigo,  therefore,  deserves  to 
rank  amongst  the  minor  symptoms  of  Brightism.  In  some  cases  the  vertigo, 
after  resisting  the  treatment  employed  in  Meniere's  disease,  has  yielded 
to  milk  diet,  Uke  most  of  the  other  minor  symptoms  of  Brightism. 

4.  Itching  — This  symptom,  which  has  been  ignored  by  some  writers, 
is  frequent,  especially  in  women.  The  itching*  may  not  differ  from  ordinary 
pruritus.  It  may  affect  different  parts  of  the  body,  and  last  for  several 
days  or  weeks.  In  some  cases  it  is  so  severe  as  to  deprive  the  patient  of 
all  sleep.  The  patients  say  that  "  they  scratch  themselves  till  they  bleed 
or  rub  off  the  skin."  The  cause  of  the  itching  is  not  clear,  for  I  do  not 
refer  to  cases  where  a  cutaneous  eruption  is  present.  Rosenstein,  who  has 
noticed  this  symptom,  sets  it  down  to  ursemia.  This  explanation  does  not 
suffice  to  solve  the  problem.  It  has  been  suggested  that  excretion  of  urea 
by  the  skin  was  the  cause  of  the  itching.  It  is  possible,  but  I  have  seen 
sweating  of  urea  without  itching.  In  another  variety  the  itching  is  com- 
pared by  patients  to  the  tickUng  provoked  by  hairs  falhng  on  to  the  neck, 
the  chest,  or  the  back.  In  a  third  variety  the  patients  compare  the  itching 
to  the  tickling  caused  by  an  ant.  The  itching  appears  at  all  stages  of  the 
disease.  In  some  cases  it  appears  at  the  onset,  and  is  then  of  importance 
in  diagnosis. 

5.  Cramps  in  the  Calves  of  the  Legs  are  common  in  Bright's  disease. 
The  spasms  may  occur  in  the  muscles  of  the  shoulder  and  the  neck,  and  in 
some  cases  opisthotonos,  with  or  without  articular  pains,  has  been  seen 
(Jaccoud).  These  latter  forms  are  exceptional,  but  cramps  in  the  calves 
are  an  earlv  and  almost  constant  comphcation  of  Brightism,  Patients 
say  the  cramps  are  so  painful  as  to  wake  them  up.  They  may  return  several 
times  during  the  same  night,  or  several  nights  following,  and  may  lead  to 
insomnia. 

*   Dienlafoy,  Oaz.  Hebd.,  1SS2,  No.  20.     Mathieu,  These  de  Paris,  1S82. 


1114  TEXT-BOOK  OF  MEDICINE 

For  some  years  my  attention  has  been  drawn  to  local  cramp  in  the 
sterno-mastoid  muscle,  I  have  called  it  torticollis  in  Bright's  disease. 
I  described  two  remarkable  instances  in  my  lectures.  It  takes  the  form 
of  a  very  painful,  permanent  contraction  in  certain  muscles  of  the  neck. 
The  pain  is  not  as  a  rule  spontaneous,  but  is  provoked  by  the  least  move- 
ment. It  differs,  therefore,  from  the  cramps,  which  are  spontaneous, 
and  last  but  a  few  moments.  I  have  repeatedly  succeeded  in  curing  the 
torticolHs  by  milk  diet.  The  intercostal  muscles  may  also  be  the  seat  of 
painful  cramps.  Writer's  cramp,  in  one  of  its  forms,  may  have  its  origin 
in  Bright's  disease  (Bonnier). 

6.  Epistaxis  assumes  various  forms  in  Bright's  disease.  We  see  pro- 
fuse epistaxis,  which  I  shall  describe  later,  and  also  haemorrhage,  which 
appears  with  the  onset  of  uraemia.  I  refer  here  to  the  shght  epistaxis  which 
appears  very  early  in  the  disease,  especially  in  the  morning.  I  have  called 
it  the  "  matutinal  epistaxis  of  Brightism." 

7.  Cry^sthesia. — Another  symptom  to  which  I  attach  some  impor- 
tance is  the  great  sensitiveness  to  cold  of  patients  suffering  from  Bright's 
disease.  They  suffer,  according  to  their  own  expression,  from  "  cold  skin 
and  cold  under  the  skin."  They  wear  a  superabundance  of  warm  clothing, 
and  are  wont  to  rub  their  thighs  and  knees  to  drive  away  the  cold.  They 
are  continually  warming  their  feet,  which  "  are  Uke  icicles,"  but  yet  all 
these  precautions  often  fail  to  keep  them  warm.  They  do  not  "  shiver 
with  cold."  The  hypersesthesia  to  cold  is  not  only  caused  by  contact  with 
cold  objects,  but  is  spontaneous,  Hke  the  sensation  of  dead  fingers,  and 
independent  of  the  surrounding  temperature.  In  order  to  emphasize  this 
symptom  in  patients  with  Bright's  disease,  I  have  proposed  the  term 
of  "  crysesthesia," 

The  trouble  usually  affects  the  lower  hmbs — the  knees,  thighs,  feet,  and 
the  region  of  the  kidneys,     I  have  pubHshed  some  typical  cases.* 

8.  Amongst  the  minor  symptoms  of  Brightism  I  would  mention  electric 
shocks,  which  chiefly  occur  during  sleep.  Since  my  attention  was  called 
to  this  sjrmptom,  which  has  not  been  previously  described,  I  have  found  it 
frequently.  The  patient  who  is  about  to  go  to  sleep,  or  has  just  gone  to 
sleep,  is  suddenly  awakened,  as  it  were,  by  an  electric  shock.  The  shock, 
which  is  single  and  violent,  is  really  a  convulsion.  It  represents,  in  a  rudi- 
mentary way,  the  convulsive  attacks  of  uraemia.  The  electric  shock,  hke 
most  of  the  other  symptoms  just  described,  may  appear  alone,  and  may 
therefore  pass  unnoticed,  unless  care  is  taken  to  look  for  it. 

9.  Sign  of  the  Temporal  Artery. — I  have  noticed  that  in  many 
people  with  Bright's  disease  the  temporal  artery  is  hard,  tortuous,  and 

*  "  Contribution  a  TEtude  Clinique  et  Experimentale  de  la  Maladie  de  Bright  sans 
Albnminurie  "  {Soc.  Med.  des  Hopit.,  1886). 


DISEASES  OF  Til K  K IDXEVS  1 1  1  '> 

dilated.  This  is  the  sign  of  the  temporal  artery.  The  diHtendod  artery 
is  readily  felt,  as  it  pursuos  its  tortuous  course  undor  the  skin.  The  con- 
dition is  not  due  to  atheroma,  but  to  excess  of  arterial  tension,  which  affects 
the  whole  arterial  system.  The  sign  is  more  evident  in  the  temporal  artery, 
because  of  its  superficial  situation.  The  tension  in  the  vessel  varies  from 
one  day  to  another.  Post-mortem  examination  of  several  ca-ses  from  mv 
wards  has  shown  that  the  condition  is  not  atheromatous. 

10.  I  have  often  noted  loss  of  the  senses  of  smell  and  taste  in  patients 
with  Blight's  disease. 

The  above  symptoms  form  the  minor  signs  of  Brightism.  They  may 
exist  at  all  stages  of  the  disease,  and  are  of  importance  because  thev 
often  give  a  clue  when  oedema,  albumin,  and  symptoms  of  uraemia  are 
wanting. 

(Edema  and  Serous  Effusion. — The  oedema  generally  commences  in 
the  face,  but  it  is  not  possible  to  assign  a  reason  for  this  fact.  The  patient, 
on  awakening,  finds  that  his  eyeUds  are  swollen.  As  the  face  is  shghtly 
puffed,  it  might  appear  as  if  the  patient  had  grown  fat.  The  oedema  mav 
be  limited  to  the  malleoh,  or  may  involve  the  legs,  the  thighs,  the  scrotum, 
and  the  labia  majora,  and,  according  to  circumstances,  it  may  take  months 
to  become  general.  It  is,  however,  rare  in  chronic  nephritis  to  find  as  much 
anasarca  as  in  acute  nephritis.  In  certain  cases  the  oedema  is  limited  to 
a  single  organ  (pulmonary  or  laryngeal  oedema).  It  has  been  hmited  to 
the  prepuce  (Rosenstein),  the  spermatic  cord  (Finger),  or  to  one  side  of  the 
face  or  the  bod}'  (Potain). 

In  cases  of  interstitial  nephritis  oedema  appears  late,  and  is  transient. 
It  may  be  limited  to  the  eyehds,  the  face,  or  the  malleoli,  whilst  it  appears 
earher  and  is  more  extensive  and  lasting  in  parenchymatous  nephritis, 
when  it  causes  not  only  anasarca,  but  also  effusions  into  the  serous  ca\'ities. 
This  distinction  is  true,  but  it  is  not  absolute.  Thus,  a  patient  may  have 
interstitial  nephritis  without  dropsy,  when  superacute  oedema  of  the  lung 
supervenes. 

When  the  oedema  is  recent,  the  tissues  are  white,  soft,  and  pit  on  pressure. 
In  the  long-run,  however,  the  tissues  become  thickened,  especially  in  the 
legs.  Because  the  oedema  is  sometimes  very  slight,  we  must  not  assume  that 
it  is  absent.  I  am  convinced  that  oedema  is  rarely  absent  during  the  course 
of  nephritis.  It  must,  however,  be  looked  for.  The  marks  left  by  the 
stethoscope  on  the  thorax,  the  folds  formed  by  the  bedclothes  on  the  skin 
of  the  face,  the  depression  caused  by  spectacles  at  the  root  of  the  nose, 
will  at  times  indicate  oedema,  which  would  otherwise  be  unnoticed. 

CEdema  of  the  viscera  and  serous  effusions  may  be  di\"ided  as  follows  : 
Out  of  406  fatal  cases  (Frerichs  and  Rosenstein)  we  find  :  Hydrothorax 
and  pleurisy,  82  ;   hydropericardium,  21  ;  hydrocephalus,  75  ;  pulmonary 


1116  TEXT-BOOK  OF  MEDICINE 

cedema,  115  ;  oedema  of  the  glottis,  4.  The  fluid  difiers  sensibly  from  the 
serum  of  the  blood.  It  is  more  rich  in  water,  but  contains  less  albumin 
and  mineral  salts,  and  more  chloride  of  sodium.  Fibrin  is  absent,  which 
proves  that  in  such  cases  of  oedema  we  are  not  deahng  with  a  simple  transu- 
dation of  serum,  as  Jaccoud  has  clearly  shown. 

Pathogenesis  of  CEdema — Pre-oedema — Retention  of  Chlorides. — What 
are  the  causes  of  oedema  in  Bright's  disease  ?  It  was  long  said  to  depend 
upon  the  loss  of  albumin  from  the  blood  (hypo-albuminosis),  but  we 
are  now  less  certain  of  this  fact.  It  is  sufficient  to  quote  cases  of  acute 
nephritis  in  which  anasarca  and  albuminuria  appear  together.  Further- 
more, how  are  we  to  reconcile  this  hypothesis  with  cases  in  which  the  ana- 
sarca is  limited  to  one  side  of  the  body  (Potain)  ?  Hydrsemia,  or  an  increase 
in  the  watery  portion  of  the  blood,  has  been  suggested ;  but  the  experiments 
of  Bernard  have  failed  to  prove  this  theory.  Lecorche  supposes  that 
the  oedema  is  due  to  atony  of  the  heart  muscle,  but  we  see  every  day  renal 
oedema  (scarlatinal  and  syphilitic  nephritis)  in  which  the  heart  takes  no  share, 
and,  besides,  renal  oedema  does  not  behave  like  cardiac  oedema.  Can  the 
oedema  be  due  to  paralysis  of  the  capillaries  (Frerichs)  ?  Is  a  reflex  action 
transmitted  from  the  kidneys  to  the  smaller  vessels  by  their  vasomotor 
nerves  (Potain)  ? 

The  pathogenesis  of  oedema  in  Bright's  disease  seemed  for  a  long  time 
to  defy  explanation.  Physiology  could  not  show  us  how  simple  renal 
lesions  could  produce  a  condition  of  oedema.  The  knowledge  of  the  laws  of 
isotonic  solutions,  the  view  that  chloride  of  sodium  plays  the  chief  part  in 
maintaining  the  osmotic  equilibrium  in  these  solutions,  had  naturally  led 
to  the  hypothesis  that  retention  of  this  salt  in  certain  tissues  might  attract 
water  from  the  organism,  and  cause  oedema  in  them. 

Cohnstein,  by  injecting  chloride  of  sodium  into  an  animal,  found  that 
the  total  amount  of  this  salt  reached  its  maximum  at  first  in  the  blood  and 
then  in  the  lymph. 

Theaulon  expressed  the  opinion  that  the  water  in  certain  cases  of  cedema 
is  attracted  to  the  tissues  by  reason  of  the  increased  molecular  concentra- 
tion of  the  lymph  plasma. 

HaUion  and  Carrion  have  produced  oedema  in  the  lungs  by  injection  of 
concentrated  salt  solutions  into  the  blood  of  animals. 

Reichel  has  shown  that  if  we  inject  salt  solution  in  a  person  suffering 
from  Bright's  disease,  the  absorption  of  the  Uquid  takes  place  slowly. 

Chaufiard,  in  a  case  of  infective  icterus,  where  the  urine  was  scanty  and 
poor  in  chlorides,  found  that  after  repeated  saline  injections,  the  weight 
of  the  patient  increased  by  the  amount  of  the  Hquid  injected.  Experimental 
oedema,  due,  -writhout  a  doubt,  to  the  retention  of  the  chlorides  in  the 
organism,  appeared  after  these  mjections. 


DISEASES  UF  TIIK  KII)>^EYS  IN, 

Arliard  and  Loeper,  thciefon*,  have  suggfsted  that  retention  of  the 
chloridos  may  play  a  part  in  the  production  of  tlie  oedema.  Widal  and 
Lemieire  deserve  the  cretlit  of  ehminating  theories  and  of  estahhshing 
facts.  They  proved  that  the  ingested  chloride  of  sodium  may  alone  lead 
to  the  a])pearance  of  (edema,  and  that  the  retention  in  the  kidnov  rcgiUates 
the  appearance  of  this  ceilema. 

In  1902  these  writers  proved  that  the  daily  ingestion  of  10  grammes 
of  cliloride  of  sodium  in  persons  with  epithelial  nephritis  will  cause  an 
"  experimental  ccdcma." 

The  appearance  of  cedema  depends  on  the  permeabiUty  of  the  kidney 
for  the  chlorides  at  the  moment  when  the  test  solution  of  chlorides  is  given. 
If  the  quantity  of  chloride  eliminated  is  equal  to  the  quantity  ingested, 
(edema  does  not  supervene,  because  the  salt  is  not  retained.  The  appear- 
ance of  the  oedema  depends,  furthermore,  upon  the  degree  of  chloride 
saturation  of  the  system,  or  upon  previous  lengthy  retention,  when  the 
supplementary  dose  of  salt  is  administered. 

It  is  especially  in  the  case  of  epithehal  lesions  that  the  ingestion  of 
chloride  of  sodium  causes  oedema,  as  Widal  and  Lesne  proved  in  1900  by 
cryoscoj)ic  examination  of  the  blood.  It  is  in  this  form  of  nephritis  that  the 
retention  is  the  most  marked.  Strauss  has  confirmed  the  facts  advanced 
by  Widal  and  Lemierre,  and  has  seen  oedema  diminish  when  polyuria,  and 
especially  polychloruria,  were  produced. 

The  appearance  of  the  oedema  is  preceded  by  a  stage  of  hydration  of 
the  system,  inappreciable  to  the  naked  eye.  Widal  and  Javal  have  called 
it  the  stage  of  pre  (Edema ;  and  the  physician  should  bear  in  mind,  that 
by  taking  the  weight  of  the  patient  daily,  it  is  possible  to  estimate  the  amount 
of  hydration. 

The  history  of  a  case  (Widal  and  Javal)  of  epithelial  nephritis,  in  which  salt  was  alter- 
nately allowed  and  excluded  from  the  diet,  is  interesting.  "  'J'he  weight  of  the  patient 
varied  between  12G  and  148  pounds.  When  on  a  diet  containing  salt,  his  weight 
exceeded  138  pounds,  and  oedema  appeared ;  inversely,  when  on  a  salt-free  diet  tlie 
weight  fell  to  136  pounds,  and  the  oedema  disappeared.  He  had,  therefore,  a  hydi'ation 
tolerance  of  13  pounds,  without  the  appearance  of  oedema.  The  scales  enabled  us  to 
foretell  almost  to  a  day  the  appearance  of  oedema,  by  indicating  the  daily  increase 
of  weight  during  the  entire  period  of  pre-oedema." 

Finally,  Widal  and  Javal  have  shown  that  salt  not  only  affects  the 
oedema,  but  also  the  albuminuria,  which  increases,  in  certain  cases,  in  a 
direct  ratio  to  the  hydration  of  the  system.  We  shall  see  later  to  what 
therapeutic  deductions  these  new  discoveries  may  lead. 

Albuminuria. — In  cases  of  interstitial  nephritis  the  urine  is  generally 
abundant,  and  the  proportion  of  albumin  is  very  small ;  it  may,  indeed, 
be  absent  for  a  time.  In  cases  of  epithelial  nephritis  the  urine  is  diminished, 
varies  in  shade,  and  may  contain  from  75  to  450  grains  of  albumin  in  twenty- 


1118  TEXT-BOOK  OF  MEDICINE 

four  hours.  The  urea,  uric  acid,  salts  of  potassium,  and  extractives  are 
generally  decreased.     The  specific  gravity  is  lowered. 

In  the  deposit  we  find  epithehal  debris,  red  and  white  corpuscles,  and 
various  casts.  The  leucocytes  are  more  numerous  during  an  acute  attack 
(Amozan).  They  are  of  the  mononuclear  and  polynuclear  types,  and 
"  their  respective  proportions  are  the  same  in  the  urine  and  in  the  blood  " 
(Achard).  Epithehal  and  blood  casts  are  rare  in  chronic  nephritis.  They 
are  chiefly  found  in  acute  nephritis.  The  hyaline  casts,  which  are  homo- 
geneous and  transparent  hke  glass,  are  unimportant.  The  eoUoid  casts 
are  rigid,  brittle,  and  of  a  yellow  straw  colour.  The  fibrinous  casts  are 
especially  frequent  in  hsematuria.  They  are  opaque,  and  formed  of  fibrinous 
clots.  The  granular  casts  diSer  from  the  fatty  ones  in  that  the  granulations 
are  formed  of  proteid,  and  not  of  fat.  As  regards  prognosis,  "  the  discovery 
of  granular  casts  is  of  value,  because  it  enables  us  to  follow  the  various 
stages  of  the  process."  The  composite  casts  are  formed  of  colloid  material, 
and  contain  the  debris  of  epithehal  ceUs  and  of  red  and  white  corpuscles. 
The  diagnostic  and  prognostic  value  of  casts  in  the  urine  has  been  some- 
what exaggerated.  Granular  casts,  however,  indicate  a  lesion  of  the 
kidneys,  as  they  do  not  exist  in  simple  albuminuria. 

The  urine  shows  weU-defijied  difEerences.  When  the  renal  lesions  are 
definitely  glandular  or  interstitial,  in  most  cases  the  lesions  blend,  so 
that  the  examination  of  the  urine  gives  every  possible  variety.  One  urine, 
for  example,  though  scanty,  contains  but  httle  albumin ;  another  urine 
contains  much  albumin,  though  the  secretion  is  increased.  During  the  past 
few  years  great  attention  has  been  paid  to  the  varieties  of  albumin  (serine, 
globuhn,  peptone)  and  their  significance  in  diagnosis.  This  interesting 
research  appears  so  far  to  have  given  no  positive  chnical  result,  and  we  shall 
see  later  that  albuminuria  has  no  longer  the  prime  importance  which  it 
formerly  possessed. 

The  causation  of  albuminuria  has  been  variously  explained.  The 
epithehal  changes  in  the  canahculi  have  been  blamed  (Lecorche).  Recent 
researches  seem  to  prove  that  the  transudation  of  albumin  takes  place  in 
the  glomerulus.  It  has  not  been  proved  that  it  is  the  increase  of  pressure 
in  the  glomerular  circulation  which  favours  the  passage  of  albumin  (Stokvis). 
The  important  point,  according  to  recent  research,  is  the  slowing  of  the  blood- 
stream in  the  capillaries  and  the  deficient  oxygenation  which  results  there- 
from. 

According  to  the  so-called  haematogenous  or  dyscrasic  theory,  the 
origin  of  the  albuminuria  is  the  primary  change  in  the  albuminoid  matter 
of  the  blood.  Jaccoud  put  forward  this  idea  :  The  albuminuria  recognizes 
as  its  cause  a  deviation  of  metabohsm  from  the  normal  type.  This  deviation 
consists  in  a  transient  or  lasting  disturbance  in  the  metabohsm  of  the 


DISEASES  OF  TFIK  KIDNEYS  111'.* 

albuiniiinid  matttu."     In  sLurt,  the  pathogenesis  of  alljuniiiiuria  in  not  yet 
dear. 

Hsematuria. — The  iirinn  in  Jiright's  disease  may  be  of  a  reddish  or 
brownish  colour.  SHght  or  aevere  hfflmaturia  may  api)ear  in  the  form  of 
attacks,  and  disappear  later.  More  rarely  the  hematuria  is  persistent. 
I  think  that  hajmaturia,  thought  to  depend  upon  interstitial  nephritis,  is 
frequently  due  to  nephritis,  comphcated  by  tuberculosis.  Nevertheless, 
certain  cases  of  nephritis,  with  hrcmaturia,  are  as  yet  unexplained.  In 
unilateral  nephritis  the  lesions  may  affect  the  glomerulus,  and  may  be  accom- 
panied by  shai-p  pain  (simulating  renal  calculus)  and  persistent  hematuria 
(simulating  tuberculosis),  while  the  ordinary  symptoms  of  Bright's  disease 
are  absent,  because  one  of  the  kidneys  is  performing  its  functions  properly. 
These  cases  are  benefited  by  nephrotomy,  which  relieves  the  pain  and  the 
haemorrhage  (see  Section  VI.). 

The  s}Tnptoms  which  we  shall  now  discuss,  in  part  blend  with  those  of 
uraemia.  Most  of  them  are  dependent  upon  the  insufficiency  of  the  urinary 
secretion. 

Headaches. — Headaches  may  occur  at  any  stage  of  Bright's  disease. 
They  often  appear  among  the  earhest  symptoms,  and  last  for  weeks  or 
months.  In  some  cases  they  are  acute,  and  simulate  the  syphiUtic  head- 
ache. In  others  they  are  called  "  migraine  "  by  the  patient.  The  pain  is 
often  much  increased  when  cerebral  symptoms  of  uraemia  appear.  Leeches 
to  the  temples  and  behind  the  ears  leheve  the  pain  in  some  cases. 

Respiratory  Troubles. — The  respiratory  distress  in  Bright's  disease 
may  be  continuous  or  intermittent,  as  the  following  examples  show :  Some 
patients  suffer  from  permanent  breathlessness,  -which  is  increased  by  exer- 
cise. At  first  sight  we  think  of  heart  mischief,  but  careful  examination 
shows  that  the  sufferers  have  chronic  nephritis,  which  does  not,  of  course, 
absolutely  exclude  cardiac  lesions.  The  distress  may  occur  in  the  form  of 
attacks,  which  are  mistaken  by  the  patient  for  asthma.  The  attack  may 
occur  by  night  or  by  day.  It  soon  becomes  acute,  and  returns  on  the  least 
movement.  It  may  recur  several  times  during  the  day,  or  only  reappear  at 
more  or  less  lengthy  intervals.  In  other  cases  the  respiration  takes  on  the 
Cheyne-Stokes  rhythm.  This  rhythm,  which  is  not  confined  to  the  dyspnoea 
of  Bright's  disease,  is  as  follows  :  The  respiratory  movements  are  at  first 
quickened  in  series.  They  then  become  slower,  and  stop  completely  for 
a  time.     After  the  pause  a  second  series  occurs. 

Dyspnoea  may  come  on  at  any  stage  of  Bright's  disease,  but  it  is  im- 
portant to  remember  that  the  distress  may  be  the  initial  symptom.  The 
attack  may  be  sudden,  hke  a  fit  of  asthma,  or  the  mischief  may  come  on 
gradually,  hke  chronic  bronchitis.  A  knowledge  of  these  facts  will  pre- 
clude the  despatch  of  a  patient  to  Mont-Dore  or  Cauterets  for  bronchial 


1120  TEXT-BOOK  OF  MEDICINE 

catarrh  and  empliysema  when  he  is  really  suffering  from  Bright's  diseaso. 
Amongst  the  rare,  though  dangerous,  respiratory  troubles  "we  must  mention 
superacute  oedema  of  the  lung  and  oedema  of  the  larynx,  which  have  been 
already  described. 

Cardiac  Troubles. — The  question  of  hypertrophy  of  the  heart  in  Bright's 
disease  is  most  comphcated.  The  h^-pertrophy,  which  may  be  considerable, 
chiefly  attacks  the  left  ventricle,  and  develops  apart  from  valvular  changes. 
The  entire  heart  may  be  affected,  and  dilatation  may  be  also  present.  When 
the  hypertrophy  is  marked,  as  in  interstitial  nephritis,  we  find  precordial 
bulging,  increased  cardiac  dullness,  and,  in  the  late  stages  of  the  disease, 
attacks  of  asystole.  The  cardiac  trotibles  are,  however,  not  pecuHar  to 
sclerosis  of  the  Iddneys.  They  exist  in  nearly  aU  forms  and  stages  of 
Bright's  disease.  They  may  precede  the  other  symptoms,  and  appear  as 
functional  troubles,  without  dilatation  or  hypertrophy  of  the  heart.  The 
patient  sufiers  from  palpitation,  precordial  distress,  and  dyspnoea.  He  feels 
his  heart,  and  complains  of  it. 

Auscultation  may  reveal  nothing.  Sometimes  the  closure  of  the  sigmoid 
valves  is  marked  (Traube),  indicating  the  high  arterial  tension.  A  hruit 
dje  galo'p  is  often  heard.  This  valuable  sign,  discovered  by  Potain,  may 
help  us  in  some  cases  to  recognize  Bright's  disease,  even  when  albumin  is 
absent.  The  hruit  de  galop,  though  more  frequent  in  interstitial  nephritis, 
may  exist  in  aU  forms  of  chronic  nephritis.  It  often  coincides  with  hyper- 
trophy of  the  heart,  but  yet  cardiac  hypertrophy  is  not  absolutely  necessary 
for  its  production.  It  is  made  up  of  three  periods — viz.,  the  two  normal 
sounds  of  the  heart  and  an  additional  sound  which  precedes  the  fijst  sound 
bv  a  short  interval.  Potain  thinks  that  the  third  sound,  which  forms  the 
gaUop  rh}H-,hm,  "  results  from  the  suddenness  with  which  the  dilatation  of 
the  ventricle  takes  place  in  the  presystohc  period."  It  is,  therefore,  said 
to  be  indirectly  "  the  consequence  of  the  excess  of  arterial  tension,"  so 
common  in  nephritis.  The  bruit  de  galop  is  not  continuous.  It  may  appear 
and  disappear.     It  has  its  maximum  of  intensity  in  the  ventricular  region. 

Valvular  lesions  are  common  in  the  course  of  Bright's  disease.  Mitral 
endocarditis  is  a  frequent  comphcation.  It  is  convenient  here  to  mention 
angina  pectoris,  in  which  lesions  of  the  aorta  may  or  may  not  be  present. 
In  two  of  mv  cases  the  attacks  of  angina  pectoris  were  for  some  time  the 
chief  trouble,  without  aortic  lesions.     Rondot  has  noted  several  cases. 

Digestive  Troubles. — Digestive  troubles  are  seen  in  all  stages  of  Bright's 
disease.  Some  patients  have  gastric  catarrh,  with  loss  of  appetite  and 
vomiting  of  mucous  liquid  ;  others,  though  not  experiencing  distaste  for 
food,  have  pains  which  simulate  ulcer  and  absolute  intolerance  of  the 
stomach,  so  that  aU  food  is  rejected.  In  some  cases  both  vomiting  and 
diarrhrsa  are  present.     These  gastro -intestinal  symptoms,  which  we  shall 


DISEASES  i)V  Tlll'i   KIDNEYS  llL'l 

discuss  liifcr  under  Urapmia,  are  found  iii  all  phjisivs  (»f  (he  disease.  Thov 
may  appear  as  the  first  sign  of  j-iriglit's  disease,  and  are  said  to  bo  due  to 
the  elimination  of  amnioniacal  products  by  the  gastnt-inteslinai  nunosa 
and  to  ulcerations  of  this  mucosa  (Treitz). 

Visual  troubles  (diminished  ainiteness  of  vision,  amblyojiia,  blindness) 
are  due  to  changes  in  the  fundus  oculi  or  to  uraBinia.  The  ophthalmoscope 
reveals  retinal  haemorrhages,  in  the  form  of  red  patches  around  the  papilla, 
whence  they  radiate  in  the  direction  of  the  bloodvessels,  and  whitish  patches 
of  inflammatory  origin.  These  visual  troubles  are  most  frequent  in  inter- 
stitial nephritis.  They  occur  at  all  stages,  and  may,  indeed,  be  present 
when  albumin  is  absent. 

Haemorrhage. — Haemorrhage  is  common  in  interstitial  nephritis. 

Eplstaxis  is  the  most  common  form  of  haemorrhage  in  Bright's  disease. 
I  have  already  mentioned  the  shght  matutinal  epistaxis  and  the  more 
abundant  bleeding  which  may  precede  or  accompany  uraemia.  The  present 
variety  of  epistaxis,  as  far  as  I  am  aware,  has  not  been  previously  described. 
For  emphasis,  I  have  called  it "  the  great  epistaxis  of  Bright's  disease,"  or 
"  epistaxis  d  tamponnement."  I  have  used  this  term  because  plugging  of 
the  nasal  fossae  is  often  required  to  arrest  the  bleeding.  It  must  not  be 
thought  that  this  epistaxis  comes  on  late  in  the  disease,  when  the  cachexia 
would  theoretically  favour  the  flow  of  blood.  The  important  feature  is 
that  this  epistaxis  appears  quite  early  in  Bright's  disease,  being  at  times  a 
prodromal  symptom.  I  am,  therefore,  accustomed  to  say  "  Brightism 
begins  with  epistaxis  a  tamfonnement." 

Some  years  ago  I  was  called  to  see  a  lady  of  about  fifty  years  of  age.  She  had  just 
been  taken  ill  with  profuse  epistaxis  that  nothing  would  stop.  I  found  her  pale  and 
alarmed  ;  the  blood  was  flowing  from  both  nostrils,  and  I  estimated  that  she  must  have 
lost  about  a  pint.  I  sent  for  Berger  to  plug  the  nares.  All  my  previous  attempts 
had  failed  completely,  but  the  epistaxis  stopped  after  plugging.  She  has  since  shown 
most  of  the  symptoms  of  Bright's  disease ;  that  she  has  been  able  to  ward  off  uraemia 
is  due  to  her  strict  milk  diet. 

Ten  years  ago,  with  Marquezy,  I  saw  a  man  of  fifty  years  of  age  ^vith  advanced 
Bright's  disease.  On  questioning  the  patient,  it  was  an  easy  matter  to  make  out  the 
course  of  events.  The  disease  seemed  to  date  back  about  eighteen  months,  but  c»  Uttle 
while  before,  the  man  who  was  suffering  from  Bright's  disease,  had  been  seized  with 
violent  epistaxis. 

In  1894  a  patient  suffering  from  Bright's  disease  was  sent  to  me  by  Grandhomme. 
Pollakiuria,  dead  fingers,  vertigo,  distension  of  the  temporal  artery,  bruit  de  galop, 
vomiting,  dyspnoea  were  the  symptoms  present.  It  was  a  case  of  chronic  interstitial 
nephritis  of  four  years'  duration.  He  said,  however,  that  these  symptoms  had  been 
preceded  by  terrible  bleeding  from  the  nose,  which  had  lasted  for  five  hours,  endangering 
liis  hfe.  The  bleeding  recurred  four  years  later  with  such  violence  that  it  necessitated 
plugging. 

Since  mv  attention  has  been  called  to  this  strange  variety  of  epistaxis 
m  Bright's  disease,  I  have  collected  several  cases  from  my  hospital  records. 


1122  TEXT-BOOK  OF  MEDICINE 

I  cannot  give  the  cause  of  tlie  bleeding,  but  we  must  remember  tlie  fact. 
If  a  healthy  person  is,  without  apparent  cause,  taken  ill  with  severe  epistaxis, 
and  the  nasal  fossae  do  not  present  any  lesion  capable  of  explaining  the 
haemorrhage,  we  must  think  of  Bright's  disease,  and  examine  for  distension 
of  the  temporal  artery,  pollakiuria,  dead  fingers,  cramps  in  the  calves  of 
the  legs,  and  a  hruit  de  galop,  even  if  we  do  not  find  albumin.  We  must 
put  the  patient  on  a  milk  diet,  for  he  is  either  suffering  from  Bright's  disease 
or  he  will  faU  a  victim  to  it. 

Cerebral  hsemorrhage  is  fairly  common  in  patients  sufiering  from  inter- 
stitial nephritis.  Grainger  Stewart  says  that  in  100  cases  of  cerebral 
haemorrhage  we  shall  find  interstitial  nephritis  fifteen  times.  In  several  cases 
observed  by  Bence  Jones  cerebral  haemorrhage  was  the  only  sign  of  inter- 
stitial nephritis,  which  had  reached  "the  atrophic  stage  without  its  existence 
having  been  previously  suspected.  This  statement  would  not  obtain  to-day. 
In  any  case,  cerebral  haemorrhage  and  its  habitual  symptoms — hemiplegia, 
aphasia,  and  apoplexy — are  seen  during  the  course  of  Bright's  disease. 

We  have  still  to  mention  meningeal  and  retinal  haemorrhages,  and 
haemorrhages  from  the  stomach,  bowels,  and  gums.  Broncho-pulmonary 
haemorrhage  is  not  uncommon  in  interstitial  nephritis.  I  have  succeeded 
in  collecting  eleven  cases.  In  the  great  majority  of  cases  post-mortem 
examinations  show  the  absence  of  tuberculosis ;  and  pulmonary  haemor- 
rhage directly  associated  with  Bright's  disease  must  not  be  confounded 
with  haemoptysis  in  phthisical  patients  who  are  sufiering  from  renal  lesions. 
I  have  often  seen  marked  haematuria  in  Bright's  disease,  and  on  two  occa- 
sions the  haematuria  was  preceded  by  profuse  epistaxis.  Some  years  ago, 
with  Peter,  I  saw  a  youth  suffering  from  Bright's  disease.  The  haemorrhage 
was  at  first  nasal  and  then  broncho -pulmonary.  The  bleeding  became 
general,  and  carried  off  the  patient. 

How  does  chronic  nephritis  cause  haemorrhage  ?  Are  vicious  composi- 
tion of  the  blood  and  reduction  in  the  albuminous  principles  at  fault  ? 
This  is  not  probable,  because  haemorrhage  is  more  frequent  in  interstitial 
nephritis  when  the  patient  is  losing  httle  albumin.  Is  there  some  change 
in  the  bloodvessels  ?  As  far  as  cerebral  haemorrhage  is  concerned,  the 
question  appears  to  be  settled,  because  in  this  case  the  most  common  lesion 
is  a  miliary  aneurysm.  As  regards  the  other  organs,  it  is  a  case  of  haemor- 
rhagic  necrosis,  due  to  uraemic  poisoning.  The  attacks  of  haemorrhage  may 
sometimes  mark  the  onset  of  Bright's  disease.  Leucocytosis  with  poly- 
nucleosis is  common  during  the  course  of  Bright's  disease ;  on  this  point 
the  experimental  researches  of  Dopter  and  Gourand  have  confirmed  clinical 
observations.  Eenon  and  Moncany  have  noted  that,  in  chronic  nephritis, 
the  leucocytosis  varies  directly  as  the  gravity  of  the  disease. 

Condition  of  the  Liver— Ascites. — In  speaking  of  serous  effusions  in 


DISEASES  OF  TIIK  KIDNEYS  11J3 

Hright's  disease,  I  omitted  to  speak  of  ascites,  becauBo  it  is  often  c'lfisociated 
with  hepatic  lesions.  They  vary  in  nature.  In  114  cases  of  Bright's 
disease  Kosenstein  found  the  following  lesions :  fatty  liver,  19 ;  cirrhotic 
liver,  15;  nutmeg  liver,  11  ;  simple  hypertrophy,  15  ;  amyloid  Uver,  5.  It 
may  be  asked  whether  the  hepatic  lesion  is  consequent  on  the  renal  lesion, 
or  whether  both  depend  on  the  same  cause.  In  one  of  my  cases  the  liver 
was  much  enlarged,  indurated,  and  painful.  Ascites  supervened.  I  with- 
drew 14  pints  of  effusion,  which  did  not  reappear. 

Cutaneous  Symptoms. — In  patients  suffering  from  Bright's  disease  the 
skin  is  dry  and  anaemic,  and  the  perspiration  is  deficient.  In  some  patients, 
however,  it  is  hmited  to  a  special  region — viz.,  the  face,  the  legs,  or  the  loins  ; 
in  others  it  is  general.  In  some  cases  the  parts  subject  to  cryassthesia  are 
chiefly  affected. 

We  find  at  times  (I  have  observed  the  fact  in  about  a  dozen  cases  of 
uraemia)  urea  in  the  sweat.  The  urea  is  deposited  in  crystals  on  the  face, 
on  the  forehead,  at  the  roots  of  the  hairs,  on  the  neck,  on  the  chest  in  the 
form  of  a  whitish  dust  analogous  to  hoar-frost.  I  consider  sweating  of 
urea  as  of  the  worst  possible  prognosis.  In  the  cases  I  have  seen  the  patient 
succumbed  in  a  short  time. 

Some  patients  with  Bright's  disease  suffer  from  ptyalism,  with  or  without 
stomatitis.     It  is  called  "  uroemic  sialorrhoea." 

Toxic  Inflammations. — We  have  seen  that  oedema  and  effusions  take 
a  large  share  in  Bright's  disease,  and  involve  the  periphery,  the  viscera 
(lungs,  lar}Tix,  brain),  the  serous  membranes  (hydrothorax,  ascites,  hydro- 
pericarditis).  The  phenomena  are  due  to  serous  transudation.  The  cases 
which  I  shaU  now  discuss  are  due  to  inflammation  of  toxi-infectious  origin. 
We  find  in  the  skin  erythema,  erysipelas,  lymphangitis,  and  celluhtis ; 
in  the  lungs,  pneumonia ;  in  the  serous  membranes,  pericarditis,  endocarditis, 
pleurisy,  and  peritonitis.  Out  of  406  cases  collected  by  Frerichs  and  Rosen- 
stein,  we  find  57  of  pleurisy,  46  of  peritonitis,  40  of  pericarditis,  and  52  of 
pneumonia. 

The  origin  of  these  inflammations  has  been  variously  interpreted.  Bright 
explained  the  endocarditis,  the  pericarditis,  and  other  lesions  of  the  serous 
membranes  by  the  blood  changes  consequent  on  the  nephritis.  His  ideas  have 
again  become  cunent,  and  many  writers  hold  that  the  lesions  just  enume- 
rated are  due  to  some  dyscrasia.  They  are  the  result  of  auto-intoxication 
secondary  to  nephritis.  Other  writers  place  more  importance  on  the  in- 
fectious agents,  and  consider  these  cases  of  inflammation  to  be  secondary 
infections.     In  reality  we  have  to  deal  especially  with  toxic  inflammation. 

Pleurisy  in  Bright's  disease  may  or  may  not  be  painful.  Percussion  and 
auscultation  show  no  diiierence  from  ordinary  pleurisy  as  regards  friction 
rub,  tubular  breathing,  segophony,  etc.     The  important  difference  is  that 


1124  .  TEXT-BOOK  OF  MEDICINE 

severe  dyspnoea  appears  early.  The  dyspnoea  is  not  due  only  to  the  effusion, 
but  also  to  the  broncho-pulmonary  oedema,  which  is  often  present  in  cases 
of  Bright's  disease.  Pleurisy  in  Bright's  disease  may  be  observed  at  any 
stage  of  the  malady.  Cyto-diagnosis  shows  that  it  is  a  form  of  mechanical 
and  aseptic  pleurisy.  It  is  characterized  by  the  presence  of  large  endo- 
thehal  plaques  (Widal  and  Ravaut). 

Pericarditis  in  Bright's  disease  is  especially  common  ia  the  ursemic  stage, 
and  makes  the  prognosis  hopeless.  It  is  generally  painless  and  apyretic. 
■As  it  comes  on  insidiously,  it  escapes  observation,  unless  careful  auscultation 
is  regularly  made.  The  rub  is  well  marked,  and  a  hruit  de  galop  may  be 
present.  The  effusion  is  scanty.  The  dullness  is  in  part  due  to  the  fluid 
and  in  part  to  the  hypertrophy  of  the  heart.  The  dyspnoea  varies  according 
to  the  presence  or  the  absence  of  pulmonary  oedema  and  pleural  effusion. 
The  fluid  may  be  yellow  or  bloody  (LetuUe). 

Uraemia. 

Pathogenesis. — The  theory  of  uraemia  is  based  on  the  fact  that  in  con- 
sequence of  lesions  in  the  kidneys  and  of  insufficient  urinary  depuration, 
products  of  metabolism  which  should  be  excreted  in  the  urine  accumulate 
in  the  blood,  and  give  rise  to  symptoms  of  poisoning.  As  Jaccoud  has 
pointed  out,  the  word  "  ursemia  "  does  not  signify  urea,  but  urine  in  the 
blood  {ovpov,  urine ;  and  al/xa,  blood).  This  theory  is  true,  but  the  diffi- 
culty arises  when  we  attempt  to  specify  which  are  the  products  of  metabohsm 
and  which  are  the  toxic  agents. 

Urea  has  been  blamed.  In  some  cases  (Bouchard,  Brouardel)  the  onset 
of  ursemia  has  coincided  with  a  diminution  of  the  urea  in  the  urine  and  with 
the  presence  of  an  enormous  quantity  of  urea  in  the  blood.  On  the  other 
hand,  however,  we  have  the  negative  series  of  blood  examinations  in  which 
no  excess  of  urea  was  present  (Wurtz  and  Berthelot,  Potain).  In  the  cases 
of  uraemia  quoted  by  Parker,  Mosler,  and  many  others,  the  urine  contained 
either  a  normal  quantity  or  an  excess  of  urea:  I  would  also  remark  that 
injections  of  urea  into  the  blood  of  animals  do  not  cause  symptoms  of 
uraemia.  Feltz  and  Ritter,  Grehant  and  Quinquaud,  have  shown  that,  in 
order  to  kill  animals  by  injections  of  chemically  pure  urea,  large  quantities 
are  necessary.  The  same  fact  is  evident  from  the  researches  of  Bouchard, 
that  urea  is  not  capable  of  reducing  the  temperature  or  of  producing  coma, 
and  that  it  only  accounts  for  a  ninth  part  of  the  toxicity  of  the  urine. 

Frerichs  supposes  that  the  urea  is  converted  in  the  blood  into  car- 
bonate of  ammonia  (Jaccoud  calls  this  condition  ammonisemia).  Ammonia 
is  present  in  the  vomit  and  the  faeces,  and  the  breath  is  sometimes  ammo- 
niacal,  as  shown  by  placing  in  front  of  the  mouth  a  piece  of  wood  soaked 
in  acetic  acid,  on  which  crystals  of  acetate  of  ammonia  are  deposited. 


DISK, ASKS  OF  'I'lli:   KlhXKVS  112." 

The  salts  of  potassium  have  Iml-h  hmkcd  upuu  hy  Keltz  and  IJitler  as 
the  essential  poison  in  the  urine.  Tliey  proposed  the  name  of  "  potassi- 
a'mia  "  for  the  intoxication  produced  by  retention  of  the  toxic  principles  of 
the  urine.  Bouchard  has  proved  experimentally  the  toxicity  of  the  salts 
of  pota.ssium,  but  he  does  not  consider  them  to  be  the  only  factor,  and 
other  important  substances  are  likewise  at  fault. 

Some  interesting  experiments  have  been  made  by  Lepine  and  Aubert 
on  the  respective  to.xicity  of  the  organic  and  saline  corLstituents  of  the 
urine.  The  colouring  matters  and  the  ptomaines  play  a  very  important 
part  in  this  question  (Bouchard). 

I  cannot  give  the  details  of  Bouchard's  experiments,  but  the  conclusion 
is  that  the  intoxication,  whether  caused  by  injections  of  urine  into  the 
veins  of  an  animal  or  by  the  retention  of  toxic  products  in  a  man  whose 
kidneys  are  diseased,  is  not  due  to  one  substance  contained  in  the  urine, 
but  to  all  the  substances  of  which  some  are  well  known,  while  others  are 
still  under  investigation. 

From  this  point  of  view  ursemia  depends  on  insufficiency  of  the  urinary 
depuration  (Jaccoud).  It  must  not,  therefore,  be  coasidered  as  a  compli- 
cation of  nephritis  ;  it  is  a  symptom.  Every  patient  with  acute  or  chronic 
nephritis  is  ipso  facto  threatened  with  ursemia.  He  escapes  the  more  serious 
symptoms  if  the  dose  of  the  toxic  agent  is  small  and  the  lesion  of  the  kidneys 
is  slight ;  but,  as  a  matter  of  fact,  ursemia,  whether  shght  or  severe,  only 
awaits  sufficient  accimiulation  of  the  toxic  agent  in  the  blood  in  order  to 
appear. 

The  minor  symptoms  of  Bright's  disease — cryaesthesia,  electric  shocks, 
cramps  in  the  calves  of  the  legs,  and  itching  -r  are,  I  think,  due  to  mild 
uremia.  The  more  marked  symptoms — headache,  dyspnoea,  gastric  troubles, 
and  temporary  prostration — are  due  to  a  more  severe  ursemic  intoxication. 
Finally,  the  major  symptoms — terrible  dyspnoea,  violent  headache,  uncon- 
trollable vomiting,  profuse  diarrhoea,  epileptiform  convulsions,  delirium, 
and  coma — are  the  consequence  of  ursemic  poisoning  in  its  worst  form. 

Ursemia  has  been  divided  into  acute  and  chronic.  It  is  better  to  say 
that  the  symptoms  are  sometimes  sudden  and  sometimes  slow  in  their 
appearance.  Some  are  transient  and  others  are  lasting.  The  symptoms 
may  appear  together  or  in  succession.  Ursemia  does  not  always  begin  with 
the  minor  symptoms,  and  pass  on  to  the  most  severe  troubles.  In  acute  or 
-subacute  nephritis  (cold,  scarlatina,  syphilis,  puerperal  fever),  when  the 
poison  causes  rapid  changes  in  the  essential  elements  of  the  kidneys,  the 
major  symptoms  may  appear  early,  without  any  prodi'omata.  On  the 
other  hand,  in  chronic  nephritis  the  major  symptoms  may  only  appear  late, 
after  a  more  or  less  complete  series  of  shght  troubles. 

Ursemia  at  times  supervenes  in  the  last  stage  of  chronic  nephritis,  when 
II.  72 


1126  TEXT-BOOK  OF  MEDICINE 

the  kidneys  are  irremediably  disorganized.  At  otlier  times  it  breaks  out 
as  an  acute  condition,  which  may  be  transient  and  curable,  exactly  hke  an 
attack  of  renal  asystole.  In  the  latter  case  its  causation  is  not  so  easy  of 
explanation.  A  patient  is  suffering  from  slowly  progressive  Bright' s  disease. 
Why  does  the  lesion  allow  sufficient  urinary  depuration  one  day,  and  a 
week  later  so  change  the  quantity  or  the  quahty  of  the  urine  that  grave 
uraemia  results  ?  And,  even  if  the  lesion  of  the  kidneys  be  so  advanced 
as  to  cause  these  grave  comphcations,  how  can  we  explain  the  fact  that 
they  may  be  removed,  the  individual  may  regain  his  health,  and  the  urinary 
depuration  prove  adequate — at  least,  for  a  time  ? 

It  is  evident  that  the  lesion  fer  se  cannot  always  explain  the  sudden 
variations  in  the  urine,  and  the  more  or  less  rapid  appearance  or  disappear- 
ance of  the  ursemic  symptoms.  I  think  that  other  factors  are  also  present. 
We  shall  see  in  the  description  of  Renal  Calculus  that  the  presence  of  a  stone 
in  one  ureter  may  cause,  by  reflex  action,  paralysis  of  both  kidneys  and 
anuria,  which  is  soon  followed  by  uraemia. 

In  Bright's  disease,  when  the  lesion  of  the  kidneys  slowly  and  pro- 
gressively narrows  the  field  of  urinary  depuration,  a  paralysis  of  the  urinary 
function  may  diminish  or  prevent  for  a  time  the  secretion  of  urine  or  its 
depuration.  This  factor  is,  I  beheve,  important  in  these  attacks  of  renal 
asystole.  I  should  be  quite  ready  to  admit  either  an  affection  of  the 
secretory  cells  of  the  kidney  by  the  ursemic  poison — i.e.,  renal  uraemia — or 
a  spasm  of  the  vessels  of  the  kidneys.  As  a  matter  of  fact,  do  we  not  know 
the  important  part  played  by  vascular  spasm  in  Bright's  disease  ?  The 
dead  fingers  which  are  so  frequent  a  symptom,  evidently  result  from  vascular 
spasm.  Certain  forms  of  ureemic  dyspnoea  {sine  materia)  might  well  be 
associated  with  spasm  of  the  smaU  bronchi  or  of  the  smaU  bloodvessels 
(Potain).  The  high  arterial  tension  which  leads  to  cardiac  hypertrophy 
in  Bright's  disease,  is  in  part  due  to  the  spasm  of  the  peripheral  arterioles. 
Whether,  then,  the  hypothesis  of  glandular  auto-intoxication  or  of  passing 
renal  congestion  be  admitted  or  rejected,  or  the  hypothesis  of  vascular 
spasm  in  the  kidneys,  I  maintain  that  the  lesion  of  the  kidneys  and  the 
obhteration  of  the  canaliculi  by  casts  will  not  explain  the  causation  of 
certain  acute  and  transitory  episodes  in  uraemia. 

In  the  above  discussion  I  have  only  considered  the  toxic  side  of  uraemia, 
but  we  may  find  other  important  factors.  Thus,  broncho-puhnonary  oedema 
is  associated  with  uraemic  dyspnoea.  Greneral  and  local  oedema  of  the 
brain  (Raymond)  and  hydrocephalus  (Coindet)  often  take  their  share  in 
the  convulsions,  the  paralysis,  and  the  coma  of  uraemia. 

Description. — I  have  already  said  that  uraemia  in  aU  its  forms  dominates 
the  history  of  Bright's  disease.  Further,  in  describing  the  symptoms  of 
Bright's  disease  we  were  constantly  brought  face  to  face  with  uraemic 


DISKASKS  OF   rill':  KIDNKVS  ITJT 

troubles.  Nevertheless,  in  order  to  confonn  to  custom,  we  have  been  used, 
vvlicti  describing  lirighi's  disease,  to  compriso  uinler  tlic  iieadirig  of  uraemia 
oiilv  the  most  marked  troubles.     These  I  shall  now  discuss. 

Cerebral  Uraemia.— In  this  form  we  find  convulsions,  dehrium,  or  codkv. 
The  conv^ulsious  may  occur  suddenly,  but  prodroraata  are  generally  present. 
The  urine  diminishes  in  quantity ;  the  patient  has  severe  headache,  epis- 
taxis,  vertigo,  giddiness,  auditory  and  visual  troubles,  sudden  bhndness 
(ura?niic  amaurosis),  and  spasmodic  movements  of  the  limbs.  At  a  given 
moment  an  attack  of  convulsions,  like  those  of  epilepsy,  comes  on.  The 
sudden  loss  of  consciousness,  the  tonic  and  clonic  convulsions,  the  biting  of 
the  tongue,  and  the  stage  of  collapse  follow  one  another,  as  in  epilepsy. 
There  is,  however,  this  difference  :  that  in  the  ursemic  attack  the  initial 
cry  is  often  wanting,  the  seizure  is  less  unilateral,  and  the  temperature  falls 
below  normal.  This  rule,  however,  is  not  absolute,  and  in  several  cases 
of  urpemia  the  convulsions  have  caused  a  rise  in  the  temperature.  This 
rise  of  temperature  may,  however,  be  due  to  secondary  infections.  The 
number  of  attacks  varies  from  one  or  two  in  twenty-four  hours  up  to  fifteen 
or  twenty  a  day,  which  end  in  coma  and  death. 

The  delirium  assumes  various  forms.  As  a  rule,  it  appears  as  an  epi- 
phenomenon  in  the  last  stages  of  the  disease.  In  some  cases,  however,  it 
is  of  special  importance.  It  may  resemble  mania.  To  this  form  I  have 
given  the  name  of  "  folie  Brightique."*  Uremic  dehrium  sometimes  re- 
sembles acute  mania,  with  excitement,  restlessness,  insomnia,  constant 
talking  and  shouting.  The  patient  cannot  sit  still,  and  becomes  violent 
when  attempts  at  restraint  are  made.  The  excitement  may  alternate  with 
phases  of  torpor  and  somnolence. 

In  some  cases  we  find  rather  hallucinations  of  hearing  and  sight.  The 
patient  sees  squadrons  of  cavalry  manoeuvring  on  the  roofs,  and  hears 
cliildren,  who  are  carrying  briUiant  Hghts  or  are  singing.  He  may  see  persons 
clad  in  rich  robes  or  hear  pistol-shots.  In  other  cases  the  disease  takes  the 
form  of  melancholia.  The  patient  will  not  move ;  his  eye  is  dull  and  his 
face  expressionless.  He  does  not  speak,  and  appears  quite  resigned.  He 
may  fear  or  welcome  death,  or  may  show  suicidal  tendencies. 

Ideas  of  persecution  may  be  marked.  He  refuses  food,  for  fear  of  poison. 
He  beheves  that  attempts  are  being  made  on  his  life  ;  hears  persons  who  wish 
to  kill  him,  or  beheves  himself  guilty  of  the  most  horrible  crimes,  and 
dreads  punishment.  More  rarely  ursemic  delirium  assumes  the  erotic  and 
the  rehgious  form.  These  varieties  of  delirium  may  exist  alone.  More 
frequently  they  follow  one  another  or  occur  together. 

The  duration  of  the  dehriimi  varied  in  the  cases  which  I  have  pubhshed 
from  nineteen  days  to  eight  months.     Ursemic  dehrium  may  break  out 
*  Dieulafoy,  Societe  de  Medecine  des  Hopitaiix,  10  Juillet,  1885. 

72 2 


1128  TEXT-BOOK  OF  MEDICINE 

suddenly,  and  be  most  acute  from  the  first,  or  be  ushered  in  by  incoherent 
words  and  gestures,  and  only  gradually  reach  its  maximum.  In  some  cases 
the  dehrium  is  practically  continuous,  and  shows  but  shght  remissions.  In 
other  cases  we  find  transient  improvement.  Certain  sufferers  from  Bright's 
disease  are  predisposed  to  dehrium  by  alcohohc  antecedents,  by  previous 
neuropathic  troubles,  and  by  heredity.  The  dehrium  sometimes  forms  one 
of  the  general  symptoms  of  Bright's  disease,  and  the  diagnosis  is  easy.  At 
other  times  it  is  the  chief  symptom,  being  so  marked  that  the  diagnosis 
is  difficult.  This  fact  is  important  to  remember,  lest  we  should  treat  as  a 
lunatic  a  patient  who  is  really  suffering  from  Bright's  disease.  The  dehrium 
does  not  supervene  only  in  confirmed  Bright's  disease  ;  it  may  appear  while 
the  other  signs  are  but  shght.  De  Fleury  has  reported  four  cases  of  mental 
troubles  in  the  early  stage  of  Bright's  disease.  "  The  patients  were  not 
improved  by  the  ordinary  treatment  of  these  affections,  but  the  symptoms 
were  markedly  reheved  by  milk  diet,  with  or  without  injections  of  pilo- 
carpine.    The  symptoms  reappeared  when  the  milk  was  discontinued." 

Coma. — The  patient  is  in  an  apoplectiform  condition.  He  suffers  from 
drowsiness,  from  which  it  is  difficult  to  rouse  him,  and  which  often  ends  in 
coma,  the  usual  termination  of  the  various  forms  of  cerebral  uraemia.  The 
coma  is  rarely  primary  ;  it  generally  follows  the  preceding  forms. 

Uraemic  Paralyses. — In  some  cases  we  find  definite  paralyses  in  patients 
suffering  from  uraemia.  The  paralyses  are  of  various  kinds — hemiplegia, 
simulating  that  due  to  cerebral  haemorrhage  ;  right  hemiplegia,  with  aphasia, 
simulating  embohsm  of  the  left  Syhdan  artery  ;  hemiplegia,  with  epilepti- 
form con^^ilsions ;  monoplegia,  with  or  without  Jacksonian  epilepsy, 
simulating  a  lesion  in  the  motor  convolutions  ;  aphasia,  without  hemiplegia  ; 
facial  hemiplegia  ;  partial  paralyses  of  the  third  and  seventh  pairs  of  nerves  ; 
crossed  hemiplegia  ;  larpigoplegia.  Some  of  these  paralyses  are  due  to 
focal  lesions  (heemorrhage  or  softening),  changes  in  the  cerebral  vessels 
being  frequent  in  the  course  of  chronic  nephritis.  I  am  not  here  alluding 
to  these  cases,  but  to  the  curable  or  fatal  cases  of  paralysis  which  are  due 
to  none  of  the  above-mentioned  lesions.  We  must  admit  that  in  such  a 
case  the  paralysis  is  due  either  to  oedema  or  to  intoxication  of  a  definite 
cerebral  region.  Cerebral  oedema,  with  or  without  serous  effusion  into  the 
ventricles,  is  found  in  a  fair  number  of  post-mortem  examinations,  renal 
lesions  being  always  present.  In  spite  of  the  opposition  of  Charcot,  cerebral 
oedema  and  the  anaemia  resulting  therefrom,  admitted  by  Frerichs,  Jaccoud, 
and  Rosenstein,  is  now  a  definite  entity,  which  post-mortem  examinations 
have  verified  (Carpentier,  Raymond,  Chantemesse  and  Tenneson). 

Nevertheless,  sufferers  from  Bright's  disease  have  succumbed  to  paralysis, 
and  post-mortem  focal  lesions,  disease  of  the  cerebral  arteries,  and  oedema 
of  the  brain  have  been  absent  (Chauffard,  Level).     It  is  probable  that  the 


DisEASER  OF  'riir:  kidni'I^'s  iil".i 

paral'.'si?;  ia  of  toxic  origin,  like  the  paralysis  due  to  sulphide  of  rarbon, 
It';ul-])oisouing,  etc.  lint  how  ran  wc  fix])lain  tho  fact  that  g«!ri(?ral  ura>niic 
])()isoiiiiig  may  cause  partial  ])aralysis  atul  liciMi])lcgia  i  Wc  arc  reduced 
to  theories. 

Dyspnoea. — T  have  already  luetitioned  respiratory  trouhle-i  due  to 
toxiiies  or  to  trdeina.  The  nature  of  the  dyspnoea  has  not  heen  clearly 
understood,  because  it  was  wrongly  thought  that  the  d3-spnoea  must  naturally 
a.ssume  the  Chevne-Stolccs  rhythm.  Now,  this  rhythm  represents  only  one 
form  of  ura)mic  dyspncea.  We  may  find  every  grade,  from  sUght  distress 
to  the  most  marked  continuous  dyspnoea,  from  breathlessness  on  exertion 
to  severe  attacks  which  come  on  suddenly,  hke  those  of  asthma  (urajmic 
asthma).  Ursemic  dyspnoea  may  be  most  severe,  and  yet  no  signs  are  found 
on  auscultation.  It  is  toxic  dyspnoea  sine  materia.  In  other  cases  we  find 
signs  of  bronchitis,  broncho-pulmonary  oedema  or  pleural  effusion,  which 
accompany  the  dyspnoea  and  modify  its  characters.  Superacute  oedema 
of  the  lungs  has  been  previously  discussed. 

Gastro-Intestinal  Uraemia. — In  some  cases  of  Bright's  disease  we  find 
vomiting  of  mucus  or  food,  as  in  chronic  gastritis  ;  uncontrollable  vomiting, 
as  in  pregnancy  ;  and  even  liaematemesis,  as  in  ulcer  of  the  stomach  (gastric 
uraemia).  We  also  find  dysenteric  diarrhoea.  These  troubles  comprise 
the  chief  features  of  gastro-intestinal  uraemia,  which  has  been  explained  by 
the  passage  of  urea  through  the  mucosse  of  the  stomach  and  of  the  intestine. 
The  digestive  passages  assist  in  the  elimination  of  urea.  Bernard  proved 
this  by  ligaturing  the  ureters  in  animals.  In  man  we  find  urea  or  its  com- 
pounds in  the  excreta.  At  the  post-mortem  examination  of  patients  who 
died  of  uraemia,  Rosenstein  has  found  numerous  ulcers  in  the  bowel.  In  a  case 
of  Bartel's  the  ulcers  had  given  rise  to  a  perforation  6  inches  above  the  ileo- 
cffical  valve.  Fatal  peritonitis  followed.  In  one  of  Mery's  cases  the  ulcers 
of  the  small  intestines  were  numerous.  One  had  perforated,  and  caused 
death  by  peritonitis.  Letulle  has  found  several  ulcers  scattered  through 
the  ileum.  They  were  irregular,  clean-cut,  and  varied  in  size  from  a  six- 
pence to  a  shilling.  They  were  all  seated  on  the  free  edge  of  the  intestine, 
and  did  not  specially  afiect  Beyer's  patches.  Two  ulcers  had  perforated, 
causing  peritonitis. 

There  is  such  a  thing  as  renal  uraemia,  although  the  term  seems  re- 
dundant. By  this  term  I  do  not  refer  to  the  lesions  of  the  kidney  or  to  the 
obstruction  of  the  tubules,  but  to  the  uraemic  poisoning  of  the  organ,  which 
diminishes  or  destroys  its  functions,  causing  oHguria  or  anuria.  This  toxic 
anuria  may,  I  beheve,  be  cured  by  subcutaneous  injections  of  nephrin,  as 
I  first  suggested  some  years  ago. 

Cardio-aortic  uraemia  exists.  It  is  characterized  by  tendency  to  collapse 
and  by  pain,  recalling  angina  pectoris, 


1130  TEXT-BOOK  OF  MEDICINE 

The  different  forms  of  uraemia,  wliicli  are  separated  for  purposes  of 
description,  may  occur  together,  or  follow  one  another  in  the  same  subject.  A 
patient  at  first  suffers  from  fits  of  suffocation,  visual  troubles,  violent  head- 
ache, and  uncontrollable  vomiting.  In  time  coma  or  convulsions  appear. 
In  some  cases,  however,  the  mischief  spends  its  force  on  one  organ,  although 
it  is  not  possible  to  explain  the  reason  of  this  selection.  Thus,  the  dyspnoea 
may  be  so  severe  as  to  kiU  the  patient,  quite  apart  from  other  uraemic 
troubles.  The  same  remark  apphes  to  gastric  uraemia,  as  in  the  following 
case,  which  I  saw  with  Potain  : 

A  patient  who  had  Blight's  disease  was  taken  ill  with  general  csdema.  The  urine 
became  scanty,  about  3  ounces  daily.  Uncontrollable  vomiting  set  in,  and  all  food  was 
vomited.  Vomiting  of  greenish  watery  fluid  occurred,  even  when  no  drink  was  given. 
The  ursemic  poisoning  was  accompanied  by  intolerable  itching.  In  spite  of  all  treat- 
ment, the  patient  succumbed  in  three  weeks ;  headache,  dyspnoea,  delirium,  convul- 
sions, and  coma  were  all  absent.     It  was  a  pure  case  of  gastric  ursemia. 

We  can  often  distinguish  clinically  moist  and  dry  forms  of  ursemia. 
The  former  is  due  to  retention  of  the  chlorides ;  the  latter  results  from 
retention  of  the  urea. 

If  in  the  course  of  Bright's  disease  the. kidneys  do  not  eliminate  the 
chlorides,  the  excess  retained  in  the  body  does  not  remain  long  in  the  blood, 
which  always  tends  to  maintain  its  molecular  equihbrium,  but  passes  into 
the  tissues  (Achard  and  Loeper).  As  salt  is  a  hygroscopic  substance,  it 
takes  up  water  from  the  tissues,  and  preserves  by  dilution  the  isotonic  con- 
dition of  the  protoplasm.  Chlorursemia,  then  (Widal),  tends  to  the  moist 
form  which  is  characterized  by  multiple  oedema.  Deformity  results  when 
the  oedema  is  superficial.  If  the  oedema  is  deep-seated,  it  leads  to  visceral 
disorders,  which  affect  the  lungs  and  the  brain,  and  reveal  themselves  by 
nervous  and  respiratory  troubles. 

When  the  free  discharge  of  urea  is  impeded  by  the  affected  kidney,  it 
does  not  pass  back  suddenly,  .as  the  chlorides  do,  into  the  tissues,  but 
accumulates  in  the  blood,  and  aU  the  molecules  tend  unceasingly  toward 
the  epithehum  of  the  tubules.  In  order  to  overcome  the  resistance  opposed 
by  the  kidneys  to  the  passage  of  the  urea,  the  blood  becomes  mechanically 
surcharged  with  a  certain  quantity  of  this  substance.  An  urea-pressure  is 
estabhshed,  which  varies  in  amount  according  to  the  extent  of  the  renal 
lesion  and  to  the  quantity  of  albumin  ingested.  Owing  to  this  regulating 
mechanism,  the  kidney  performs  its  functions  better,  and  practically  regains 
the  permeability  necessary  to  assure  the  free  passage  of  the  urea  that  it  has 
to  eliminate. 

We  see,  therefore,  that  the  molecules  of  urea  foUow  in  order  to 
accumulate  in  the  blood,  an  inverse  course  to  that  which  the  molecules 
of  the  chlorides  pursue  in  order  to  accumulate  in  the  tissues.      The  reten- 


DISEASES  OK  THE  KIDNEYS  li:;i 

tion  of  tlie  molecules  of  urea  does  not  give  rise  to  <jedeiiia,  bul  only  to  dry 
uraemia. 

A  patient  with  Briglit's  disease,  therefore,  may  be  of  the  azotoemic  or 
chlorurseraic  type.  The  signs  of  azotemia  are  loss  of  appetite,  which  miiy 
amount  to  invincible  distaste  for  food,  fatigue,  and  torpor,  which  may  end 
ill  complete  coma.  The  presence  of  an  excess  of  urea  in  tlie  blood  is  the 
best  evidence  of  the  retention  of  this  substance  (Widal  and  Javal). 

Just  as  retention  of  chlorides  may  exist  alone  for  a  lengthy  period,  so 
may  retention  of  urea  appear  at  any  stage  of  the  disease,  quite  apart  from 
any  retention  of  chlorides.  Patients  may  die  of  uraemia,  although  they  have 
never  shown  any  trace  of  oedema.  These  cases  are  exceptional,  for  in  most 
instances  we  find  that  the  retention  of  both  substances  has  an  influence  on 
the  renal  insufficiency. 

We  see,  therefore,  that  there  are  several  varieties  of  uraemia.  The 
disease  may  be  sudden  in  its  onset,  or  may  come  on  insidiously,  simulating 
some  other  malady,  and  causing  difficulties  in  diagnosis,  which  we  shall  now 
discuss. 

Diagnosis. — The  following  remarks  on  diagnosis  are  applicable  both  to 
the  symptoms  of  Bright's  disease  and  to  the  most  marked  forms  of  uraemia. 
As  I  have  already  remarked,  Bright's  disease  in  its  slow  and  insidious  forms, 
which  are  the  most  common,  shows  itself  by  headaches,  which  are  wrongly 
spoken  of  as  migraine  ;  by  gastric  troubles  and  by  fits  of  vomiting,  which 
are  wrongly  put  down  to  dyspepsia  or  alcohoHc  gastritis  ;  by  fits  of  suffoca- 
tion, which  are  confounded  with  attacks  of  asthma  ;  by  difficulty  in  breathing, 
which  is  called  emphysema  ;  by  cardiac  troubles,  which  are  mistaken  for 
heart  disease  ;  by  pleural  effusion,  which  simulates  ordinary  pleurisy ;  by 
bronchial  catarrh  of  undetermined  nature ;  by  mental  troubles,  which  are 
mistaken  for  mania,  and  for  which  the  patient  is  sent  to  an  asylum ;  by 
auditory  troubles  and  vertigo,  which  are  confounded  with  Meniere's  disease  ; 
by  nervous  phenomena,  which  are  charged  to  neurasthenia  ;  by  frequent 
micturition,  which  is  attributed  to  some  lesion  of  the  bladder  or  of  the 
prostate. 

A  thorough  knowledge  of  the  symptoms  of  Bright's  disease  reveals  its 
nature,  and  allows  us  to  group  around  some  symptom  which  has  attracted 
the  attention  of  the  patient  other  symptoms  which  have  passed  almost 
unnoticed.  In  this  way  we  arrive  at  the  diagnosis.  I  am  well  aware  that, 
as  far  as  the  diagnosis  is  concerned,  there  are  two  signs  of  the  utmost  im- 
portance— oedema  and  albuminuria.  As  regards  albuminuria,  however,  I 
must  mention  certain  restrictions.  Albuminuria  has  been  looked  upon  as 
so  important  in  the  diagnosis  of  nephritis  that  we  cannot  rid  our  minds  of 
tbis  idea.  It  commenced  with  Bright  himself.  Under  the  influence  of 
Bright  and  of  Rayer,  whose  great  authority  I  delight  in  acknowledging, 


1132  TEXT-BOOK  OF  MEDICINE 

albuminuria  was  for  a  long  time  considered  as  the  decisive  factor  in  the 
diagnosis  of  nephritis.  I  am  of  opinion  that  this  view  is  incorrect,  although 
I  am  neither  the  first  nor  the  only  one  to  think  so. 

In  acute  nephritis  albuminuria  is  of  the  utmost  importance.  In  chronic 
interstitial  nephritis,  on  the  other  hand,  albuminuria  is  an  inconstant 
sign.  Not  only  may  albuminuria  be  absent  in  the  initial  phase  of  Brightism, 
but  it  may  be  wanting  when  Bright's  disease  is  confirmed,  and  even  in  the 
grave  forms  of  uraemia. 

In  my  communication  to  the  Societe  Medicale  des  Hopitaux  on  the 
chnical  and  experimental  study  of  Bright's  disease  without  albuminuria,* 
and  in  my  communication  to  the  Academic  de  Medecinef  regarding  Brightism 
and  the  dissociation  of  the  morbid  processes  in  the  kidneys,  I  quoted 
cases,  some  verified  by  post-mortem  examinations,  in  which  the  albumin 
had  completely  disappeared  for  some  considerable  time. 

It  is,  therefore,  proven  that  albuminuria  has  a  somewhat  secondary  value 
in  Bright's  disease.  It  is  only  an  unrehable  sign,  because  it  may  either  be 
absent,  or  because  it  may  exist  apart  from  any  condition  of  Bright's  disease. 

We  should,  then,  be  very  hable  to  errors  in  diagnosis  if  we  looked  upon 
albuminuria  as  being  the  decisive  sign. 

The  remarks  which  I  have  just  made  on  albuminuria  also  apply  to 
(Bdema.  Sufferers  from  Bright's  disease,  especially  if  they  have  arterio- 
sclerosis, may  show  no  trace  of  oedema  for  a  long  time,  whilst  oedema  of 
rheumatic  origin  (Potain)  simulates  that  due  to  Bright's  disease,  though  it 
has  nothing  to  do  with  Bright's  disease,  and  is  of  good  prognosis. 

In  order  to  distinguish  the  defaced  forms  of  Bright's  disease  (oedema  and 
albuminuria  being  absent),  and  to  recognize  its  initial  stage  or  its  presence 
when  the  more  marked  symptoms  are  absent,  I  have  tried  for  many  years 
to  bring  into  relief  certain  signs  which  I  have  named  the  "  minor  symptoms 
of  Brightism."  I  have  described  them  in  the  course  of  this  article.  They 
have  Httle  value  when  they  are  isolated.  Because  a  patient  presents  isolated 
pollalduria,  crysesthesia,  dead  finger,  cramps  in  the  calves  of  the  legs,  electric 
shocks,  or  auditory  troubles,  we  must  not  at  once  put  him  down  as  sufiering 
from  Bright's  disease.  If,  however,  a  patient  complains  of  violent  headache 
of  which  we  cannot  find  the  cause,  of  attacks  of  dyspnoea  which  are  not 
due  to  asthma,  of  gastric  troubles  or  vomiting  due  to  some  unknown  cause, 
etc. ;  and  if  he  also  suffers  from  pollalduria,  dead  fingers,  cramps  in  the  calves 
of  the  legs,  morning  epistaxis,  crysesthesia,  auditory  troubles,  itchings, 
electric  shocks,  etc. — ^in  short,  if,  after  a  minute  inquiry,  we  succeed  in 
grouping  some  of  these  signs,  whether  they  have  shown  themselves  succes- 
sively or  simultaneously,  if  the  arterial  tension  is  raised,  if  we  find  the  bruit 

*  Societe  de  Medecine  des  Hopitaux,  Seances  du  11  Juin  et  du  22  Octobre,  1886. 
t  Bvlletin  de  V Academie  de  Medecine,  6  Juia  et  20  Juin,  1893. 


DISEASES  OK  'rilh:  KIDNEYS  11:;:; 

(Jr  galop,  wo  have  tliiMi  i^ood  roason  to  say  tlial  he  has  Brightism,  ovon 
wlieii  oEHlema  is  ahseiit  and  the  urine  does  not  contain  allminin.  Tlir  iniiior 
symptoms  of  Hii«»htism  a])j)ear  in  the  first  period  of  liright's  disease  in 
suhjt'cts  who  have  not  yet  suffered  from  the  more  severe  sym])toms,  ami 
who  will  perhaps  never  have  them.  They  are  often  present  tlirougliout 
the  whole  of  the  disease.  They  are  not  recognized  because  they  are  not 
looked  for.  1  am  convinced  that  many  people,  thougli  lu^althy  in  a]))iear- 
ance,  are  really  affected  with  Brightism. 

I  think  these  facts  should  be  included  in  our  descriptions  of  Hright's 
disea.se.  Many  gouty  per.sons,  who  perchance  suffer  from  renal  colic  or 
albuminuria,  are  for  a  long  time  afflicted  with  the  minor  symptoms  of 
Brightism  before  the  appearance  of  the  grave  symptoms  of  ur;cmia.  Many 
sypliilitic  patients  show  symptoms  which  are  put  down  to  syphilis,  while 
they  are  really  due  to  Brightism,  and  form  the  prelude  to  more  severe 
mischief,  unless  appropriate  measures  are  employed.  In  many  people, 
after  an  infectious  disease  (typhoid  fever,  pneumonia,  and  especially  .scar- 
latina), the  symptoms  of  Brightism  run  an  insidious  course,  until,  for  want  of 
treatment,  the  more  severe  troubles  of  Bright's  disease  appear.  Many  women 
who  appear  to  suffer  from  anaemia,  with  pallor,  headaches,  breathlessness, 
palpitation  of  the  heart,  etc.,  and  are  considered  chlorotic,  are  really  suffer- 
ing from  chloro-Brightism,  a  special  form,  which  I  shall  discuss  later.  In 
manv  cases,  therefore,  a  knowledge  of  the  slight  symptoms  of  Brightism 
and  of  the  existence  of  high  tension  and  of  a  hriiit  cle  galop  helps  us  to  make 
the  diagnosis  of  incipient  Bright's  disease,  even  in  the  absence  of  oedema 
and  albuminuria.  In  my  oavu  wards  I  constantly  see  patients  in  whom  the 
minor  s}Tnptoms  are  present  without  oedema  or  albuminuria.  Some  months 
later  the  diagnosis  is  verified,  when  the  patient  returns  with  obvious 
symptoms  of  Bright's  disease,  including  oedema  and  albuminuria. 

Renal  Insufficiency  and  Laboratory  Researches.— The  three  methods 
which  we  are  about  to  consider  are  employed  in  the  diagnosis  of  renal  in- 
sufficiency, and  in  the  estimation  of  its  amount  (Achard).  They  comprise 
the  study  of  the  urinary  toxicity,  the  study  of  the  permeability  of  the 
kidneys,  and  cryoscopy. 

Urinary  Toxicity. — Bouchard,  as  the  result  of  many  experiments,  has 
shown  that  if  the  urine  of  a  healthy  adult  be  collected  for  twenty-four  hours 
and  injected,  after  filtration  and  neutralization,  into  the  veins  of  a  rabbit 
weighing  3J  pounds,  death,  follows  after  the  injection  of  about  3  ounces. 
These  figures  are,  of  course,  relative,  as  normal  urine  may  vary  in  its  to.xic 
power.  A  rabbit  weighing  3^  pounds  may  die  after  the  injection  of  from  1  to 
2  ounces.  On  the  other  hand,  it  may  not  die  till  after  the  injection  of  4  ounces, 
for  manv  conditions,  even  in  the  normal  state,  modify  the  toxicity  of  the 
urine.     Under  correct  experimental  conditions,   with   proper  precautions, 


1134  TEXT-BOOK  OF  MEDICINE 

it  may  be  said  that  a  rabbit  weighing  1  pound  will  be  killed  by  1  ounce  of 
normal  urine. 

I  have  repeated  these  experiments  with  similar  results — nam';ly,  that 
as  the  quantity  of  the  injection  is  increased,  the  animal  suffers  from  myosis, 
acceleration  of  the  respiratory  movements,  weakness  or  abohtion  of  the 
eye  reflexes,  lowering  of  the  temperature,  tetanic  rigidity,  sahvation,  con- 
vulsive movements,  and  exophthalmos.  The  less  toxic  the  urine  the  greater 
must  be  the  quantity  injected  in  order  to  Idll  the  animal.  It  might  a  priori 
be  supposed  that  as  the  urine  in  Bright's  disease  is  less  toxic,  because  the 
urinary  depuration  is  imperfect,  we  should  have  to  inject  a  large  quantity 
to  kill  an  animal.  This  is,  as  a  matter  of  fact,  just  what  Bouchard  found. 
The  urine  of  patients  suffering  from  Bright's  disease  (in  various  degrees 
and  under  certain  conditions)  has  but  httle  toxic  power.  These  experiments, 
repeated  with  the  urine  of  patients  who  had  Bright's  disease  but  no  albu- 
minuria, have  helped  me  to  a  correct  diagnosis*  in  many  difficult  cases. 

A  complete  investigation  of  the  toxicity  must,  however,  take  both  the 
urine  and  the  blood  into  account,  says  Achard.  The  conclusion  is,  says 
this  writer,  that,  "  besides  practical  difficulties,  the  investigation  is  also 
liable  to  theoretical  objections.  As  the  results  obtained  with  the  same 
liquid  are  Uable  to  variation,  no  exact  value  can  be  attributed  to  a  single 
trial.  In  practice  it  is  impossible  to  make  more  than  one  experiment  in 
each  case.  The  uncertainties  and  the  technical  difficulties  must,  therefore, 
limit  this  method  to  the  laboratory,  and  prevent  it  from  becoming  an  ordinary 
cUnical  method." 

Renal  Permeability  through  Provoked  Elimination.— It  has  long  been 
known  that  certain  drugs,  and  also  the  normal  constituents  of  the  urine,  are 
not  so  readily  ehminated  by  the  kidney  in  cases  of  nephritis.  Various  authors 
had  investigated  the  elimination  of  certain  substances,  when  Achard  and 
Castaigne  proposed  a  practical  method,  based  on  the  use  of  methylene  blue. 
This  method  has  led  to  systematic  researches  on  renal  permeabiUty.  A 
hypodermic  injection  of  1  grain  of  methylene  blue  is  given,  and  the  urine 
is  then  examined  repeatedly  for  traces  of  the  pigment. 

The  passage  of  the  blue  into  the  urine  shows  the  following  features : 
(1)  Under  normal  conditions  it  begins  to  appear  within  half  an  hour;  in 
pathological  conditions  it  may  be  delayed  for  several  hours.  (2)  The  ehmi- 
nation  in  normal  subjects  varies  from  thirty-five  to  sixty  hours ;  in  patho- 
logical conditions  it  is  either  shortened  or  prolonged.  (3)  The  quantity  of 
the  substance  ehminated  is,  according  to  Achard  and  Clerc,  the  most  im- 
portant element  of  the  test.  This  is  difficult  to  estimate.  The  whole  of 
the  urine  must  be  carefuUy  collected,  and  the  amount  of  the  blue  eliminated 

♦  Dieulafoy,  "  Etude  Clinique  et  Experimentale  de  la  Maladie  de  Bright "  (Societe 
de  Medecine  dea  Hopitaux,  Seances  du  11  Juin  et  du  22  Octobre). 


DISEASES  OF  TITE  KIDNEYS  11:;- 

must  be  estimated  by  cUromometric  tests.  Under  normal  conditioiLS  the  rate 
«)f  eliinijiatiou  in  the  first  twenty-four  hours  (mothylone  blue  and  chromofjen 
united)  nrnounts  at  least  to  half  of  the  <|uantity  injected.  Tlu!  (pjantity 
eliminated  in  the  first  twenty-four  hours  is  the  most  interesting.  The 
jiinounts  are,  nevertheless,  estimated  every  twenty-four  hours,  if  need  bfi, 
until  the  end  of  the  ehmination.  (4)  The  rhythm  of  the  ehmination,  which, 
under  normal  conditions,  at  first  increases  regularly  and  then  decreases, 
after  having  attained  a  maximum.  ChaufTard  has  shown  that  intermittent 
ehmination  is  characteristic  of  hepatic  insufficiency. 

The  pathological  results  furnished  by  the  methylene  blue  test  are  as 
follows  :  In  interstitial  nephritis  the  permeability  is  diminished,  though 
some  cases  have  been  recorded  in  which  it  was  practically  normal.  Tlw. 
explanation  given  is  that  a  small  portion  of  the  parenchyma  capable  of 
ehminating  the  dye  still  remains.  In  parenchymatous  nephritis,  on  the 
contrary,  Bard,  and,  later,  Leon  Bernard,  Widal,  Achard  and  Glerc,  have 
shown  that  the  permeabihty  remains  normal,  or  may  be  increased. 

The  test,  therefore,  often  gives  a  general  idea  of  the  permeabihty  of  the 
kidneys  ;  but,  as  Bernard  and  Widal  have  pointed  out,  the  variations  in  the 
elimination  in  nephritis  are  far  from  being  always  proportional  to  the  degree 
of  the  renal  lesion  and  to  the  intensity  of  the  ursemic  symptoms.  Widal 
lias  reported  a  case  of  s}'phihtic  nephritis  in  which  the  permeability  was 
normal,  in  spite  of  severe  uraemia.  To  interpret  these  facts  we  must  remember 
that  the  permeabihty  of  the  renal  epithelium  varies  for  different  substances. 
On  the  other  hand,  we  must  remember  that  methylene  blue  is  a  substance 
wliich  may  undergo  considerable  reduction  in  the  body.  Bard  and  Bonnet 
have  shown  that,  in  certain  cases,  there  may  be  disassociation  between  the 
ehmination  of  the  blue  and  that  of  the  iodide  of  potassium.  Widal  and 
Ravaut  have  shown  a  similar  dissociation  for  the  ehmination  of  sahcylate 
of  soda.  On  the  other  hand,  they  have  shown  that  sahcylate  of  soda  in- 
jected in  doses  under  the  skin  has  the  advantage  of  being  eliminated  more 
rapidly  than  methylene  blue  or  iodide  of  potassium — viz.,  in  fifteen  to 
twenty  hours  under  normal  conditions.  The  quantity  ehminated  may  be 
tested  with  great  accuracy  in  the  urine  discharged  at  each  micturition. 
Taken  as  a  whole,  the  ehmination  of  these  substances  by  the  kidneys  does 
not  furnish  in  the  diagnosis  of  renal  insufficiency  results  precise  enough  to 
enable  us  to  estimate  the  degree  of  this  insufficiency. 

It  is  not  the  same  with  the  elimination  by  the  kidneys  of  a  natural  sub- 
stance hke  chloride  of  sodium.  In  epithehal  nephritis  the  ehmination  of 
methylene  blue  may  be  normal,  while  the  ehmination  of  the  chlorides  is 
much  disturbed. 

Widal  has  shown  that  differences  of  permeabihty  might  be  noticed  even 
between  substances  naturally  eliminated — between  urea  and  chloride  of 


1136  TEXT-BOOK  OF  MEDICINE 

sodium,  for  instance — and  that  there  was,  as  far  as  the  kidneys  were  con- 
cerned, a  very  special  mechanism  for  ehmination  of  the  chlorides,  which 
might  be  disturbed,  while  the  other  mechanisms  were  still  intact. 

The  permeabiUty  of  the  kidneys  for  chlorides  is  most  interesting,  be- 
cause the  retention  of  this  salt  may,  as  we  have  already  seen,  lead  to  oedema. 
If  we  know  the  approximate  quantity  of  chloride  of  sodium  in  the  diet  taken 
for  some  days  by  the  patient,  and  compare  it  with  the  quantity  of  the 
chlorides  ehminated  in  the  urine,  we  can  deduce  the  degree  of  renal  per- 
meability. 

Toxicity  of  the  Serum. — Researches  into  the  toxicity  of  normal  or  patho- 
logical serum  injected  into  the  veins  or  the  subcutaneous  cellular  tissue  have 
so  far  given  contradictory  results.  Widal,  Sicard,  and  Lesne  have  experi- 
mented with  the  serum  of  normal  or  ureemic  subjects  by  the  method  of  intra- 
cerebral  injections.  They  have  shown  that  in  healthy  people  or  in  persons 
suffering  from  symptoms  of  uraemia  there  exists  a  convulsive  poison,  which 
causes  certain  symptoms  when  injected  into  the  brain  of  a  guinea-pig  but 
none  in  the  case  of  the  rabbit.  The  nerve  cells  of  allied  species  of  animals, 
such  as  the  guinea-pig  and  the  rabbit,  may  thus  react  quite  differently  to 
the  same  systemic  poison.  If  the  serum  of  ursemic  patients  injected  into 
the  brain  of  rabbits  is  not  more  toxic  than  the  serum  of  normal  subjects, 
we  may  ask  whether  this  anomaly  is  not  due  to  the  fact  that  poisons  which 
affect  the  nerve  cell  of  man  do  not  affect  the  cell  of  a  different  species,  such 
as  the  rabbit. 

The  following  experiment  of  Widal  and  Lesne  is  in  favour  of  this  hypo- 
thesis. They  produced  parenchymatous  nephritis  in  a  rabbit  by  the  in- 
jection of  chromic  acid.  The  serum  of  the  animals  thus  treated  was  toxic 
when  used  as  an  intracerebral  injection — for  the  guinea-pig  in  a  dose  of 
■Yo  c.c,  and  for  the  rabbit  in  a  dose  of  |  c.c.  Before  the  appearance  of  the 
renal  lesion  the  serum  was  harmless  to  the  guinea-pig  after  intracerebral 
injection  of  J  c.c,  and  for  the  rabbit  after  injection  of  J  c.c. 

Cryoscopy. — "  The  object  of  cryoscopy,"  says  Achard,  "  is  to  overcome 
the  insurmountable  difficulty  which  the  chemical  comparison  of  the  blood 
and  of  the  urine  presents,  by  substituting  the  estimation  of  a  physical 
quahty  for  a  chemical  value.  Instead  of  estimating  the  relative  proportion 
of  the  substances  in  the  blood  and  the  urine,  this  method  estimates  the  total 
quantity  of  the  molecules  contained  in  these  two  hquids,  and  does  not  dis- 
tinguish their  nature.  The  relatively  simple  procedure'  which  yields  the 
molecular  concentration  of  a  hquid  consists  in  determining  its  freezing- 
point.  As  a  matter  of  fact,  according  to  Raoult's  law  the  lowering  of  the 
freezing-point  of  a  solution  is  proportional  to  the  number  of  molecules  dis- 
solved in  unit  volume  of  the  solvent,  irrespective  of  the  size  and  nature  of 
these  molecules.     Given  the  molecular  concentration  of  the  urine  and  of 


DISKASKS  OK  Till;   KIDNKVS  j1;j7 

the  blood-scrum,  it  is  easy  to  establish  their  relation.  The  variations  in 
the  latter  will  indicate  the  differences  of  concentration  which  result  from 
the  pathological  (K)udition  of  the  Icidneys."  These  researches  and  all  the 
calculations  which  they  necessitate  (Claude  and  Balthazard)  have  little 
|ir;icti(%al  value,  and  are  too  complicated  for  everyday  use. 

Duration.  —The  duration  of  Bright's  disease  is  very  variable  :  one  or 
two  years,  and  still  less,  in  parenchymatous  nephritis  ;  five,  six,  or  seven 
years,  and  even  more,  in  interstitial  nephritis  and  in  cases  of  mixed  nephritis. 
Remissions  are  fairly  frequent.  We  meet  with  patients  who  appear  cured, 
and  in  whom  the  disease  returns  after  a  few  years.  It  may  be  asked 
whether  the  return  of  the  disease  is  not  the  result  of  some  fresh  cause. 

Cases  of  cure  wliich  are  frequent  in  instances  of  acute  nephritis  are  less 
common  in  Bright's  disease,  especially  if  the  arterio-sclerosis  is  more  or 
less  general.  Death  may  result  from  haemorrhage,  apoplexy,  cardiac  and 
pulmonary  lesions.  In  some  cases  cutaneous  and  visceral  inflammation 
and  gangrene  (secondary  infections)  hasten  the  end,  and  if  the  patient 
escape  these  complications,  he  may  be  carried  off  by  uraemia,  dyspnoea, 
apoplexy,  epileps3%  or  coma. 

Prognosis. — We  must  remember,  in  deahng  with  the  prognosis,  that 
albuminuria  may  last  for  years  without  being  due  to  Bright's  disease,  or 
may  be  the  only  e\adence  ;  and,  on  the  other  hand,  Bright's  disease  may  run 
its  course  without  albuminuria.     The  follomng  examples  illustrate  this  : 

I  bad  under  my  care  a  youth  who  has  suffered  for  many  years  from  scarlatinal 
albuminuria,  without  Eright's  disease.  I  placed  him  on  a  milk  diet ;  and  I  may  remark, 
in  passing,  that  milk  diet,  which  is  so  efficacious  in  uraemia,  is  of  less  benefit  in  albumin- 
uria. I  am  at  present  attending  a  cloild  ten  years  of  age  who,  after  scarlatina,  has 
had  albuminiuria  for  several  years.  The  face  is  pale,  and  the  eyelids  are  sometimes 
puffy,  but  no  symptom  of  Bright's  disease  has  appeared.  I  saw  a  lady  in  consultation 
with  a  colleague  ;  she  has  had  scarlatinal  nephritis  for  sev^en  years.  The  albumin 
disappeared  at  intervals,  and  then  reappeared,  but  no  symptoms  of  uraemia  had  ever 
appeared.  As  opposed  to  these  cases,  I  can  quote  two  others  :  one  refers  to  a  woman 
of  twenty-five  years,  and  the  other  to  a  youth  of  seventeen  years  of  age.  Both  have 
scarlatinal  nephritis  with  albuminuria ;  the  symptoms  of  Bright's  disease  persist, 
although  the  albuminuria  has  disappeared  for  some  time. 

This  dissociation  of  the  morbid  acts  of  the  kidneys  is  fairly  common  in  chronic 
nephritis.  Caussade  told  me  of  a  naval  surgeon  who  had  been  suffering  from  pneumo- 
coccal nephritis  for  the  past  five  years.  During  these  five  years  albuminuria  had  been 
the  only  symptom.     The  minor  troubles  of  Brightism  then  began  to  appear. 

Sjrphilis  also  presents  analogous  forms.  It  is  common  to  find  during 
the  first  year  after  infection  albuminuria  without  other  s}'mptoms  of  Bright's 
disease.  On  the  other  hand,  we  see  syphihtic  patients  suffering  from  s}'Tnp- 
toms  of  uraemia,  while  albuminuria  is  for  the  time  being  absent. 

We  shall  study  this  dissociation  of  the  morbid  acts  of  the  kidneys^ 
under  Chloro-Brightism,  Syphilo-Brightism,  and  Gouty  Brightism.    A  subjp.ct 


1138  TEXT-BOOK  OF  MEDICINE 

with  articular  gout  may  have  albuminuria  for  years  without  any  other 
symptoms  of  Blight's  disease.  I  am  acquainted  with  gouty  persons  who 
have  passed  albumin  for  several  years,  and  yet  have  none  of  the  minor 
troubles  of  Brightism.  I  have  often  spoken  to  a  foreign  doctor  who  attended 
my  chnic  at  Necker  Hospital.  He  was  very  gouty,  and  for  seven 
years  passed  large  quantities  of  albumin,  without  having  experienced  the 
least  symptom  of  Bright's  disease.  I  recently  saw  a  young  man  who  was 
subject  to  attacks  of  acute  articular  gout,  and  who,  to  his  own  knowledge, 
had  for  three  years  passed  albuminous  urine.  His  urine  actually  contained 
30  grains  of  albumin  to  the  quart,  but  its  toxicity  was  absolutely  normal. 
I  have  questioned  him  most  minutely,  and  find  that  he  has  had  no  signs  of 
Bright's  disease.  There  is,  therefore,  a  gouty  albuminuria,  which  may  last 
for  years  without  leading  to  Bright's  disease.  These  facts  are  important 
from  the  point  of  view  of  the  prognosis. 

A  patient  suffering  from  albuminuria  due  to  gout,  syphiHs,  scarlatina, 
etc.,  has,  consequently,  nothing  to  fear  as  long  as  the  urinary  depuration 
is  sufficient — that  is  to  say,  as  long  as  the  albuminuria  is  not  accompanied 
by  the  minor  troubles  of  Brightism,  or  by  a  lowering  of  urinary  toxicity. 
I  say  there  is  nothing  to  be  feared,  provided  that  he  diets  himseK  and 
avoids  as  far  as  possible  infectious  conditions,  influenza,  colds,  etc.,  which 
may  hght  up  a  latent  nephritis  in  which  albuminuria  has  been  the  only  sign. 

On  the  other  hand,  a  patient,  although  he  has  no  albumin  in  the  urine, 
but  only  the  minor  symptoms  of  Brightism,  must  be  continually  on  the 
alert,  because  his  urinary  depuration  is  insufficient. 

The  presence  of  these  minor  symptoms  does  not  absolutely  imply  a  grave 
prognosis.  Fortunately,  many  syphihtic,  gouty,  or  ansemic  persons  have 
only  Brightism,  and  fatal  uraemia  does  not  set  in.  When,  however,  a  patient 
is  suffering  from  these  minor  symptoms  of  Brightism,  it  is  a  warning  that 
he  must  be  careful  whether  albuminuria  be  present  or  not. 

Summary. — My  view  of  the  question  is  as  follows  :  Every  case  of  sub- 
acute or  chronic  nephritis  impHes  a  greater  or  less  change  in  the  urinary 
depuration.  It  matters  httle  whether  the  nephritis  is  interstitial,  epithehal, 
or  mixed,  and  whether  the  lesion  is  hmited  to  the  kidneys  or  whether  other 
organs  are  more  or  less  affected  :  the  condition  is  Bright's  disease. 

Bright's  disease  may  follow  on  acute  nephritis,  but  in  most  cases  it  is 
chronic  from  the  outset.  Exacerbations  and  remissions  may  or  may  not 
occur.  Finally,  it  may  be  cured.  Whatever  the  order  and  the  course  of 
the  lesions  and  of  the  symptoms,  the  patient  is  suffering  from  Bright's 
disease ;  the  renal  lesion  and  the  insufficient  urinary  depuration  then  expose 
him  to  the  minor  and  the  major  troubles  which  I  have  enumerated  above. 

We  must  not,  however,  look  upon  the  urinary  insufficiency  and  the 
consequent  poisoning  as  the   only  symptoms.     Other  comphcations  are 


DISEASES  OF   rilK  Kll)x\EYS  Jl;;'.t 

dependent  on  the  nephritis,  or  march  side  hv  side  with  it  :  {jedemii  of  the 
lungs  and  of  the  brain ;  effusions  into  the  pleura,  the  peritoneum,  and  the 
pericardium ;  hypertrophy  and  fibrosis  of  the  heart ;  miliary  aneurysms, 
cerebral  and  retinal  hiemorrhage;  lesions  of  the  liver,  secondary  infectioas, 
pneumonia,  suppuration,  and  gangrene,  are  complications  which  may  be 
present  and  which  may  modify  tlie  complex  symptomatology  of  Bright's 
disease. 

When  these  symptoms  are  present,  the  albuminuria  is  of  minor  im- 
portance, and,  therefore,  the  names  ''  albuminuric  dyspnoea,"  "  convulsions," 
and  "  retinitis  "  are  bad.  Instead  of  remarking  that  a  man  is  suffering 
from  Bright's  disease,  we  often  say  he  is  albuminuric.  This  is  incorrect, 
because  many  people  suffering  from  albuminuria  have  not  Bright's  disease, 
and  in  certain  cases  of  Bright's  disease  albuminuria  may  not  be  present  at 
times. 

The  terms  "  albuminuria  "  and  "  Bright's  disease  "  are  not  only  not 
synonymous,  but  albuminuria  itself,  during  the  course  of  Bright's  disease, 
gives  only  uncertain  information  as  to  the  course  and  the  prognosis  of  the 
disease.  As  a  matter  of  fact,  it  is  not  in  the  cases  with  the  most  marked 
albuminuria  that  we  find  the  major  troubles.  The  albumin  sometimes 
disappears  at  the  gravest  moment,  and,  on  the  other  hand,  it  may  persist 
in  spite  of  the  apparent  cure  of  Bright's  disease. 

In  a  word,  the  key  to  the  whole  situation  is  not  what  passes  through 
the  kidneys,  but  what  does  not  pass.  It  is  not  because  the  kidneys  allow 
some  albumin  to  pass  every  day  that  there  is  danger.  The  danger  hes  in 
the  fact  that  the  diseased  kidneys  do  not  allow  the  elements  of  depuration 
to  pass  in  proper  quantity.  The  poison  retained  in  the  system  may  accumu- 
late rapidly  and  in  large  amount  if  the  urinary  depuration  be  much  affected, 
and  the  major  s}Tnptoms  of  uraemia  then  appear.  If  the  effect  on  the  urinary 
depuration  is  slight,  the  poison  takes  longer  to  accumulate  in  the  system, 
and  the  patient  is  threatened  with  the  condition  which  I  have  just  described 
under  the  name  of  "  Brightism,"  or  "  minor  uraemia." 

The  appearance  or  the  disappearance  of  albumin  in  all  stages  of  Bright's 
disease  condemns  the  theory  of  Mahomed,  who  had  described  a  pre-albumin- 
uric  period,  as  if  Bright's  disease  must  perforce  commence  with  a  stage  in 
which  albumin  was  absent. 

Treatment. — Milk  diet  is  of  prime  importance  in  Bright's  disease  in 
most  cases.  The  patient  should  take  5  or  6  pints  of  milk  at  equal  intervals 
and  in  equal  quantities — for  instance,  J-  pint  every  two  hours.  If  the  patient 
does  not  like  the  milk,  it  may  be  sweetened  or  be  flavoured  with  a  spoonful  of 
coffee.  If  the  milk  does  not  agree  well,  small  quantities  should  be  given  at 
first,  care  being  taken  to  make  it  alkaline  with  hme-water  or  Vichy.  Accord- 
ing to  the  taste  of  the  patient,  cow's  milk,  goat's  milk,  ass's  milk,  koumiss, 


lUO  TEXT-BOOK  OF  MEDICINE 

kephrr,  or  milk  aerated  with  carboiiic  acid  by  meaas  of  a  sparklet,  may  be 
given.  In  some  cases  the  milk  diet  must  be  absolute.  A  few  eggs  may, 
however,  be  allowed,  as  weU  as  a  Httle  cream-cheese,  milk  foods,  cream 
flavoured  with  vanilla  or  chocolate,  and  some  fruit.  As  milk  diet  readily 
produces  constipation,  simple  enemata  or  laxatives  such  as  manna  or 
cascara  should  be  prescribed. 

The  result  is  that  the  urine  becomes  more  abundant,  the  cedema 
diminishes,  and  the  dyspnoea  disappears.  It  is  a  remarkable  fact  that  milk 
diet,  which  has  such  a  marked  action  on  the  toxic  symptoms  and  the  oedema, 
has  less  effect  on  the  albuminuria.  I  have  oft^n  seen  patients  suffering 
from  Brighfs  disease  in  whom  an  absolute  milk  diet  for  months  worked 
marvels,  but  yet  moderate  albuminuria  persisted. 

Some  patients  are  hterally  poisoned  as  soon  as  they  substitute  a  meat 
diet  for  a  milk  one.  One  of  my  colleagues,  whose  health  is  excellent  as 
long  as  he  strictly  follows  his  milk  diet,  suffers  from  headache,  breathless- 
ness,  and  vomiting  if  he  swallows  even  a  few  cups  of  broth. 

Experiments  have  been  made  to  account  for  the  good  effects  of  milk. 
Gilbert  and  Dominici  have  shown  that  the  number  of  bacteria  in  the  in- 
testinal tract  is  much  diminished  with  a  milk  diet.  There  is,  therefore, 
a  quasi-asepsis  of  the  digestive  tube,  and  the  auto-intoxication  is  diminished 
in  proportion.  "We  shall  see  later  that  one  advantage  of  the  milk  cure  is  to 
reduce  the  chlorides  in  the  food. 

The  milk  diet  should  be  continued  for  months  ;  if  it  does  not  agree  well, 
it  should  be  replaced  by  a  mixed  diet  of  fresh  vegetables,  farinaceous  foods, 
cakes,  fruits,  with  some  white  meat.  Tonics  and  injections  of  cacodylate 
of  soda,  may  prove  useful  at  this  period. 

The  skin  should^  be  stimulated  by  massage,  but  I  do  not  ad^4se  vapour 
baths.  The  cutaneous  stimulation  must  be  methodical  and  constant 
(Semmola).  Blisters  over  the  kidneys  aud  dry-cuppings  are  also  indicated. 
Iodide  of  sodium  or  of  potassium  which  is  recommended  when  the 
arterio -sclerosis  is  present  does  not  appear  to  me  to  be  necessary.  Both  have 
the  disadvantage  of  upsetting  the  patient.  They  cause  a  "  bad  mouth  and 
stomach,"  and  their  curative  value,  except  in  syphiHs,  is  questionable,  in 
my  opinion. 

Other  drugs,  such  as  tannin,  gallic  acid,  or  fuchsin,  which  have  been  so 
highly  lauded,  are  of  no  value. 

If  the  oedema  is  persistent,  the  heart  is  failing,  in  spite  of  the  milk  diet, 
and  the  urine  too  scanty,  diuretics  should  be  employed.  We  may  give 
Trousseau's  wine,  digitalis,  digitahn,  diuretin,  or  theobromin.  The  last- 
named  drug,  in  doses  of  30  grains  daily,  is  best.  It  produces  diuresis  and 
dechlorination.  In  many  cases  the  urine  becomes  abundant,  the  chlorides 
diminish,  and  the  cedema  disappears.     "  Furthermore,  the  diuretics  most 


DISKASES  OF  Til K  K 1 1)N K VS  1 1  U 

[jowcrfiil  ill  liiight's  disease  have  proved  themselves  to  be  tlic  l>cst  agents 
iti  causing  dechlorination.  Theobromin  is  a  renal  diuretic,  which  re- 
establishes the  passiige  of  chloridfs  through  the  kidneys,  produces  polyuria, 
and  rids  the  body  of  the  excess  of  chlorides."  These  condusiorLS  are  de- 
duced from  the  convincing  researches  of  Widal  and  Javal.  Digitalis  should 
be  given  if  the  heart  is  at  fault.  If  the  serous  effiLsions  are  abundant,  they 
must  be  drawn  off. 

We  may  here  consider  the  dechlorination  cure  proposed  by  Widal  and 
Javal.  It  refers  especially  to  Bright's  disease  \vith  oedema.  In  some 
patients  it  also  seems  to  have  an  influence  on  the  albuminuria.  We  have 
already  seen  that  Widal  and  his  pupils  have  proved  the  role  of  chloride  of 
sodium  in  the  production  of  oedema  in  Bright's  disease.  The  practical 
deductions  followed  quite  naturally.  As  they  have  proved  that  the  salt 
is  the  dangerous  element  in  many  cases,  it  is  natural  to  restrict  it  in  the 
diet  of  persons  with  Bright's  disease. 

Milk,  which  has  long  been  known  for  its  good  effect  in  nephritis,  no  doubt 
owes  a  part  of  its  quaUties  to  its  small  chloiination.  Widal  and  Javal  have 
shown  that  the  addition  of  chloride  of  sodium  rendered  the  milk  injurious 
as  a  food,  and  that  in  the  same  subject  a  mixed  diet,  though  rich  in  pro- 
teids,  sugar,  and  fats,  did  not  hinder  (if  salt  were  not  added)  the  disappear- 
ance of  oedema  and  albuminuria,  and  might,  therefore,  help  in  the 
dechlorination  cure.  Rice,  pastry,  and  food  pastes  give  similar  results^ 
pro\'ided  no  salt  be  added  in  their  preparation.  As  these  foods  contain 
only  traces  of  chlorides,  we  can  employ  them  to  vary  the  diet  in  certain 
cases  of  Bright's  disease.  We  know  that  chloride  of  sodium  is  absolutely 
prejudicial  to  patients  suffering  from  Bright's  disease,  especially  to  those 
who  have  oedema,  and  the  salt  must,  therefore,  be  excluded  from  their  diet. 
As  to  the  diet :  milk  alone,  or  lacto-vegetarian  diet,  to  which  meat  may 
be  added.  It  is  varied  to  suit  the  patient,  and  is,  indeed,  almost  a  question 
of  experiment. 

In  ursemia  with  acute  dehrium,  epileptiform  convulsions  or  coma, 
and  acute  oedema  of  the  lungs,  bleeding  should  be  employed  up  to  about 
10  ounces,  and  repeated  as  may  be  necessary.  Bleeding,  if  properly 
employed,  gives  excellent  results,  and  often  arrests  the  convulsions,  which 
are  prone  to  be  fatal.  The  improvement  obtained  is  due  to  two  causes : 
first,  bleeding  f  acihtates  the  absorption  of  the  visceral  oedema ;  and,  secondly, 
it  withdraws  a  considerable  quantity  of  the  uraemic  poison.  In  the  absence 
of  blood-letting,  leeches  may  be  appUed  behind  the  ears  or  in  the  lumbar 
region. 

I  formerly  asked  myself  whether  transfusion  might  not  be  of  ser\-ice 
in  ura3mia,  and  whether  the  pure  blood  so  introduced  might  not  modify  the 
vicious  composition  of  the  blood  in  the  body.  I  have  performed  trans- 
IL  73 


1142  TEXT-BOOK  OF  MEDICINE 

fusion  on  ten  occasions.  My  cases  are  too  few  for  any  definite  conclusions, 
but  they  seem  to  show  that  the  transfusion  of  3  or  4  ounces  of  blood  has  a 
beneficial  influence  on  uraemia,  and  may  hold  it  in  check  for  a  period  which 
varies  with  the  nature  and  the  severity  of  the  lesions.  This  result  was  very 
clear  in  my  first  case.*  It  is  evident  that  the  transfusion  of  4  ounces  of 
blood  could  not  modify  the  renal  lesions,  but  the  headache,  vomiting, 
convulsions,  and  coma  were  kept  in  check.  For  the  time  being  we  cannot 
draw  any  other  conclusions,  but  we  may  well  ask  what  might  happen 
if,  instead  of  performing  a  single  transfusion,  a  series  of  them  were 
performed. 

In  Stohr's  case  transfusion  was  performed  for  acute  uraemia.  The 
patient  succumbed  thirteen  days  later  from  pleuro-puhnonary  trouble,  but 
the  operation,  says  Bartels,  was  a  brilhant  success  as  far  as  the  ursemic 
symptoms  were  concerned.  Behna  Swiouthowsky  performed  transfusion 
in  a  woman  with  puerperal  eclampsia,  and  the  success  was  complete  and 
lasting. 

In  uraemie  dyspnoea,  which  may  be  most  severe,  we  may  use  various 
means,  especially  bleeding.  Small  injections  of  morphia  should  be  given, 
each  injection  containing  i  to  J  grain.  I  do  not  share  the  prejudice  of 
certain  physicians  as  to  the  use  of  morphia  in  Bright's  disease.  It  gives 
good  results  when  it  is  properly  used. 

Some  years  ago  I  decided  to  try  ipecacuanha  in  ursemic  dyspnoea.  The 
drug  succeeded  the  better  because  the  dyspnoea  is  rather  toxic,  and  not  so 
much  dependent  on  oedema  of  the  lung.  I  gave  pills  of  ipecacuanha  and 
opium  every  two  hours.  The  drug  is  stopped  as  soon  as  vomiting  threatens, 
and  is  given  again  on  the  following  days,  if  necessary.  I  have  seen  several 
cases  which  were  much  reheved.  Inhalations  of  oxygen  have  also  been 
extolled  in  ursemic  dyspnoea. 

Uraemie  headache  is  reheved  by  the  apphcation  of  leeches  behind  the 
ears  and  by  antipyrin  in  doses  of  15  to  30  grains  daily. 

Uraemie  vomiting  is  sometimes  very  difficult  to  reheve.     The  patient 

must  be  placed  on  starvation  die't— no  water,  no  milk.     He  may  be  allowed 

a    few    pieces    of    ice ;    enemata,    containing   5   ounces   water,    ^    ounce 

lactose,    the   yolk    of   an   egg,    and    3  drachms   peptone,   are  prescribed. 

As    soon    as    the    stomach    has    become    more    tolerant,    a   wineglassful 

of  iced  water,  preceded   by  a  teaspoonful   of   the   foRowing  solution,  is 

given : 

lime-water         ..  ..  ..  ..  ..  ,.3  ounces. 

Hydroclilorate  of  cocaine  . ,  . .  , .  . .     1  grain. 

Hydrochlorate  of  morphia  . .  . .  . .  •  •     i  grain. 

*  Dieulafoy,  "  Etude  sur  la  Transfusion  du  Sang  dans  la  Maladie  de  Bright " 
{Gaz.  Hebd.,  18  Janvier,  1884). 


DISKASES  OF  THE  KIDNEYS  1143 

Oliguria  and  anuria  aro  fairly  frequently  met  with  in  Bright's  disease. 
They  are  tlie  diivct  cause  of  the  uneiiiic  symptoms.  As  I  remarked  above, 
it  is  not  the  extent  of  the  lesion  which  of  itself  is  the  cause  of  oliguria  or 
anuria  in  Bright's  disease.  If  the  oliguria  ran  a  parallel  course  with  the 
renal  lesions,  we  should  not  have,  as  is  sometimes  seen,  periods  of  oliguria 
alternating  ^^'ith  periods  in  wliich  the  secretion  in  normal  or  in  excess.  It 
is,  therefore,  evident  that  in  Bright's  disease  the  urinary  secretion  is  not 
only  dependent  on  the  lesions  of  the  kidneys  and  the  obstruction  of  the 
tubules,  but  also  on  an  intoxication  which  at  times  afiects  or  destroys  the 
functions  of  the  kidneys.  Anuria  in  Bright's  disease  is,  therefore,  difficult 
to  reheve  by  blood-letting  or  by  means  of  diuretics,  and  it  is  because  I  had 
failed  in  anuria  or  ohguria  due  to  Bright's  disease  with  the  known  diuretics 
that  I  was  anxious  to  try  as  a  diuretic  an  extract  of  the  cortical  substance  of 
the  kidney. 

With  this  object  in  view,  my  assistant  prepared  the  following  solution, 
to  which  I  have  given  the  name  of  nephrin  :  A  fresh  bullock's  kidney  is 
placed  in  a  sterile  vessel ;  the  cortical  substance  is  removed  with  every 
antiseptic  precaution.  It  weighs  about  200  grammes.  The  cortical  sub- 
stance is  pounded  in  a  mortar,  and  to  it  are  added  300  grammes  of  neutral 
glycerin  and  200  grammes  of  sterile  water  containing  05  per  cent,  of  sea-salt. 
The  w^hole  is  then  macerated  for  five  hours  in  a  vessel  surrounded  by  ice. 
The  filtration  is  carried  out  in  two  parts  :  (1)  filtration  of  the  whole  mass 
through  a  filter  of  Chardin  paper ;  (2)  filtration  of  the  Hquid  thus  obtained 
through  a  Chamberland  candle  (stBrOized  in  the  autoclave  at  115°  C). 
This  filtration  is  made  with  compressed  air  at  a  variable  pressure  by  means 
of  D'Arsonval's  ingenious  apparatus.  We  thus  obtain  50  to  55  grammes 
of  a  yellowish,  transparent,  viscid,  and  absolutely  sterile  Hquid,  and  eight, 
ten,  or  twelve  subcutaneous  injections  are  given  daily,  each  injection  con- 
taining 50  centigramjnes  of  nephrin  and  50  grammes  of  sterilized  water. 

We  are  so  helpless  in  cases  of  ohguria  and  of  anuria  that  I  felt  compelled 
to  try  this  new  means,  in  the  hope  that  it  might  be  not  altogether  useless. 
It  is  not  possible  to  pass  judgment  after  a  single  case.  If,  however,  the 
reader  will  peruse  the  account  of  this  case,  he  "will  see  that  the  urinary 
secretion,  wliich  had  stopped  completely  for  five  days,  reappeared  after 
the  injections  of  nephrin.  At  the  same  time  as  the  urinary  secretion  re- 
appeared, there  was  a  notable  improvement  in  the  patient's  condition. 
The  stupor  passed  off,  and  he  took  his  milk ;  the  sweating  of  urea 
diminished.  I  noticed  that  after  each  injection  of  nephrin,  especially 
after  the  first  ones,  the  symptoms  were  improved.  It  is,  therefore,  per- 
missible to  beheve  that  subcutaneous  injections  of  nephrin  may  be  of 
some  sersace  in  cases  of  anuria,  especially  in  Bright's  disease.*  Nephrin 
*  Dieulafoy,  Societe  de  Medecine  des  Hopitaux,  Seance  du  14  Octobre,  1892. 

To— 2 


1144  TEXT-BOOK  OF  MEDICINE 

has  since  been  employed  in   many  cases.     Gonin   reports   the   following 
case  : 

In  a  woman  forty-nine  years  of  age,  with.  Bright's  disease,  symptoms  of  ursemia 
appeared :  dyspnoea,  uncontrollable  vomiting,  oliguria,  and  abundant  albuminuria. 
As  the  condition  did  not  yield  to  bleeding  and  other  measures,  an  injection  of  nephrin 
was  given  every  day.  The  urine  gradually  rose  to  80  ounces,  and  vomiting  ceased. 
When  the  remedy  was  discontinued,  the  former  symptoms  reappeared,  and  again  gave 
way  to  the  remedy. 

Scliiperovitsch,  of  St.  Petersburg,  has  given  fresh  kidney  extract  to  thirty-five 
patients  suffering  from  nephritis,  with  or  without  ursemia.  The  patients  were  not  given 
any  other  drug,  and  took  a  meat  diet.  The  conclusions  arrived  at  by  the  author  are : 
In  40  per  cent,  of  the  cases  the  albumin  disappeared  from  the  urine.  The  remedy 
caused  marked  improvement  in  the  general  condition,  and  cessation  of  the  uraemic 
symptoms.  When  the  remedy  was  suspended,  the  symptoms  returned  after  a  period 
which  varied  in  each.  case.  The  kidneys  of  animals,  therefore,  possess  diuretic 
properties. 

Injections  of  serum  are  very  harmful,  on  account  of  the  chloride  of 
sodium  contained  in  the  serum.     I  advise  injections  of  sterihzed  water. 

These  different  remedies  may,  therefore,  be  of  service  in  ursemia.  Drastic 
purgatives  must  not  be  given  to  ursemic  patients,  because  the  purgative 
robs  the  system  of  fluid  necessary  for  the  secretion  of  urine.  Bhsters 
should  be  avoided.  Opiates  must  be  given  in  strict  moderation,  and  injec- 
tions of  morphia  should  be  reserved  for  dyspnoea.  We  must  not  forget  that 
remedies  given  in  excessive  doses  and  imperfectly  eliminated  by  the  diseased 
kidney  may  cause  symptoms  of  poisoning  (Bouchard,  Chauvet).  This  fear, 
however,  must  not  be  exaggerated,  and  in  syphihtic  nephritis  there  must 
be  no  hesitation  in  prescribing  mercury  and  iodide  of  potassium,  whilst 
carefully  watching  the  action  of  the  remedies.  The  surgical  treatment  of 
Bright's  disease  will  be  discussed  in  the  next  section. 

Sufferers  from  Bright's  disease,  on  account  of  their  insufficient  urinary 
depuration,  must  avoid  food  rich  in  ptomaines— game,  certain  lands  of 
fish,  mussels,  shell-fish,  etc.  I  witnessed,  in  company  with  Potain  and 
Boncour,  the  onset  of  fatal  trouble  in  a  patient  with  Bright's  disease  who  was 
poisoned  by  bad  shell-fish.* 


VI.  DISCUSSION  ON  UNILATERAL  NEPHRITIS— SURGICAL 
TREATMENT  OF  NEPHRITIS. 

Can  one  of  the  kidneys  remain  healthy  whilst  its  fellow  is  attacked  by 
nephritis,  or,  in  other  words,  can  unilateral  nephritis  occur  ? 

These  questions  are  the  more  important  in  that  surgery  now  claims  a 

large  share  in  the  treatment  of  nephritis.     At  first  its  intervention  was 

*  Dieulafoy,  "  Brightism  ct  Toxhemie  Alimentaire  "  (La  Presse  Medicale,  1896, 
p.  205). 


DISEASES  OF  THE  KIDNEYS  11  15 

limited  to  certain  easf^s  of  unilateral  nephritis — tuberculosis,  suppurating 
infarcts,  and  abscess  of  the  kidneys,  stone  in  tlie  kidney,  and  floating 
kidney.  Since  then  it  has  intervened  in  acute  and  chronic  nephritis.  Nu- 
merous papers  on  this  subject  have  been  pubhshed  in  France  and  abroad. 
It  will  suffice  to  quote  the  names  of  Pousson  (France;),  Israel  and  Ilo.se 
(Germany),  Rovsing  (Denmark),  Fergus.son  and  Edcbohls  (United  States), 
Newman  and  Harrison  (England),  to  show  the  importance  of  the  work  which 
has  been  undertaken  in  this  direction.  These  works  should  fix  our  attention, 
and  we  physicians  must  ask  ourselves  what  is  the  exact  value  of  surgical 
intervention,  and  how  far  is  it  beneficial  in  acute  and  chronic  nephritis. 

In  unilateral  nephritis  the  conditions  are  particularly  favourable  for 
surgical  intervention,  and  in  such  cases  an  operation  is  often  indicated. 
We  must,  therefore,  review  the  pathological  conditions  which  favour 
unilateral  lesions  in  the  kidney,  and  see  which  cases  lend  themselves  best 
to  operation. 

1.  Ascending  infection  frequently  affects  one  kidney  alone.  The  in- 
fectious agents  which  start  from  the  genito-urinary  passages,  especially 
from  the  bladder,  sometimes  affect  both  Iddneys  ;  at  other  times  one  kidney 
only.  Statistics  show  that  the  lesion  is  unilateral  19  times  in  150  cases 
(Godhardt),  19  times  in  71  cases  (Weir).  Unilateral  nephritis  has  been 
experimentally  reproduced  (Albarran).  It  is  favourable  for  surgical  inter- 
vention, as  in  the  following  examples  : 

Pousson  had  a  patient  who  suffered  for  a  long  time  from  purulent  cystitis ;  acute 
inflammation  of  the  right  kidney  supervened  ;  pain  intense,  fever  very  high,  lumhar 
region  indiu-ated  and  very  painful  on  pressure.  Pousson  operated.  The  perirenal  cellular 
tissue  was  healthy,  but  at  the  upper  end  of  the  kidney  a  small  abscess  was  found, 
and  incision  along  the  convex  edge  disclosed  a  large  number  of  small  mihary  abscesses, 
due  to  the  coli  bacillus.     The  operation  was  followed  by  recovery. 

Pousson  quotes  several  other  cases  of  unilateral  ascending  nephritis  cured  by  surgical 
intervention.  A  case  of  Jordan  refers  to  a  man  who,  after  gonorrhoea,  was  taken  ill 
with  pains  in  the  right  kidney,  high  fever,  albumin  and  pus  in  the  urine.  Weir  opened 
the  kidney,  and  foxuid  it  riddled  with  small  abscesses.  He  performed  nephrectomy. 
The  coh  bacillus  was  present.     A  few  weeks  later  the  patient  was  cured. 

Potherat  performed  a  successful  nephrotomy  in  nephritis  of  the  right  kidney, 
following  on  gonorrhceal  cystitis. 

Wilms  operated  on,  and  cured,  a  young  girl  suffering  from  acute  ascending  pyelo- 
nephritis which  was  secondary  to  cystitis.  The  incision  of  the  kidney  disclosed  pvu*ulent 
tracts.     The  coli  bacillus  was  the  infective  agent. 

Le  Nouene  has  collected  eleven  cases  of  abscess  secondary  to  infection 
of  the  bladder,  and  treated  by  surgical  intervention.  The  coli  bacillus  was 
the  most  common  agent.  These  eleven  cases  are  as  follows  :  Eight  cases  of 
nephrotomy,  seven  recoveries,  and  one  death  ;  two  cases  of  nephrectomy,  one 
cure  and  one  death  ;  one  case  of  decapsulation,  cured.  In  one  of  the  fatal 
cases  the  nephritis  was  double  ;  in  the  other  it  was  probably  double  and 


1146  TEXT-BOOK  OF  MEDICINE 

tubercular.  It  is  certain  that  the  chance  of  a  cure  is  much  greater  when 
the  nephritis  is  unilateral.  The  clinical  symptoms  (locahzation  of  the  pain, 
swelHng  of  the  region)  do  not  show  that  the  nephritis  is  unilateral.  It  is 
necessary,  when  possible,  to  separate  the  urine  by  Luys's  segregator,  which 
indicates  the  condition  of  each  kidney. 

2.  Infection  by  the  blood-stream  is  also  hkely  to  cause  a  unilateral  lesion. 
Castaigne  and  Eathery  quote  the  following  examples  : 

In  a  patient  who  died  on  the  nineteenth  day  of  typhoid  fever  the  post-mortem 
examination  revealed  two  abscesses  as  big  as  a  large  nut  in  the  right  kidney,  but  no 
pus  in  the  left  kidney.  In  the  case  of  a  young  man  who  died  of  staphylococcic  infec- 
tion, due  to  osteomyelitis,  the  left  kidney  was  riddled  with  miliary  abscesses.  Finally, 
in  the  case  of  a  patient  who  died  of  pneumococcal  infection  with  suppurating  pneu- 
monia, they  found  three  small  abscesses  in  the  left  kidney,  whilst  the  right  kidney  was 
healthy. 

Surgical  intervention  has  sometimes  given  good  results  ia  cases  due  to  blood  infec- 
tion. Israel  operated  successfully  for  nephritis  of  the  left  kidney,  secondary  to  a 
carbuncle.     He  removed  the  kidney,  which  contained  miliary  abscesses. 

Monod  has  reported  the  case  of  a  young  girl  who  was  taken  iU  "  with  quick  pulse, 
temperature  104°  F.,  and  incessant  vomiting,  and  painful  mobile  tumour  in  the  region 
of  the  right  kidney."  The  urine  contained  neither  albumin  nor  pus.  Monod  per- 
formed nephrectomy,  and  recovery  followed.  The  kidney  was  enormous,  and  contained 
miliary  abscesses. 

Pousson  performed  nephrotomy  on  a  woman  with  acute  nephritis  of  the  right 
kidney,  probably  due  to  influenza.  The  urine  contained  pus,  and  the  pain  was  acute 
in  the  right  lumbar  region.  Pousson  found  an  enlarged  kidney,  of  a  dead-leaf  colour, 
with  an  abscess  at  its  upper  end.  Incision  of  the  kidney  showed  no  pus  anywhere  else. 
The  case  was  followed  for  four  years,  and  recovery  was  maintained. 

Koutier  has  communicated  the  following  case  to  the  Societe  de  Chirurgie  : 

A  young  woman  was  sent  to  him  with  the  diagnosis  of  pyelo-nephritis.  Her  tempera- 
ture was  very  high.  The  urine  was  not  purulent,  and  did  not  show  any  trace  of  albumin. 
Much  pain  in  the  right  renal  region.  A  lumbar  incision  disclosed  a  somewhat  enlarged 
kidney  ;  on  opening  it,  scattered  points  of  pus  were  found. 

In  nephritis  due  to  blood  infection  and  to  ascending  infection  it  is 
necessary  to  segregate  the  urine  in  order  to  ascertain  the  condition  of  the 
kidneys.  We  may  not  find  any  pus  in  the  urine  from  the  affected  kidney, 
but  it  is  rare  not  to  find  albumin. 

In  some  cases  of  infective  nephritis  pus  does  not  appear.  We  find 
simply  congestion  of  the  kidney,  which  is  perhaps  an  early  stage. 

3.  Tuberculosis  of  the  kidney  is  often  unilateral.  This  question  will 
be  discussed  in  Section  IX.  Vigneron,  collecting  the  statistics  of  Eoberts, 
Dickinson,  Gaultier,  Morris  and  Gergon,  found  that  the  lesions  were  unilateral 
in  99  out  of  205  cases  of  tuberculosis  of  the  kidney.  Albarran  found  that 
the  lesions  were  bilateral  in  15  to  20  per  cent,  of  the  cases.  According  to 
Tamayo,  the  lesions  were  unilateral  in  32,  and  bilateral  in  59  cases.  Unilateral 
tubercular  nephritis,  if  operated  upon  early,  is  amenable  to  surgical  inter- 


DISEASES  OF  THE  KIDNEYS  II  ^7 

vention.  It  is  essential  to  examine  the  urine  from  each  kidney  separately, 
in  order  to  know  the  condition  of  the  kidney  which  is  healthy,  or  is  sujjposed 
to  be  so.  The  healthy  kidney  may  show  compensatory  hypertrophy,  and 
as  pain  is  present,  we  might  make  a  mistake  in  the  absence  of  segregation 
of  the  urine. 

4.  I  shall  refer  in  greater  detail  to  unilateral  nephritis,  which  is  sometimes 
associated  with  a  movable  kidney.  This  question  is  still  under  discussion, 
and  I  must,  therefore,  give  details.  For  a  long  time  a  movable  kidney  was 
considered  to  be  exempt  from  lesions.  Tuffier  has,  however,  said  that,  if  in 
operating  for  movable  kidney,  we  find  the  capsule  of  the  organ  to  be  fibro- 
lipomatous or  indurated,  we  must  think  of  an  infective  lesion.  This 
point  must  never  be  lost  sight  of  in  these  cases.  In  certain  cases  we  find 
albuminuria.  The  organ  is  often  enlarged,  and  may  show  nephritis.  A 
few  years  ago,  in  company  with  Guyon  and  Robin,  I  saw  a  lady  whose  right 
kidney  was  movable.  The  kidney  was  enlarged,  painful,  and  the  albumin 
was  abundant.  (Edema  and  other  complications  led  me  to  suppose  that 
both  Iddneys  were  affected  by  nephritis.  This  question  of  nephritis  in 
movable  kidney  has  entered  a  new  phase  since  the  works  of  Edebohls,  Box 
and  Newmann.  These  writers  performed  nephropexy  in  subjects  suffering 
from  floating  kidney  and  albuminuria,  and  found  that  the  albuminuria 
disappeared  after  the  operation.  Box  quotes  a  case  of  floating  Iddney  with 
chronic  nephritis  and  albuminuria.  After  the  operation  every  sign  of 
nephritis  disappeared. 

The  most  complete  work  in  this  field  is  due  to  Edebohls.*  He  had 
occasion  to  perform  nephropexy  in  five  cases  of  floating  kidney  with  coexist- 
ing chronic  nephritis.  The  nephritis  was  undeniable,  being  proved  de  visu. 
The  urine  contained  albumin  and  casts.  In  three  out  of  the  five  cases 
operated  on,  the  kidney  was  fij^ed,  and  the  nephritis  was  also  cured,  the 
albumin  and  the  casts  disappearing  from  the  urine.  Edebohls  performed 
bilateral  nephropexy  on  a  woman  in  whom  one  kidney  was  affected  by 
chronic  nephritis.  The  urine  became  normal,  and  she  was  cured  simul- 
taneously of  all  her  trouble. 

Although  the  cases  reported  by  Edebohls  do  not  give  all  the  medical 
details  of  the  question,  it  is  none  the  less  true  that  people  with  movable 
kidney  have  albuminuria.  The  albumin  is  present  in  14  per  cent.,  according  to 
SchiUing.  There  are  also  people  who  have  albuminuria,  casts  and  coexisting 
nephritis,  as  proved  by  surgeons.  It  must,  therefore,  be  admitted  that  a  direct 
relation  exists  between  movable  kidney  and  the  development  of  nephritis. 
"  It  is  incontestable,"  says  Lepine,  "  that  a  displaced  kidney  is  predisposed 
to  the  development  of  nephritis.  Kinldng  of  the  ureter  may  cause  not  only 
changas  in  the  excretion  of  urine,  but  also  stasis  of  the  urine  in  the  canaHcuh, 
*  Medical  News,  April  22,  1899. 


1148  TEXT-BOOK  OF  MEDICINE 

which  is  very  favourable  to  infection  of  the  kidneys."  In  conclusion,  the 
association  of  nephritis  and  of  floating  kidney  is  one  of  the  most  interesting 
facts  in  the  pathogenesis  of  chronic  unilateral  nephritis  on  the  one  hand 
and  the  surgical  treatment  of  chronic  nephritis  in  general  on  the  other. 
When  Edebohls  found  that  he  could  cure  chronic  nephritis  by  fixing  the 
kidney,  he  hoped  to  employ  this  mode  of  treatment  successfully  in  all  forms 
of  chronic  nephritis.  We  find,  however,  chronic  unilateral  nephritis  and 
chronic  bilateral  nephritis  (Bright's  disease),  which  is  very  different. 

5.  Chronic  unilateral  nephritis  (leaving  aside  calcuh,  tuberculosis,  and 
sjrphiHs  of  the  kidney)  is  found  not  only  in  floating  Iddney,  but  also  under 
other  conditions. 

A  kidney  may  be  infected  without  the  infection  leading  to  the  formation 
of  pus.  The  toxines  may  cause  an  infecting  sclerosis  which  leads  to  the 
death  of  the  renal  cells  and  to  the  proliferation  of  the  connective  tissue. 
This  process  may  be  confined  to  one  kidney  only  and  we  have  a  unilateral 
nephritis. 

f  In  many  cases  surgeons  have  been  able  to  examine  these  cases.  Thus, 
Edebohls,  on  exposing  both  kidneys,  has  often  found  that  only  one  kidney 
was  attacked  by  nephritis.  On  referring  to  the  statistics  of  nineteen  cases 
of  chronic  nephritis  operated  on  by  him,  we  see  that  in  several  cases  where 
both  kidneys  were  exposed,  the  chronic  nephritis  was  unilateral.  The  exist- 
ence of  chronic  nephritis  was  here  beyond  doubt,  because,  in  addition  to  the 
albumin  and  the  casts  found  in  the  urine,  the  condition  of  the  decapsulated 
kidney  was  verified,  and  histological  examination  made  of  the  portions  re- 
moved during  the  operation.  Several  of  the  patients  operated  on  recovered, 
while  others  were  much  improved. 

In  some  of  the  pubhshed  cases  of  chronic  unilateral  nephritis  the  chief 
symptoms  were  pain  and  hsematuria.  The  pains  are  at  times  very  acute, 
and  the  haBmaturia  is  often  persistent  or  abundant.  In  these  cases  of  mixed 
nephritis  the  lesions  chiefly  afiect  the  glomerular  system  and  the  con- 
nective tissue.  I  am  of  opinion  that  some  of  these  cases  are  due  to  tuber- 
culosis. In  some  of  the  pubhshed  cases,  nevertheless,  it  does  seem  that 
tuberculosis  was  not  present,  and  that  they  were  reaUy  cases  of  chronic 
unilateral  nephritis,  with  pain  and  hsematuria.  They  were  cured  by  the 
operation. 

6.  We  now  come  to  a  side  of  the  question  which  has  not  yet  been  eluci- 
dated. Our  discussion  so  far  has  referred  principally  to  unilateral  nephritis 
and  its  surgical  treatment.  On  reading  the  reports  of  the  surgical  treat- 
ment, we  find  that  the  operation  has  been  frequently  performed  in  Bright's 
disease.  The  term  "  Bright's  disease  "  imphes  the  idea  of  bilateral  nephritis. 
The  presence  of  albumin  and  casts  in  the  urine  is  not  sufl&cient  to  prompt 
the  diagnosis  of  Bright's  disease.     Albumin  and  casts  may  be  found  when 


DISEASES  OF  THE  KIDNEYS  1149 

only  one  kidney  is  aflected.  If  the  other  kidney  is  healthy,  the  urinary 
depuration  is  sufficient,  and  there  is  no  need  to  fear  uraemia.  This  con- 
dition ia  not  Briglit's  disease.  We  mu.st,  therefore,  not  speak  of  having 
operated  on  a  case  of  Briglit's  disease  when  only  one  kidney  is  involved. 
This  confusion  is  sometimes  made  by  surgeons.  It  may  falsify  our  ideas. 
A  case  is  called  Bright's  disease  (which  presupposes  bilateral  nephritis),  and, 
on  reading  the  report,  we  find  that  it  is  a  case  of  unilateral  nephritLs. 

Surgical  intervention  has,  however,  been  frequent  in  Bright's  disease 
(chronic  bilateral  nephritis).  This  question  is  well  put  by  Bassan.  I  quote 
verbatim  : 

"  In  an  article  which  appeared  in  the  British  Medical  Journal  of 
November  23,  1902,  Edebohls  compared  decapsulation  of  the  kidney  with 
nephrotomy  and  nephrectomy.  He  carried  out  decapsulation  in  40  cases 
of  Bright's  disease — 23  cases  in  women,  1  case  in  a  child,  and  16  cases  in 
men,  of  whom  6  were  doctors.  In  16  cases  Edebohls  removed  the  capsule 
and  fixed  the  kidney.  In  4  cases  the  right  kidney  was  operated  on,  and 
in  the  other  12  cases  both  kidneys  were  decapsulated.  In  the  24  other 
cases  double  and  total  decapsulation  was  performed,  which  brings  the 
number  of  bilateral  interventions  carried  out  by  Edebohls  to  36.  In 
other  words,  36  persons  were  operated  on  by  him  for  Bright's  disease 
(bilateral  chronic  nephritis),  and  from  that  time  Edebohls  announced  new 
facts." 

What  is  the  nature  of  these  operations  ?  It  is  not  usual  in  a  text- 
book of  medicine  to  describe  operative  technique,  and  I  shall  therefore  rest 
satisfied  with  pointing  out  that  these  operations  were  nephrotomv,  decapsula- 
tion, nephropexy,  etc.  By  nephrotomy  we  remedy  the  increased  tension  in 
the  kidney.  The  loosening  of  the  inextensible  capsule  frees  the  kidney  and 
favours  proper  circulation  and  functional  acti\aty.  According  to  Edebohls, 
the  operation  assists  the  insufficient  circulation  of  the  blood  in  the  kidney. 
With  this  object  in  view,  he  performs  decapsulation  or  decortication  of  the 
kidney  (partial  or  extensive  ablation  of  the  capsule).  He  calls  this  operation 
"  nephrocapsectomy." 

According  to  Edebohls,  "  decortication  renders  the  circulation  of  the 
kidney  more  active,  and  brings  more  arterial  blood  to  the  diseased  organ 
through  the  bloodvessels  of  the  perirenal  fat,  the  vessels  being  increased 
in  size  and  in  number.  Decapsulation,  which  places  the  entire  cortical 
surface  in  direct  contact  with  this  area,  rich  in  vessels,  is  said  to  result  in 
the  formation  on  a  large  scale  of  a  vascular  network  between  the  kidnev 
and  the  fatty  tissue.  In  this  way  there  arises  an  active  arterializatlon  of 
the  diseased  kidney,  which,  by  the  creation  of  a  new  circulation,  would 
tend,  if  not  to  an  absolute  cure,  at  least  to  an  improvement  of  the  lesions  in 
Bright's  disease.'" 


1150  TEXT-BOOK  OF  MEDICINE 

It  is  certain  tliat  the  results  of  surgical  intervention  are  often  excellent 
in  a^  case  of  acute  or  ckronic  unilateral  nephritis,  and  they  appear  to  be 
worthy  of  consideration  in  Bright's  disease.  It  is,  however,  indispensable 
to  state  clearly  the  indications  and  the  contra-indications  of  surgical  inter- 
vention, and  to  select  cases  that  are  amenable  to  operation.  Eor  the  time 
being  we  are  unable  to  answer  this  question,  because  many  of  the  pubhshed 
cases  are  incomplete  from  a  medical  point  of  view.  I  am  convinced,  how- 
ever, that  this  gap  will  soon  be  filled.  In  Bright's  disease,  which  makes 
progress  in  spite  of  treatment,  we  are  so  often  at  a  loss  that  we  must  try 
to  ascertain  as  clearly  as  possible  the  proper  time  for  surgical  intervention. 


VII.  CASES  OF  ALBUMINUEIA  NOT  DUE  TO  BRIGHT'S 

DISEASE. 

We  have  seen  that  albuminuria  may  be  absent  for  a  time  in  Bright's 
disease.  The  opposite  is  also  true,  and  just  as  in  Bright's  disease  albuminuria 
may  be  absent,  so  also  may  albuminuria  occur,  quite  apart  from  Bright's 
disease.  Cases  of  albuminuria  not  due  to  Bright's  disease  have  become 
more  and  mora  numerous  since  they  have  been  sought  for.  This  question 
has  been  discussed  by  Senator,  Lepine,  Noorden,  and  other  writers. 

Physiological  albuminuria  may  occur  aside  from  any  lesion  of  the  kidneys 
and  any  general  affection.  It  is  probable  that  absolutely  physiological 
albuminuria  does  not  exist,  and  that  in  a  final  analysis  these  cases  of 
so-called  physiological  albuminuria  are  associated  with  a  vicious  process 
in  the  proteids  or  in  the  uropoietic  system.  If,  however,  they  are  not 
physiological  in  the  true  sense  of  the  word,  they  are  at  least  compatible 
with  good  health,  which,  clinically  speaking,  leaves  nothing  to  be  desired. 
To  quote  examples : 

I  attended  a  young  man  wlio  for  some  years  had  noticed  a  fair  amomit  of 
albumin  in  his  urine.  He  examined  his  urine  himself,  and  drew  up  a  comparative 
table  of  the  albiuninuria,  according  to  the  time  of  day,  the  hom's  of  rest  or  work,  and 
the  nature  of  the  food  taken  at  meals.  The  quantity  of  albumin  varied,  but  his  health 
was  good,  and  symptoms  of  Bright's  disease  never  appeared. 

A  doctor  who  was  expert  in  laboratory  work  tested  his  own  urine,  and  was  surprised 
to  find  albumin.  His  health  is  excellent ;  his  urine  shows  a  normal  toxic  coefficient, 
as  I  have  satisfied  myseK  by  experiment ;  and  he  has  never  experienced  any  symptom 
of  Bright's  disease. 

A  friend  of  mine  was  anxious  about  his  httle  daughter,  because  she  had  had  albumin- 
uria since  she  was  four  years  old.  This  condition  lasted  for  sixteen  or  seventeen  years. 
She  has  now  been  married  for  some  years,  and  has  never  had  any  sign  of  Bright's  disease. 

Amongst  these  cases,  I  know  of  none  more  interesting  than  those  reported  to  the 
Clinical  Society  of  London  by  Hawkins.  A  robust  man,  forty-nine  years  of  age, 
had  albuminm'ia  for  twenty-five  years.  A  doctor  passed  albumin  for  forty-three  years, 
but  remained  free  from  Bright's  disease,  though  Bright,  whom  he  had  consulted  thirty 
years  previously,  had  predicted  early  death. 


DISEASES  OF  THE  KTDNRYS  11  "l 

Our  ditBculty  commences  when  we  try  to  interpret  the  facts.  Noorden 
has  classified  tliose  cases  into  several  "roiijw,  according  as  albumin  alone  is 
found  in  the  urine  or  associated  with  glolnilin  or  mucin  ;  according,  also,  as 
the  albumin  is  met  with  in  the  morning  or  at  any  hour  of  the  day  ;  or 
as  it  appears  independently  of  any  external  cause  ;  or  as  it  varies 
with  meals,  exercise,  malaise,  fatigue,  etc.  (intermittent  allmmiiiuria,  cyclic 
albuminuria). 

Te.ssier  classifies  these  cases  as  follows  :  (1)  intermittent  albuminuria 
in  apparently  healthy  subjects ;  (2)  albuminuria  in  youths,  which  is 
generally  intermittent  and  cyclical ;  (3)  albuminuria  of  a  digestive  or 
hepatic  kind ;  (4)  neuropathic  albuminuria,  and  especially  albuminuria 
of  the  erect  position  or  orthostatic  albuminuria. 

These  cases  of  albuminuria  may  be  shght,  intermittent,  or  continuous, 
and  may  have  different  origins,  but  they  are  perfectly  compatible  with 
good  health.  It  is  important  to  find  out  whether  albuminuria  is  or  is  not 
due  to  Bright's  disease,  because  the  prognosis  is  different.  Absence  of 
granular  casts  and  of  the  minor  sjTnptoms  of  Brightism,  together  with 
normal  toxicity  of  the  urine  and  physiological  permeabihty  of  the  kidney, 
shows  that  the  albuminuria  is  not  due  to  Bright's  disease. 

Linossier  and  Lemoine  give  the  following  differential  characteristics : 

1.  In  absolutely  normal  kidneys  orthostatism  only  reveals  its  noxious 
action  by  moderate  diminution  of  the  watery  secretion.  The  excretion  of 
the  sohds  undergoes  no  regular  modification.  The  urea  only  is  eliminated 
in  greater  abundance,  but  this  is  due  rather  to  increased  production  than 
to  excessive  ehmination. 

2.  If  the  kidneys  are  incompetent,  the  diminution  in  the  watery 
secretion  by  the  erect  position  is  much  more  marked  than  when  the 
kidneys  are  normal,  so  that  an  exaggeration  of  the  orthostatic  oliguria 
may  be  looked  upon  as  a  sign  of  functional  insufficiency  of  the  kidney. 
In  this  case  it  is  combined  with  diminished  secretion  of  the  sohds,  and 
especially  of  the  urea.  There  is,  therefore,  oliguria  and  also  orthostatic 
hypo-azoturia. 

3.  If  the  Iddneys  are  even  more  incompetent,  the  influence  of  ortho- 
statism is  still  further  revealed  by  the  appearance  of  albumin  or  by  the 
exaggeration  of  an  already  existing  albuminuria. 

Nevertheless,  it  is  at  times  very  difficult  to  diagnose  between  simple  albu- 
minuria and  that  due  to  a  renal  lesion.  Nephritis  limited  to  a  part  of  the 
kidney  (tubercular  lesion)  may  have  albuminuria  as  its  sole  sign.  We  only 
discover  later  that  this  simple  albuminuria  was  in  reahty  the  precursor  of 
renal  tuberculosis. 

Some  cases  of  nephritis,  especially  of  unilateral  nephritis,  may  for  a 
long  time  give  no  sign  save  albuminuria.     We  have  no  proof  that  some  forms 


1152  TEXT-BOOK  OF  MEDICINE 

of  Bright's  disease  are  not  primarily  limited  to  one  kidney,  the  lesion  passing 
later  to  the  other  one. 

In  a  difficult  case  of  albuminuria  it  is  well  to  segregate  the  urine  by 
Luys's  apparatus,  in  order  to  study  the  conditions  of  each  kidney. 

The  treatment  of  simple  albuminuria  varies.  The  milk  cure  is  not  so 
essential  as  it  is  in  Bright's  disease.  The  diet  must  be  carefully  regulated, 
and  the  food  selected  on  the  basis  of  practical  experience.  Rest,  or  even  the 
supine  position,  must  be  prescribed,  and  tonics,  alkahs,  or  the  cure  at  Evian 
be  recommended. 

VIII.  AMYLOID  KIDNEY. 

Pathological  Anatomy. — ^We  mean  by  amyloid  degeneration  the  deposit 
in  certain  organs  (kidney,  spleen,  hver,  intestinal  mucosa)  of  a  transparent 
homogeneous  substance,  which,  by  its  chemical  reaction,  is  alHed  to  the 
carbohydrates,  but  which,  by  the  presence  of  nitrogen,  is  also  allied  to  the 
proteids.  This  substance  is  readily  detected  in  the  kidney  and  other  organs 
by  certain  reactions.  A  section  of  the  kidney  is  made,  and  the  surface 
washed  with  water.  An  aqueous  solution  of  iodine  and  iodide  of  potassium 
is  poured  over  it.  The  healthy  parts  assume  a  pale  yellow  tint ;  the 
affected  parts  become  a  mahogany  colour,  distinct  strise  (arterioles)  and 
points  (glomeruh)  being  visible.  Several  writers  include  the  amyloid  kidney 
under  Bright's  disease,  and,  as  a  matter  of  fact,  amyloid  disease  of  the  kidney 
is  in  many  cases  associated  with  parenchymatous  or  interstitial  nephritis. 
Corriil  and  Ranvier  even  state  that  in  diffuse  subacute  nephritis  with  enlarged 
kidney  amyloid  lesions  are  always  present  in  the  vessels  and  the  walls  of 
the  tubules,  the  parenchymatous  nephritis  preceding  the  amyloid  degenera- 
tion. These  mixed  forms  are  included  in  Bright's  disease.  In  other  cases 
(Cohnheim,  Weigert,  Straus)  the  amyloid  change  occurs  alone,  and  therefore 
deserves  special  mention.  The  amyloid  kidney  may  be  enlarged  or  of 
normal  size.  Its  surface  is  smooth  and  whitish  or  yellowish.  On  section,  it 
is  waxy,  and  its  capsule  is  easily  detached.  Atrophy  is  rare.  The  atrophy, 
if  present,  is  anterior  to  the  amyloid  degeneration. 

The  microscopic  examination  is  made  easy  by  the  use  of  gentian  violet, 
which  stains  the  amyloid  substance  violet  and  the  normal  tissue  pale  blue. 
Amyloid  degeneration  attacks,  in  order  of  frequency,  the  glomeruh,  the 
vasa  recta,  and  the  interlobular  capillaries.  The  membrana  propria  of 
the  canahculi  is  not  invaded  except  in  advanced  cases.  The  disease  may 
exist  for  a  long  while  before  the  function  of  the  kidney  is  affected.  When 
parenchymatous  nephritis  is  also  present,  we  find  the  lesions  previously 
described  under  Nephritis.  When  the  Iddneys  are  affected,  we  generally 
find  that  the  spleen,  the  hver,  and  the  muscular  coat  of  the  intestine  are  also 
involved. 


DISK  ASKS  OF  TIIK  KIDNEYS  1153 

Description. — Tlie  syin{)torns  may  be  the  same  as  in  Briglit's  diBeatie. 
At  otlier  times  they  are  practically  absent.  This  diversity  in  the  appearance 
and  the  succession  of  the  symptoms  is  due  to  the  anatomical  condition  of 
the  kidney,  and  varies  according  as  the  amyloid  degeneration  is  pure  or 
associated  with  more  or  less  marked  parenchymatous  lesioas.  When  it  is 
j)ure,  the  symj)toms  may  be  limited  to  urinary  troubles  (polyuria,  diminution 
of  urea,  uric  acid,  phosphoric  acid,  and  of  most  of  the  salts)  (Lecorche). 
\\Tien  it  is  mixed,  other  s^-mptoms  appear.  The  permeabihty  for  methy- 
lene blue,  according  to  Achard  and  Loeper,is  normal  or  increased  in  amyloid 
disease.  This  fact  may  help  in  the  diagnosis  between  it  and  chronic 
nephritis. 

The  question  of  albuminuria  in  amyloid  degeneration  of  the  kidney 
deserves  special  mention.  According  to  certain  writers,  it  is  always 
present.  Others  maintain  that  it  only  supervenes  when  inflammatory 
lesions  are  also  present. 

Straus,  in  his  interesting  monograph,  has  collected  cases  of  amyloid 
degeneration  in  which  albuminuria  was  both  present  and  absent.  Straus 
explains  this  apparent  contradiction  by  the  occurrence  of  the  degeneration 
in  the  vasa  recta  in  the  former  case,  and  in  the  glomeruh  in  the  latter  case. 
In  some  cases  as  much  as  10  to  20  grammes  of  albumin  have  been  found  per 
litre.  Urinary  casts  only  appear  at  an  advanced  phase  of  the  disease. 
They  are  colloid,  but  they  never  give  the  true  amyloid  reaction. 

Uraemia  is  rare  in  amyloid  kidney.  The  patient  is  carried  off  by  other 
complications — uncontrollable  diarrhoea,  pubnonary  tuberculosis,  pneu- 
monia, cachexia  or  coma.     The  prognosis  is  fatal. 

As  regards  diagnosis,  in  amyloid  kidney  we  must  look  for  its  cause. 
Persons  with  tubercular  or  syphiUtic  cachexia,  children  with  caries,  abscess 
of  bone,  or  tubercular  glands,  are  liable  to  suflter  from  amyloid  disease.  Ex- 
amination of  the  other  organs  helps  us  in  the  diagnosis  :  enlargement  of 
the  Uver  and  the  spleen ;  diarrhoea,  due  to  amyloid  disease  of  the  intestine. 

Amyloid  degeneration  of  the  kidneys  is  usually  due  to  caries,  prolonged 
suppuration,  tuberculosis,  or  syphilis.  Gout,  chronic  rheumatism,  malaria, 
and  alcohohsm  have  also  been  incriminated. 

Charrin,  in  his  experiments  on  the  Bacillus  fyocyatieus,  found  that 
after  inoculation,  rabbits  and  guinea-pigs  were  attacked  by  paralysis, 
nephritis,  and,  in  the  long-run,  by  amyloid  degeneration,  though  there  was 
no  suppuration. 

IX.  TUBERCULOSIS  OF  THE  KIDXEY. 

Acute  mihary  tuberculosis,  which  accompanies  general  infection,  merely 
deserves  mention.  In  general  tuberculosis,  especially  in  children,  both 
kidneys  are  often  riddled  with  mihary  tubercles.     Tubercles  are  found  in 


1154  TEXT-BOOK  OF  MEDICINE 

the  cortical  and  medullary  substance.  They  are  small,  transparent,  and 
white  or  greyish.  They  occur  in  "  the  perivascular  connective  tissue,  along 
the  bloodvessels,  and  in  the  glomeruli,  or  the  space  corresponding  to  several 
adjacent  tubules "  (Brault).  This  form  of  mihary  tuberculosis  often 
spares  the  ureters,  the  bladder,  and  the  genito-urinary  organs. 

I  shaU  now  describe  chronic  tuberculosis  of  the  kidney.  The  infection 
may  reach  the  kidney  by  the  blood-stream  (primary  form),  or  may  begin 
in  the  bladder,  prostate,  testicle,  or  epididymis  (ascending  or  secondary 
form).  It  may  invade  both  kidneys,  or,  as  usually  happens,  it  may  be 
limited  to  one  kidney.     In  any  case  the  lesions  finally  end  in  caseation. 

Pathological  Anatomy. — The  removal  of  the  kidney  is  not  always  easy, 
because  numerous  adhesions  fix  the  organ  to  the  lymphatic  glands  of  the 
hilum  and  of  the  lumbar  chain,  to  the  renal  vein,  the  vena  cava,  and  the 
aorta,  in  the  case  of  the  right  kidney ;  to  the  intestine  and  the  peritoneum, 
in  the  case  of  both  kidneys.  The  tumour,  after  removal,  is  bulky,  because 
it  comprises  the  kidney  and  the  perirenal  fat.  The  kidneys  have  not  the 
shapeless  look  5een  in  certain  cases  of  cancer.  The  surface  is  smooth  or  at 
times  nodular  from  the  projection  of  cavities,  and  is  perforated  by  sinuses 
which  connect  the  cavities  with  the  perirenal  tissue.  The  capsule  is 
thickened,  fibrous,  and  adherent  to  the  perirenal  fat,  which  is  of  great 
importance  in  certain  diseases  of  the  kidney.  By  reason  of  the  overgrowth 
of  fibrous  and  adipose  tissue  the  perirenal  fat  may  be  some  inches  in  thick- 
ness, especially  in  the  pelvis,  where  it  forms  Hpomata.  The  fibro-fatty 
tissue  around  the  kidney  prevents  the  renal  lesions  from  spreading  to  the 
rest  of  the  body,  but  this  barrier  is  not  insurmountable,  and,  either 
by  direct  propagation  or  by  the  lymphatics,  infection  from  the  kidney 
may  reach  the  perirenal  tissue.  In  this  way  a  perinephritic  abscess  is 
formed. 

The  abscess  is  sometimes  hmited,  and  of  small  size.  At  other  times  it 
extends  into  neighbouring  regions,  reaches  up  to  the  diaphragm,  opens  into 
the  thoracic  cavity,  and  causes  a  vomica,  or  else  the  pus  descends  towards 
the  ihac  fossa,  and  points  at  the  crural  ring  or  small  trochanter.  It  may 
open  into  the  intestine  or  into  the  bladder.  The  fluid  in  these  collections 
is  sero-purulent  or  sanguinolent,  evil-smelhng,  and  mixed  with  caseous 
debris.  A  guinea-pig  inoculated  with  this  pus  contracts  tuberculosis.  On 
section  of  the  kidney,  we  find  the  following  lesions  :  tubercular  granula- 
tions ;  caseous  foci,  which  are  beginning  to  soften ;  cavities  containing 
caseating  matter  ;  cavities  which  look  hke  abscesses  ;  and  transformation  of 
the  kidney  into  a  putty-hke  mass,  the  ureter  being  obhterated. 

Tubercular  lesions  in  the  kidney  run  a  different  course,  according  as  the 
infection  takes  place  by  the  blood-stream — the  bacillus  first  affecting  the 
cortex,  and  being  transported  thence  by  the  renal  or  capsular  arteries — or 


DISEASES  OF  THE  KIDNEYS  11G5 

as  it  takes  place  by  the  ascending  putii  of  the  bladder,  ureter,  pelvis,  and 
calices,  thus  affecting  first  the  medullary  substance. 

The  tubercles  may  be  few  or  many,  and  may  exist  in  every  part  of  the 
organ.  They  usually  invade  the  cortical  substance  in  the  case  of  blood 
infection,  whilst  they  first  become  localized  in  the  medullary  substance,  in 
the  case  of  ascending  infection.  In  cortical  tuberculosis  Durand-Fardel 
found  tubercle  bacilli  in.  the  parenchyma,  prior  to  the  formation  of 
tubercles.  The  bacilh  are  usually  found  in  the  glomeruU  and  the  terminal 
arterioles  of  the  cortex,  and  may  reach  the  uriniterous  tubules,  which  they 
may  invade  from  without  inwards. 

The  fused  tubercles  or  the  infiltrated  tubercular  tissue  form  caseous 
masses  of  the  size  of  a  hazel-nut  or  of  a  walnut.  These  masses  soften  and 
give  rise  to  cavities.  The  cavities  are  anfractuous  and  well  defined.  They 
contain  debris,  pus,  and  at  times  phosphatic  calcuh.  The  topography  of 
these  ca\TJ:ies  presents  some  variation,  according  to  the  process  which  has 
caused  them.  AVhen  the  tuberculosis  is  cortical,  the  cavities  are  formed 
in  the  cortex,  and  open  by  narrow  or  broad  orifices  into  the  pelvis,  which 
is  not  dilated.  When  the  tubercular  infection  follows  the  ascending  path, 
the  pelvis,  which  is  first  invaded,  is  much  dilated,  and  we  find,  instead  of 
several  more  or  less  gaping  cavities,  one  large  festooned  excavation,  formed 
at  the  expense  of  the  dUated  peMs  and  the  p^nramidal  substance  of  the 
kidney.  The  caUces  and  the  pehis  are  bathed  in  piinilent  caseous  Hquid, 
and  in  some  places  the  organ  is  reduced  to  a  fibrous  shell,  infiltrated  with 
Ume  salts. 

In  some  cases  the  kidney,  including  the  cahces  and  the  pelvis,  is  trans- 
formed into  a  putty-hke  mass,  compared  by  Tuffier  to  the  contents  of  a 
large  dermoid  cyst.  This  degeneration  en  masse  is  due  to  the  obliteration 
of  the  ureter,  w^hich  is  blocked  up  by  the  tubercular  debris.  I  found  this 
condition  in  a  patient  who  died  in  my  wards.  The  kidney  was  transformed 
into  a  caseous,  putty-Hke  mass,  and  surrounded  by  a  fibrous  shell. 

This  obliterating  ureteritis  may  cause  true  hydronephrosis.  In  a  case 
published  by  Tuffier  the  obhteration  of  the  ureter  was  absolute,  the  pehis, 
the  cahces,  and  the  kidney  being  converted  into  a  pseudo-cystic  cavity, 
containing  transparent  sterde  fluid.     Similar  cases  have  been  published. 

Renal  tuberculosis  may  then  present  the  follo^ving  forms  :  (1)  The 
tubercular  infiltration  is  confined  to  the  cortex  (blood  infection),  and  causes 
foci,  cavities,  or  abscesses,  which  empty  into  the  pehis.  (2)  The  tubercular 
lesions  are  ascending,  and  cause  pyelonephritis.  We  may  find  obstruction 
of  the  ureter,  distension  of  the  gland,  retention  of  pus  and  urine,  and  tuber- 
cular lesions  in  the  medullary  substance  and  in  the  cortex.  (3)  Tubercular 
ureteritis  leads  to  obhteration,  and  is  associated  with  tubercular  degenera- 
tion of  the  kidney  en  masse.     (4)  Ureteritis  obhterans  is  associated  with 


1156  TEXT-BOOK  OF  MEDICINE 

tubercular  hydronephrosis.  (5)  The  cellulo-fatty  layer  which  surrounds 
the  kidney  is  attacked  by  sclero-hpomatous  or  by  suppurative  perinephritis. 
All  these  lesions  are  seen  in  the  tubercular  kidney,  and  if  their  topography 
differs  at  first,  according  as  the  infection  is  cortical  or  ascending  (secondary), 
we  may  say  that  at  a  given  moment  the  lesions  become  fused. 

The  ureter  is  usually  affected.  In  ascending  tuberculosis  it  is  always  so. 
It  is  enlarged,  indurated,  constricted,  or  obhterated,  and  sometimes  ad- 
herent to  the  peritoneum,  to  the  utero-ovarian  vessels,  or  to  the  ileum  on 
the  right  and  to  the  sigmoid  on  the  left  side.  It  forms  a  large  hard  cord, 
which  can  be  felt  through  the  abdominal  wall. 

In  the  bladder  we  find  tubercles  at  any  part  of  the  mucosa.  In  de- 
scending tuberculosis  we  may  see  tubercles  at  the  level  of  and  below  the 
ureter  of  the  diseased  kidney  (Albarran,  Israel).  Ulcers  eventually  appear, 
but  their  evolution  is  very  slow. 

In  the  male,  the  vesiculse  seminales,  prostate,  vas  deferens,  and  epididymis 
are  frequently  attacked.  Genital  tuberculosis  is  one  of  the  most  common 
origins  of  secondary  disease  in  the  kidney.  On  the  other  hand,  tuberculosis 
of  the  genital  system  in  woman  is  exceedingly  rare. 

I  have  already  stated  that  tuberculosis  of  the  kidney  is  often 
unilateral.  From  post-mortem  examinations — i.e.,  when  the  infection  has 
had  time  to  become  general— we  find  that  the  lesion  is  unilateral  in  haK  of 
the  cases.  From  the  statistics  of  surgical  intervention  we  see  that  the  second 
kidney  is  immune  in  three-quarters  of  the  cases— a  point  in  favour  of 
operative  interference.  Albarran  estimates  that  in  15  to  20  per  cent,  of 
the  cases  both  kidneys  are  tubercular.  And  though  the  second  kidney  is 
not  tubercular,  at  a  fairly  advanced  period  it  frequently  shows  other  lesions 
— e.g.,  pyelonephritis,  calculous  pyehtis,  and  amyloid  degeneration.  Koch's 
bacillus  is  found  in  the  early  stages  of  the  renal  lesion.  Later  we  usually 
find  the  coh  bacillus,  streptococcus,  and  staphylococcus. 

The  lungs  are  often  infected,  either  before  or  after  the  invasion  of  the 
kidney. 

Description. — Tuberculosis  of  the  kidneys  is  insidious  and  latent  in  its 
commencement.  It  may  remain  almost  latent  until  an  advanced  period, 
especially  if  the  ureter  be  obhterated.  When  I  say  that  it  remains  almost 
latent,  it  would  be  more  correct  to  say  that  it  may  fail  to  be  recognized,  as 
it  is  sometimes  masked  by  tuberculosis  of  the  bladder.  In  some  cases,  after 
remaining  latent  for  a  time,  the  mischief  reveals  itseK  by  certain  symptoms. 
The  patient  passes  pus  or  blood  ;  he  has  acute  pains ;  a  perinephritic  abscess 
appears.  In  any  case,  bladder  symptoms — hsematuria,  pyuria,  albuminuria, 
pain,  and  renal  tumour — are  the  most  common  s\Tnptoms. 

Bladder  Symptoms. — Albarran  has  shown  that  tuberculosis  may 
at  first  simulate  cystitis.     Frequency  of  micturition,  pain,  and  diminution 


DISEASKS  OK  'IMIK   KIDNKY8  Un? 

of  the  capacity  of  the  bladder  are  the  syiiiptoms.  Tlicy  may  lie,  diic.  to 
concomitant  cystitis,  hut  in  most  cases  tlicy  are  only  reflex.  It  is  not  rare 
to  see  patients  who  have  urinary  troubles,  and  who  cornj)lain  of  fre(j[uent  aud 
painful  micturition  when  the  bladder  is  absolutely  healthy,  as  a  cysto- 
scopic  examination  will  prove.  I  recently  saw  a  case  with  Albarran.  The 
bladder  symptoms  were  marked,  while  the  kidney  alone  was  aflcctcd. 

HiEMATURiA. — Haematuria  is  a  frecpient  symptom.  Here,  as  in  pul- 
monar}'  tuberculosis,  hemorrhage  may  be  the  first  sign.  We  find  cases  of 
early  ha)maturia,  which  precedes  the  appearance  of  renal  tuberculosis  by 
months  and  years,  just  as  "  defensive  haemoptysis  "  precedes  the  appear- 
ance of  phthisis.  The  haematuria  is,  as  a  rule,  neither  abundant  nor  obsti- 
nate. We  do  not  find,  as  in  cancer,  long  fibrinous  clots  in  the  ureter,  which 
cause  pain  or  retention  of  urine.  Tubercular  haematuria  supervenes  with- 
out appreciable  cause.  It  is  not  brought  on,  like  calculous  haematuria,  by 
violent  exercise,  riding,  or  driving.  When  it  is  over,  it  may  not  appear 
again,  or  it  may  reappear  only  at  intervals  of  several  weeks  or  months. 

Such  is  the  usual  course  of  events,  and  tubercular  haematuria  has  not 
the  same  importance  as  the  haemorrhage  seen  in  cancer.  We  must  not, 
however,  trust  too  much  to  this  feature.  In  some  cases  the  haematuria  is 
abundant ;  it  may  last  from  two  or  three  months  up  to  four  years. 

RotTTTER's  Case. — A  young  woman  was  taken  ill,  without  cause  and  without  pain, 
with  haematuria.  The  urine  was  blackish,  and  the  quantity  of  blood  lost  considerable. 
After  five  weeks  she  was  pale  and  cachectic,  and  could  not  stand.  She  repeatedly  liad 
renal  colic,  followed,  not  by  the  expulsion  of  calcuh,  but  of  clots.  The  right  kidney 
was  painful  and  enlarged.  Cj'stoscopy  showed  that  the  blood  came  from  the  right  ureter. 
She  was  threatened  with  death.  Nephrectomy  was  performed  by  Routier  six  weeks 
after  the  appearance  of  the  haematuria.  The  bleeding  stopped,  and  the  patient  regained 
her  health.  Her  husband  wrote  a  few  months  later  :  "  The  urine  is  always  clear  ;  she 
looks  splendid,  and  has  grown  fat."  The  kidney  examined  by  PUhet  showed  only 
one  tubercular  focus,  in  a  calyx,  on  a  level  with  the  arterial  arch  of  the  kidney,  but 
this  focus  had  caused  profuse  haematviria,  due  to  the  erosion  of  the  vessels  and  to  the 
arterial  tension.  It  was,  in  short,  a  case  of  primary  tuberculosis,  which  was  circum- 
scribed and  favourable  for  operation. 

Poussox's  Case. — In  a  young  man  the  first  symptom  was  haematuria,  which  lasted 
for  seven  months  and  a  half  without  interruption,  and  increased  in  severity.  He  had 
sharp  attacks  of  haematinia,  with  blackish  urine  and  renal  cohc,  caused  by  the  expulsion 
of  the  clots  and  retention  of  urine  due  to  obhteration  of  the  ureter.  Rest  or  exercise 
had  no  influence  on  the  ha?maturia.  Other  symptoms,  such  as  pyuria  or  enlargement  of 
the  kidney,  were  absent.  Koch's  bacillus  was  found  in  the  urine.  Exploration  of  the 
ureters,  the  bladder,  the  vesiculae,  the  prostate,  etc.,  was  absolutely  negative.  It  was, 
therefore,  a  case  of  primary  or  cortical  tuberculosis  of  the  right  kidney,  which  was  painful 
during  the  attacks  of  bleeding.  The  haematuria  was  gradually  replaced  by  pyuria ; 
the  infection  took  a  descending  com^e.  The  patient  declined  operation,  and  the  tuber- 
culosis spread  to  the  vesiculae  seminales  and  the  neck  of  the  bladder. 

Tuffier's  Case. — A  woman,  without  premonitory  symptoms,  was  taken  ill  with 
abundant  haematui'ia.  It  was  quite  temporary,  because  the  urine  soon  regained  its 
normal  colour,  but  for  lour  years  and  a  hall  the  attacks  recurred  every  few  months, 

II.  74 


1158  TEXT-BOOK  OF  MEDICINE 

lasting  on  each  occasion  for  ten  or  twelve  days.  In  the  intervals  the  urine  was  abso- 
lutely nonnal.  She  had  no  pain.  The  final  attack  was  so  severe  that  the  patient  had 
to  stop  for  two  weeks  in  a  railway-station.  She  was  pale  and  cachectic.  Cystoscopy 
showed  that  the  blood  came  from  the  left  ureter.  Tuffier  decided  to  remove  the  left 
kidney.  The  operation  was  most  successful.  The  kidney  was  of  normal  size  ;  on  the 
convex  edge  and  at  the  two  extremities  tubercular  abscesses  were  present ;  the  fluid, 
when  inoculated,  caused  tuberculosis.  On  section,  three  other  abscesses  were  seen  at 
the  junction  of  the  cortex  and  the  medulla  ;  they  did  not  communicate  with  the  pelvis. 
The  pelvis  and  the  ureter  were  absolutely  healthy.  It  was,  therefore,  a  case  of  primary 
or  cortical  tuberculosis,  which  had  revealed  itself  by  hsematuria.  These  recurrent 
attacks  had  caused  no  symptoms ;  pain,  pyuria,  albuminuria,  fever,  and  tumour  beiag 
absent. 

These  cases  prove  that  we  may  find  tlie  classical  form  of  the  disease,  in 
which,  the  hsematuria  is  painless,  transient,  and  of  httle  importance,  and 
also  other  forms.  The  latter  show  numerous  intermediary  stages,  in  which 
hsematuria  is  the  sole  or  the  chief  symptom.  It  may  be  profuse  and  painful, 
the  clots  in  the  ureter  simulating  renal  cohc  or  causing  retention  of  urine. 
The  patient  loses  flesh,  and  becomes  cachectic,  and  the  symptoms  thus 
recall  those  seen  in  hsematuria  due  to  cancer.  These  cases  constitute  the 
hsematuric  form.  In  some  cases  the  bleeding  is  continuous,  and  the  patient 
passes  blood  without  interruption  for  several  months.  In  other  cases  the 
bleeding  is  intermittent,  and  the  patient  passes  blood  during  periods  of 
three  days  or  more  for  years  (Tuffier).  And  as  these  attacks  of  profuse 
hsematuria  are  almost  always  associated  with  primary  tuberculosis  due  to 
blood  infection,  and  as  the  lesion  is  limited  to  the  cortex — ^for  some  time, 
at  least — and  does  not  invade  the  cahces  and  the  pelvis,  it  follows  that  this 
form  can  produce  only  one  symptom — viz.,  hsematuria.  The  other  symp- 
toms of  pyuria,  pyelonephritis,  and  fever  are  here  absent,  though  they  are 
rarely  so  in  tubercular  pyelonephritis  of  the  ascending  type. 

The  nature  and  the  amount  of  the  hsemorrhage  -per  se  are  not,  then,  of 
much  help  in  showing  the  nature  of  the  renal  lesion  (cancer,  calculus,  cyst, 
essential  hsematuria),  but  they  furnish  valuable  information  when  we  have 
to  decide  upon  an  operation.  Surgical  intervention  is  very  successful  in 
hmited  cortical  tuberculosis. 

Pyueia. — Pus  in  the  urine  is  especially  associated  with  ascending  tuber- 
culosis when  the  lesion  assumes  the  aspect  of  suppurative  tubercular  pyelo- 
nephritis. Pyuria  likewise  occurs  in  cortical  tuberculosis  when  the  cavities 
or  abscesses  have  opened  into  the  pelvis,  or  when  the  cahces  and  pehds 
take  part  (descending  infection)  in  the  process.  In  a  general  way,  pyuria, 
which  is  an  early,  or,  indeed,  the  chief  symptom  in  ascending  tuberculosis 
of  the  kidney,  is,  on  the  contrary,  an  inconstant  or  late  symptom  in  the 
cortical  form.  It  may,  indeed,  be  absent,  as  in  some  of  the  cases  already 
cited. 

The  urine  is  turbid  or  clearly  purulent,  and  sometimes  rich  in  caseous 


DISEASES  (»K  THE  KIDNEYS  1150 

matter.  When  we  allow  the  urine  collected  during  twenty-four  hours  to 
stand  in  a  test-tuhe,  the.  deposit  of  ])us  and  phospiiatos  is  somelirues  con- 
siderable. It  is  much  larger  in  pyelonephritis  than  in  cystitis.  The  pus 
may  vary  in  amount  at  different  times,  but  once  it  is  installed,  it  never 
disappears,  unless  the  ureter  is  obUterated.  In  half  the  cases  Koch's  bacillus 
is  found  in  the  urine. 

Pain. — Many  people  with  renal  tuberculosis  do  not  feel  the  least  pain. 
Others  experience  a  sensation  of  heaviness  or  of  tearing,  and  the  pain  may 
radiate  to  the  other  kidney,  to  the  bladder,  to  the  groin,  or  to  the  testicles, 
which  are  retracted,  as  in  renal  cohc  (Guyon). 

These  pains  are  sometimes  spontaneous,  and  appear  to  be  the  result  of 
nephralgia.  Under  other  circumstances  here,  as  in  pericholecystitis  with 
adhesions,  perihepatitis,  perigastritis,  or  peri-appendicitis,  the  pains  may 
have  their  origin  in  the  adhesions.  In  some  cases,  too,  they  are  due  to  the 
passage  of  caseous  fragments,  phosphatic  concretions,  or  fibrinous  clots 
consequent  on  nephrorrhagia.  In  some  patients  the  pains  are  so  severe 
and  persistent  as  to  form  the  chief  symptom.  They  constitute  a  painful 
type  of  renal  tuberculosis  (Tuffier),  and  supply  a  motive  for  surgical  inter- 
vention.    These  cases  are  quite  exceptional.     To  quote  examples : 

Tuffier  reports  a  case  treated  for  some  years  for  renal  colic.  The  pains  began  in  the 
lumbar  region,  spread  into  the  flanks  and  the  groin,  with  repeated  fits  of  vomiting, 
and  ceased  after  a  few  hours.  These  crises  returned  several  times  every  month.  Urine 
contained  pus,  but  not  gravel.  Slight  haematxma  appeared.  As  the  pains  recurred  at 
shorter  intervals  and  became  more  severe,  the  patient  asked  for  an  operation.  Tuffier 
removed  the  kidney,  and  the  operation  confirmed  the  diagnosis.  The  kidney  showed 
diffuse  tuberculosis  and  some  caseous  centres.  The  pelvis  was  quite  healthy.  It  was 
a  case  of  primary  tuberculosis  of  the  kidney  ;  caseoUs  foci  in  the  cortex  had  opened  into 
the  pelvis.     The  patient  was  ciired  of  all  pain,  and  resumed  his  work. 

In  Cormak's  case  (reported  by  Tuffier),  renal  coUc  had  appeared  four  years  previously, 
and  the  pain  had  remained  the  chief  symptom.  Some  months  prior  to  the  operation 
the  m-ine  had  contained  pus  and  blood,  but  no  bacUh.  A  calculus  in  tlie  right  kidney 
was  suspected.  The  patient  was  operated  on,  and  the  kidney  was  foimd  to  be  studded 
with  tubercles.  A  small  cavity  existed  in  the  cortex.  The  pelvis  and  the  ureter  were 
healthy.  This  was  also  a  case  of  primary  tuberculosis  of  the  kidney.  The  patient 
recovered  quickly. 

There  is,  therefore,  a  painful  as  well  as  a  haematuric  form  of  renal  tuber- 
culosis. Continuous  or  paroxysmal  pain  is  the  chief  element.  It  ma)'  be 
the  only  symptom,  pyuria,  haematuria,  and  renal  tumour  being  absent. 
When  pain  is  present  and  the  baciUi  are  absent,  we  may  think  of  renal 
calculus  ;  but  the  crises  are  not  followed  by  the  expulsion  of  gravel,  unless 
the  patient  pass  phosphatic  concretions  formed  in  the  tubercular  centres. 
The  urine  must  be  repeatedly  centrifugahzed  and  examined  for  baciUi. 

Renal  Tumour. — The  tumour  is  not,  as  a  rule,  of  large  proportions.  It 
is  partly  due  to  the  distension  of  the  organ  and  partly  to  the  sclero-hpo- 

74—2 


1160  TEXT-BOOK  OF  MEDICINE 

matous  perinephritis.  The  tumour  projects  below  the  costal  margin  by 
some  inches  ;  it  may  even  extend  below  the  umbihcus.  It  may  be  more  or 
less  movable  or  it  may  be  fixed  by  adhesions.  Bimanual  palpation  will 
reveal  the  size,  situation,  and  mobihty  of  the  renal  tumour  (Gruyon). 

General  Symptoms. — I  have  just  reviewed  the  various  symptoms  which 
may  accompany  the  evolution  of  renal  tuberculosis.  WTien  the  renal  trouble 
is  secondary,  the  extent  or  the  age  of  the  lesions  (bladder,  prostate,  vesiculse 
seminales,  ureter)  accelerates  the  course  and  the  gravity  of  the  symptoms. 
When  the  condition  is  primary,  the  patient's  general  health  remains  good 
for  a  long  time.  Fever  is  usually  absent — or,  at  least,  it  does  not  appear 
until  later.  Shght  symptoms  of  fever,  with  a  rise  in  temperature  to  100°  F., 
indicate  mild  infection ;  but  severe  rigors,  sweating,  pyrexia  of  103°  F.  and 
pyuria,  point  to  comphcations,  and  indicate  here,  as  in  all  cases  of  pyelo- 
nephritis, either  the  onset  of  perinephritic  abscess  or,  more  frequently,  the 
formation  of  a  closed  cavity  in  the  kidney. 

As  long  as  the  pus  can  make  its  exit  through  the  ureter,  retention  of  the 
organisms  and  toxines  does  not  take  place,  and  the  fever  is  shght.  If  the 
ureter  becomes  blocked,  or  an  abscess  is  shut  off  in  the  Iddney,  the  reten- 
tion of  the  infectious  agents  in  a  closed  cavity — just  as  occurs  in  appendi- 
citis— betrays  itself  by  renal  pain,  rigors,  and  attacks  of  intermittent  fever, 
followed  by  sweating  and  by  rapid  loss  of  strength.  An  apparent  improve- 
ment in  the  urine  often  coincides  with  this  aggravation  of  the  symptoms. 
The  urine,  which  was  turbid,  ammoniacal,  and  purulent,  becomes  clear, 
because  it  is  derived  from  the  healthy  kidney  alone.  If  the  ureter  again 
becomes  patent,  or  if  a  quantity  of  pus  is  passed,  the  comphcations  will 
cease  for  a  time.  Similar  comphcations  occur  in  calculous  pyelonephritis. 
As  the  disease  progresses,  the  patient  grows  weak  and  loses  his  appetite. 
The  cachectic  stage  commences  with  oedema,  diarrhoea,  and  sweating,  and 
becomes  the  more  marked  as  the  tuberculosis  invades  the  other  parts  of 
the  genito-urinary  system  and  the  lungs. 

Complications. — Perinephritic  inflammation  may  appear  early  or 
late  in  tubercular  kidney.  It  is  sometimes  the  first  indication  of  insidious 
or  latent  renal  tuberculosis.  Suppuration  in  the  fatty  tissue  around  the 
kidney  is  not  always  accompanied  by  acute  fever.  It  may  be  apyretic  and 
insidious,  hke  a  cold  abscess,  or  may  begin  with  pain,  rigors,  fever,  and 
induration  or  swelhng  in  the  loin.  Under  Pathological  Anatomy  I  have 
already  mentioned  the  various  terminations  of  perinephritic  abscess. 

Tuberculosis  of  the  bladder  is  a  collateral  phenomenon  rather  than  a 
comphcation.  Still,  in  almost  every  case  of  primary  renal  tuberculosis 
which  is  locahzed  to  the  cortex  and  is  not  accompanied  by  descending  lesions 
the  bladder  is  free.  This  condition  also  obtains  in  cases  where  early 
obliteration  of  the  ureter  prevents  the  renal  infection  from  passing  down  to 


DISEASES  OF  THR  KIDNEYS  11  Gl 

the  bladder.  On  the  other  hand,  in  ascending  or  surgical  tuberculoHJH  the 
disease  of  the  hhidder  first  attracts  attention.  It  may,  indeed,  he  .so  marked 
that  the  secondary  mischief  in  the  kidney  is  not  discovered.  Tiie  chief 
symptom  is  painful  and  frequent  micturition.  I  saw  with  Guyon  a  young 
girl  who  had  tuberculosis  of  the  bladder.  She  passed  water  more  than 
100  times  a  day.  She  passed  at  each  micturition  a  few  dro])s  of  turbid, 
bloody  urine,  while  the  spasms  of  the  neck  of  the  bladder  were  most  acute, 
and  the  pain  radiated  to  the  bladder,  the  anus,  and  the  urethra.  The  un- 
fortunate patient  attempted  in  vain,  by  various  changes  in  position,  to  le.s.sen 
the  agonizing  ])ain  of  these  spasms.  This  painful  form  is,  fortunately,  the 
exception.  It  vdW  be  understood  that  it  masks  the  onset  of  ascending 
renal  tuberculosis. 

Tuberculosis  of  the  bladder  is  not  always  easy  to  recognize  at  its  outset. 
Micturition  is  frequent  and  painful.  The  passage  of  a  catheter  causes  pain, 
and  rectal  examination  reveals  the  induration  at  the  lower  part  of  the 
bladder.  "  In  a  patient  from  twenty  to  thirty-five  years  of  age,  suffering 
from  the  bladder  without  appreciable  cause,  examine  the  condition  of  the 
chest,  palpate  the  epididymis,  and  explore  the  prostate  and  the  vesiculse 
seminales.  Inquire  into  his  past  liistory  for  scrofulous  manifestations  in 
childhood,  and  ask  about  the  health  of  his  parents  and  his  relatives  " 
(Guyon).     These  points  must  not  be  forgotten  in  a  difficult  case. 

Tubercular  and  Paratubercular  Nephritis. — The  complications  of 
Brights  disease  now  demand  our  attention,  and  I  make  use  of  the  oppor- 
tunity to  present  this  question,  as  I  did  during  my  course  of  lectures  at  the 
Faculte  :*  Are  persons  with  renal  tuberculosis  hable  to  comphcations  and 
to  uraemia,  Uke  those  who  are  suffering  from  chronic  nephritis  ?  In  other 
words :  Is  there  such  a  thing  as  tubercular  Bright's  disease  ?  The  kidney 
may  be  affected  with  cavities,  tubercular  pyelonephritis,  or  degeneration 
en  masse;  it  may  be  destroyed,  with  total  loss  of  function,  and  yet 
the  patient  does  not  show  either  the  symptoms  of  Bright's  disease  or  of 
uraemia,  because  the  other  kidney  is  usually  able  to  do  the  work.  The 
urinary  insufficiency  seen  in  nephritis  and  the  symptoms  of  Brightism 
and  of  uraemia  depend  on  the  fact  that  in  nephritis,  whether  it  be  due 
to  infection,  diathetic  causes,  or  poisoning,  the  lesion  always  affects 
both  kidneys.  As  the  glandular  substance  of  both  kidneys  is  affected, 
we  have  not  a  healthy  kidney  to  supplement  its  diseased  fellow,  and  the 
insufficiency  or  the  suppression  of  the  function  brings  minor  or  major 
uraemia. 

In  renal  tuberculosis,  when  one  of  the  kidneys  is  compromised,  the  other 
one  is  healthy  or  sufficiently  sound  to  carry  out  the  urinary  depuration. 
The  patients  do  not  show  symptoms  of  Bright's  disease,  and  do  not  succumb 
*  Dieulafoy,  "  Cours  de  Pathologie  Interne,"  Fevrier,  1896. 


1162  TEXT-BOOK  OF  MEDICINE 

to  uraemia.  If  uraemia  does  occur  (this  is  very  rare),  it  is  because  the  other 
kidney  is  injured  by  amyloid  degeneration  or  other  lesions.  Hence,  in  spite 
of  the  destruction  of  the  tubercular  kidney,  the  patient  hardly  ever  dies 
from  uraemia,  because  the  other  kidney  can  carry  out  the  work  of  urinary 
depuration.  I  hold  the  same  opinion  as  regards  cancer  and  other  unilateral 
lesions,  which,  in  spite  of  the  destruction  of  one  kidney,  do  not  cause 
Brightism  or  uraemia,  provided  the  other  kidney  is  sufficiently  healthy. 

But,  it  will  be  asked,  can  there  not  be  tubercular  nephritis  in  the  true 
sense  of  the  word,  both  kidneys  being  attacked  simultaneously  with  diffuse 
nephritis,  as  they  are  in  infectious,  syphihtic,  or  scarlatinal  nephritis  ?  In 
phthisis,  it  will  be  asked,  do  we  not  see  patients  suffering  from  symptoms 
of  Bright's  disease — viz.,  oedema  and  albuminuria — the  albuminuria  having 
here  nothing  to  do  with  haematuria  or  pyuria  ?  Are  these  cases  of  Bright's 
disease  or  of  tubercular  nephritis  ?  In  the  first  place,  it  is  a  well-estabHshed 
fact  that  phthisical  patients — and  they  are  numerous — very  rarely  die  of 
uraemia.  The  infection  does  not  easily  spread  to  the  kidneys  and  cause 
nephritis.  We  see  a  difference  from  other  infectious  diseases — scarlatina 
and  syphihs,  for  example — which  may  cause  acute  or  chronic  nephritis. 
We  do  not  see  this  result  in  phthisis.  We  do  not  find  phthisical  patients 
contracting  chronic  tubercular  nephritis  with  symptoms  of  Brightism 
and  of  uraemia.  I  have  seen  but  few  tubercular  patients  who  suffered 
from  acute  nephritis  with  much  oedema  and  symptoms  of  uraemia.  It  is, 
therefore,  certain  that  tubercular  infection  does  not,  as  a  rule,  lead  to 
nephritis,  and  yet  patients  suffering  from  tuberculosis  often  have  albu- 
minuria. A  pretubercular  form  of  albuminuria  has  been  described.  They 
also  suffer  from  oedema,  which  is  not  the  result  of  venous  thrombosis  or 
cachexia.  Their  kidneys  may  show  diffuse  epithehal  and  amyloid  lesions, 
and,  therefore,  tubercular  nephritis  exists  in  the  true  sense  of  the  word.  It 
would,  however,  be  more  correct  to  call  it  nephritis  in  tubercular  patients 
—in  fact,  I  should  prefer  the  epithet  "  paratubercular,"  which  is  similar  to 
Fournier's  "  parasyphilitic "  troubles.  This  paratubercular  nephritis  is 
due  to  the  action  of  the  tubercuhn  on  the  kidneys,  as  experiments  have 
proved.  The  kidneys  are  tuberculinized  rather  than  tubercuHzed,  and 
Koch's  bacillus  is  absent  (Du  Pasquier).  This  form  of  nephritis  causes 
albuminuria  and  oedema,  but  it  is  usually  an  indefinite  condition,  and  rarely 
ends  in  uraemia.  The  conclusion,  therefore,  is  that  renal  tuberculosis  is 
common,  whereas  tubercular  nephritis  is  very  rare. 

Diagnosis. — The  previous  description  of  renal  tuberculosis  clearly  shows 
the  difficulties  in  diagnosis.  In  ascending  tuberculosis,  when  we  have 
found  the  bacillus  in  the  urine  or  the  pus,  the  diagnosis  is  much  simpUfied. 
The  presence  of  the  bacilh,  although  ehminating  all  doubts  as  to  the  nature 
of  the  disease,  does  not  always  indicate  its  exact  seat      This  examination 


DISEASES  OF  TIIR  KIDNF.YS  !](',:) 

ia  iiiufli  more  delicate  than  the  examination  of  the  ])}ithisical  sputum,  and 
the  absence  of  bncilh,  even  in  centrifuj^ahzed  urine,  does  not  chniinatc  all 
idea  of  urinary  tuberculosis.  Al})arran  has  shown  that  the  search  for  the 
bacillus  must  be  made  in  acid  urine— that  is  to  say,  in  a  fresh  specimen, 
and  not  in  a  specimen  taken  from  the  total  urine  discharged  during  the 
day. 

Experiments  may  help  us  in  difl&cult  cases.  We  should  make  cultures 
of  the  tubercle  bacillus  on  glycerinated  blood,  as  already  described.  The 
urine  must  be  absolutely  free  from  the  organisms  of  secondary  infection . 
These  microbes  develop,  as  a  matter  of  fact,  more  rapidly  than  Koch's 
bacillus,  and  would  invade  the  entire  surface  of  the  culture  medium  before 
the  colonies  of  tubercle  bacilU  have  time  to  appear.  It  is  a  good  plan  to 
centrifugalize  the  urine,  and  to  sow  only  the  deposit. 

Nattan-Larrier's  method  is  often  of  service.  He  injects  1  c.c.  of  the 
suspected  urine  into  the  mammar}'  gland  of  a  suckhng  guinea-pig.  A  few 
days  later  tubercular  mammitis  appears,  and  Koch's  bacilh  can  be  found  in 
the  milk,  collected  by  squeezing  the  gland. 

The  diagnosis  is  still  more  difficult  when  the  trouble  is  limited  to  the 
cortex,  and  reveals  its  presence  by  pains  like  those  due  to  calculus  or  by 
haematuria,  as  is  seen  in  cancer  of  the  kidneys.  It  has  been  suggested  that 
tuberculin  might  help  in  diagnosis,  but  Guyon  and  Albanan  condemn 
this  method  as  being  both  harmful  and  inconstant.  It  is  better  to  employ 
radioscopy.  In  several  cases  the  presence  of  calculi  has  been  thus  revealed 
(Albarran  and  ContremouHn).  According  to  these  writers,  calcuh  may  be 
thus  classified  in  order  of  decreasing  opacity  :  oxahc,  phosphatic,  and  uric 
acid.  Cystoscopy  is  of  value  when  tbe  bladder  itself  is  invaded  by  tubercu- 
losis ;  in  such  a  case  examination  with  the  cystoscope  may  reveal  a  patch 
or  a  tubercular  swelling  at  the  mouth  of  the  ureter. 

Catheterization  of  the  ureter  may  also  assist  us  in  the  differential 
diagnosis  between  tuberculosis  and  calculosis.  The  catheter  passes  readily 
in  calculus,  whereas  tubercular  lesions  of  the  ureter,  which  are  common  in 
renal  tuberculosis,  make  the  ureter  practically  impermeable  (Guyon  and 
Albarran). 

In  order  to  complete  the  diagnosis,  it  is  necessary  to  ascertain  which  kidney 
is  affected  and  the  condition  of  the  other  kidney.  The  diagnosis  of  the 
diseased  kidney  is  difficult  when  neither  kidney  is  painful  nor  hypertrophied. 
It  is  even  more  difficult  when  the  healthy  kidney  is  painful  and  affected  by 
compensatory  hvpertrophy  (Albarran).  In  such  a  case  cystoscopic  ex- 
amination may  show  blood  or  pus  issuing  from  the  ureter  on  the  diseased 
side.  The  ureter  may  be  catheterized  in  order  to  collect  the  urine  from 
the  affected  kidney,  but  it  is  better  to  use  the  ingenious  apparatus  of  Luys, 
which  segregates  the  urine  of  each  kidney.     Amongst  other  services  ren- 


1164  TEXT-BOOK  OF  MEDICINE 

dered  by  the  segregator  in  tubercular  nephritis  Luys  quotes  the  following 
case  : 

A  young  woman  whose  urine  contained  pus  and  tubercle  bacilli  complained  of  her 
right  kidney,  which  was  enlarged.  As  the  left  kidney  was  painless  and  not  perceptible 
on  palpation,  the  right  kidney  might  have  been  removed  for  tuberculosis,  if  the  segre- 
gator had  not  shown  that,  contrary  to  the  clinical  evidence,  the  m-ine  came  almost 
entirely  from  the  right  ureter.  It  was  therefore  clear  that,  in  spite  of  the  clinical 
signs,  the  left  kidney  was  much  affected ;  nephrectomy  revealed  atrophy  of  the  organ. 
We  can  imagine  what  might  have  happened  if  the  operator,  relying  on  the  chnical 
evidence  alone,  had  removed  the  right  kidney.  As  a  general  rule,  segregation  of  the 
urine  should  always  be  performed,  and  no  operation  be  performed  until  the  diagnosis 
has  been  thus  confirmed. 

This  method  shows  that  in  early  renal  tuberculosis  the  diseased  kidney 
sometimes  secretes  more  urine  than  the  healthy  kidney.  Furthermore,  the 
urine  secreted  by  the  diseased  kidney  is  not  so  rich  in  urea,  phosphates,  and 
chlorides.     It  generally  contains  pus  and  some  bacilh. 

The  condition  of  the  other  kidney  (which  is  supposed  to  be  healthy) 
must  be  ascertained  prior  to  any  operation.  It  is  not  permissible  to  remove 
a  tubercular  kidney  unless  we  are  sure  that  the  other  kidney  is  carrying  out 
its  functions  normally  (Albarran).  Absolute  precision  in  diagnosis  can  only 
be  obtained  by  ureteral  catheterization.  I  have  recently  proved  this  fact 
in  a  patient  whom  I  saw  with  Albarran. 

A  young  man  who  had  no  hereditary  antecedents,  and  was  free  from  pulmonary  or 
genital  tuberculosis,  had  for  four  months  complained  of  painful  poUakiuria.  The  urine 
was  turbid  and  contained  pus  ;  bacteriological  examination  revealed  the  presence  of 
Koch's  baciUus.  The  kidneys  were  neither  enlarged  nor  painful  on  pressure.  The 
bladder  was  of  normal  size,  and  cystoscopic  examination  showed  that  it  was  healthy. 
By  catheterization  of  the  left  ureter,  Albarran  in  an  hour  and  a  half  collected  2  ounces 
of  tiu-bid  urine,  whilst  the  right  kidney  only  secreted  1|  ounces  of  clear  urine.  Pus 
and  Koch's  bacilh  were  found  in  the  urine  from  the  left  kidney ;  neither  pus  nor  bacilh 
in  the  urine  from  the  right  kidney.  Urea,  phosphates,  and  chlorides  were  30  per  cent, 
higher  in  the  urine  from  the  left  or  diseased  kidney  than  in  the  virine  from  the  right 
kidney.  It  was  evident  that  the  left  kidney  only  was  tubercular,  and  that  the  lesions 
were  not  advanced.  Albarran  removed  the  left  kidney.  At  first  sight  it  appeared  to 
be  healthy,  but  on  section  he  found  the  following  lesions  :  a  hard  tubercle  at  the  base  of 
a  pyramid,  a  small  cavity  of  the  size  of  a  pea  in  the  cortical  region,  tubercular  granu- 
lations in  the  pelvis.     The  patient  recovered. 

The  prognosis  is  much  graver  in  the  secondary  than  in  the  primary  form. 
Eecovery  is  possible,  because  the  cicatrices  of  ca^^ties  have  been  met  with. 
The  disease  generally  lasts  for  one  or  more  years  if  early  intervention  has 
not  been  made,  and  the  patient  succumbs  to  hectic  fever,  tubercular  inva- 
sion of  the  genito -urinary  organs,  septic  fever,  or  tubercular  comphcations 
in  the  respiratory  system. 

Treatment. — The  medical  treatment  of  renal  tuberculosis  is  reduced  to 
hygienic  considerations.  As  surgical  treatment,  which  is  the  only  rational 
one,  has  no  detailed  place  in  a  text-book  of  medicine,  I  refer  the  reader  to 


DISEASES  OF  THE  KIDNEYS  IHJ.' 

works  on  surgery.  This  article,  however,  gives  some  idea  of  the  principal 
indications  for  operation.  We  have  seen  that  the  cases  of  primary  tubercu- 
losis of  the  kidney  are  more  favourable  for  intervention  than  the  .secondary 
ca.scs,  in  wliioh  the  bladder,  the  ureter,  and  other  orgaas  are  already  in- 
fected. 

Two  different  operations  are  performed  in  tubercular  kidney  :  (1)  Nephro- 
tomy, or  simple  incision  of  the  kidney,  the  object  being  to  evacuate  the  pus 
which  has  accumulated  in  the  pelvis  in  case  of  retention.  It  is  an  operation 
of  necessity  which  has  the  great  drawback  of  leaving  a  permanent  fistula. 
(2)  Nephrectomy,  or  extirpation  of  the  kidney.  The  results  of  this  operation 
have  much  improved,  owing  to  the  more  accurate  diagnosis  rendered  possible 
by  ureteral  catheterization.  Vigneron  in  1892  found  the  mortality  to 
be  34  per  cent.  Albarran  lost  only  one  patient,  who  died  of  meningitis,  out 
of  thirty-one  cases  of  nephrectomy.  These  results  are  the  more  remarkable 
in  that  several  patients  had  fever  or  advanced  cachexia.  Several  of  the 
cures  have  been  maintained  for  five  or  six  years. 

X.  RENAL  SYPHILIS— SECONDARY  SYPHILITIC  NEPHRITIS- 
TERTIARY  SYPHILIS  OF  THE  KIDNEY. 

According  to  a  certain  theory  (Giintz),  mercurial  treatment  is  largely 
responsible  for  the  nephritis  which  occurs  in  syphilitic  patients.  In  a 
monograph  on  syphilosis  of  i:he  kidney  Mauriac  rightly  protests  against  this 
statement.  To  refute  it,  we  have  only  to  study  mercurial  poisoning  in 
workmen  who  employ  this  metal.  Except  in  acute  poisoning,  due  to  the 
ingestion  of  large  quantities  of  the  drug,  niercurial  intoxication  does  not 
affect  the  kidney.  Gilders,  looking-glass  manufacturers,  miners,  and 
many  other  workmen  who  use  mercury,  may  suffer  from  stomatitis,  disease 
of  the  jaws,  tremors,  and  other  symptoms,  but  their  kidneys  remain  healthy. 
Mercury  differs  from  lead,  which  does  cause  nephritis.  In  this  section  I 
shall  cite  cases  of  acute  nephritis  in  syphilitic  persons,  appearing  three  or 
four  months  after  the  chancre,  when  they  had  not  taken  mercury.  I  shall 
also  speak  of  cases  in  whom  syphihs  of  the  kidney  appeared  fifteen  years 
after  the  chancre.  The  patients  had  not  taken  any  mercury  for  many  years. 
The  question  is  therefore  settled.  The  cause  of  this  nephritis  is  not  mercury, 
but  syphihs. 

The  syphihtic  toxine  is  ver\^  poisonous  to  the  renal  filter.  It  exercises 
a  harmful  or  even  deadly  action  on  the  kidneys,  but  it  acts  differently, 
according  as  the  kidney  is  attacked  in  the  secondary  or  in  the  tertiary  stage 
of  the  disease.  This  fact  is  easily  seen  from  an  analysis  of  the  cases,  and  I 
shall,  therefore,  follow  the  di\asion  indicated  by  writers,  and  also  employed 
in  mv  pathological  and  chnical  lectures. 


1166  TEXT-BOOK  OF  MEDICINE 

Early  infection  causes  nephritis  in  the  true  sense  of  the  word.  Both 
kidneys  are  attacked,  as  they  are  in  acute  infective  nephritis — e.g.,  scar- 
latinal nephritis.  This  early  form  may  show  itself  by  slight  or  moderate 
symptoms.  In  some  cases  the  sjnnptoms  are  acute,  and  the  mischief  proves 
fatal. 

Late  infection,  which  supervenes  in  the  tertiary  stage,  does  not  reveal 
itself  only  by  the  lesions  of  nephritis,  in  the  true  sense  of  the  word.  It 
engenders  gummatous  or  amyloid  lesions,  which  are  sometknes  predomi- 
nant, or  are  at  other  times  associated  with  the  lesions  of  ordinary  nephritis. 

In  these  various  cases,  therefore,  the  clinical  picture  differs.  Syphilitic 
nephritis  is  most  suitable  for  the  early  cases,  and  tertiary  syphilis  of  the 
kidneys  for  the  late  cases.  Between  these  two  extremes  there  are,  of  course, 
intermediate  types. 

1.  Early  Syphilitic  Nephritis. 

In  a  first  category  of  cases  the  nephritis  is  so  shght  as  to  pass  unnoticed. 
It  appears  a  few  months  after  infection,  and  albuminuria  is  ahnost  the  only 
symptom  (Jaccoud).  From  3  to  5  grains  of  albumin  are  found  daily. 
The  urine  is  of  normal  toxicity ;  the  amounts  of  urea  and  extractives  are 
normal ;  and  histological  examination  reveals  the  presence  of  hyahne 
casts.  The  albumin  is  present  for  a  longer  or  shorter  period,  which  may 
be  lessened  by  specific  treatment,  and  then  disappears  without  further  com- 
pHcations.  In  this  form  of  nephritis  the  functions  of  the  kidneys  are  not 
deranged.  The  urinary  depuration  is  sufficient,  and  the  patient  does  not 
suffer  from  "  symptoms  of  Brightism."  Another  sjrmptom,  however,  often 
accompanies  the  albuminuria — viz.,  shght  puffiness  of  the  eyehds  or  of  the 
face.     There  may  also  be  shght  oedema  over  the  maUeoh. 

This  attenuated  form  of  nephritis,  reveahng  itself  only  by  albuminuria 
and  perhaps  shght  oedema,  is  not  strange,  for  we  find  in  influenza,  typhoid 
fever,  scarlatina,  or  pneumonia,  that  the  renal  changes  may  for  a  time 
be  indicated  only  by  albuminuria,  with  or  without  oedema.  I  am  of  opinion 
that  this  mild  form  is  due  to  the  weakness  of  the  toxi-infectious  agent,  and 
perhaps  to  the  previous  integrity  of  the  kidneys.  These  cases  must  be 
carefully  treated  by  antisjrphihtic  remedies,  and  must  be  closely  watched, 
because  they  do  not  always  recover  at  once.  They  sometimes  recur  in  a 
more  severe  form. 

Syphihtic  nephritis,  however,  does  not  always  run  such  a  favourable 
course.  It  is  sometimes  very  much  more  severe.  I  shall  cite  cases  which 
prove  that  early  syphihtic  nephritis  may  be  as  severe  as  the.  other  forms  of 
infective  nephritis.  It  may  run  an  acute  and  fatal  course,  and  at  the  post- 
mortem examination  we  find  diffuse  nephritis,  the  kidney  being  enlarged  and 
pale  or  showing  haemorrhages.     The  histological  examination  shows  swelling 


DISEASES  OF  THE  KID^^EY3  1107 

and  necrosis  of  the  glandular  tissue,  and  sometimes  enlargement  of  the 
glomcnili,  irritative  lesions  of  the  capsules  and  the  bloodvessels,  and 
glomerular  hoemorrhage.  It  would  be  wrong  to  suppose  that  acute  syphiUtic 
nephritis,  wliicli  is  often  fatal,  and  the  lesions  of  which  are  especially  hmited 
to  the  secretory  and  excretory  elements  of  the  kidneys,  is  only  seen  in 
malignant  syphilis.  It  usually  appears  during  the  first  months  of  an  ordinary 
attack  of  syphihs,  wliile  the  other  manifestations  are  only  roseola  and 
mucous  patches. 

Case  I. — Tho  best  example  which  I  can  give  is  a  case  mentioned  in  my  clinical 
lectures.*  A  young  man  was  sent  to  me  by  Mauriao.  Puffiness  of  tlie  face  and  oedema 
of  the  legs  had  appeared  suddenly  two  days  previously.  On  admission,  tho  eyehds  were 
swollen  and  the  oedema  of  tho  lower  limbs  was  considerable.  The  oedema,  which  was 
white  and  soft,  extended  as  far  as  the  loins.  Abimdant  albuminuria.  Tlio  urine,  which 
was  fairly  coloured,  was  normal  in  amount ;  no  haematuria.  It  contained  6  drachms  of 
albumin  in  the  twenty-four  hours.  No  other  symptoms.  It  was  a  case  of  acute  neph- 
ritis, which  had  come  on  suddenly,  without  pain  in  the  loins,  rigors,  or  fever.  I  agreed 
with  Mauriac  that  it  was  a  case  of  early  syphiUtic  nephritis.  As  a  matter  of  fact,  ho 
had  had  a  chancre  on  the  penis  two  months  previously.  The  slight  induration  of  the 
tissues,  their  colour,  and  the  hard,  painless  glands  in  the  groin  were  corroborative 
evidence.     Mucous  patches  were  present  in  the  throat  and  round  the  anus. 

As  this  acute  nephritis  appeared  nine  weeks  after  the  chancre  in  a  man  who  previously 
had  not  had  a  chill,  scarlatina,  influenza,  typhoid  fever,  or  any  infection  capable  of 
affecting  the  kidneys,  it  was  quite  natural  to  set  it  down  to  syphilis.  It  was  no  doubt 
a  case  of  acute  nephritis,  and  not  an  outburst  of  nephritis  during  the  course  of  chronic 
Brightism,  because  no  symptoms  of  Brightism  were  discovered  in  the  previous  history. 
There  could,  therefore,  be  no  possible  doubt  as  to  the  diagnosis. 

Although  alarming  symptoms  were  absent,  I  gave  a  guarded  prognosis,  because 
experience  has  led  me  to  beware  of  early  syphiUtic  nephritis.  I  prescribed  milk  diet 
and  a  dessertspoonful  of  the  foUowing  preparation  night  and  morning : 

Iodide  of  potassium     . .  . .  . .  . .  . .       1  ounce. 

Biniodide  of  mercury  . .  . .  . .  . .  . .       3  grains. 

DistiUed  water  . .  . .  . .  •  •  . .     12  ounces. 

The  effects  were  rapid  and  successful :  in  a  fortnight  the  oedema  had  completely  dis- 
appeared. As  the  oedema  diminished,  the  patient  lost  weight  in  proportion.  The 
amount  of  fluid  taken  and  the  quantity  of  urine  passed,  were  measured  daily.  The 
latter  exceeded  the  former,  and  the  excess  passed  by  the  kidney  agreed  with  the  loss 
of  weight  due  to  the  diminution  in  the  oedema.  In  a  fortnight  he  got  rid  of  21  poimds 
of  Uquid  from  the  tissues.     The  albumin  had  all  disappeared  by  the  seventeenth  day. 

I  have  seen  him  several  times  since  he  left  the  Hotel -Dieu  ;  his  recovery  is  maintained. 
I  kept  him  on  mUk  diet  for  two  months,  and  then  I  aUowed  him  to  take  soup,  vege- 
tables, and  bread.  The  mixture  was  given  for  a  fortnight,  and  then  suspended  for  a 
fortnight.  Six  months  later  he  was  perfectly  weU,  and  could  eat  ordinary  diet.  The 
albumin  never  reappeared. 

Case  II. — On  March  16,  1898,  a  man,  thirty-four  years  of  age,  was  admitted  for 
anasarca.  About  a  month  before,  whilst  in  perfect  health,  he  noticed  that  his  eyeUds 
were  ptiffy.  Next  day  his  whole  face  was  oedematous,  and  in  twenty-four  hours  the 
oedema  had  reached  the  lower  limbs.     The  anasarca  showed  a  tendency  to  become 

*  "  Nephrite  SyphiUtique :  SyphiUs  Tertiaire  du  Rein "  (Clinique  MediccUe  de 
Hotel-Dieu,  1898,  IS™"  et  14°"  lemons). 


1168  TEXT-BOOK  OF  MEDICINE 

general.  His  doctor  examined  his  urine,  and  prescribed  milk  diet.  In  spite  of  the 
milk  diet,  the  anasarca  spread,  and  reached  the  scrotum.  It  was  solely  for  dropsy  that 
he  came  to  the  Hotel-Dieu,  as  he  had  no  other  symptoms.  At  first  sight  he  looked  hke  a 
healthy  man  with  a  clear  and  rosy  complexion.  His  arms  were  muscular,  but  the  abdo- 
men, the  scrotum,  and  the  lower  limbs  were  oedematous.  The  urine  was  rather  high- 
coloured  ;  4  pints  were  collected  in  twenty-four  hours,  and  contained  120  grains  of 
albumin  per  pint.     We  diagnosed  acute  nephritis. 

The  only  discoverable  cause  for  this  nephritis  was  recent  syphilis  (eight  months  old). 
In  Jime,  1897,  he  had  been  treated  at  the  Hopital  du  Midi  by  I\Iauriac  for  a  chancre  on 
the  penis  with  pills  of  proto -iodide ;  a  few  months  later  he  returned  to  the  hospital 
with  mucous  patches  in  his  throat.  In  the  absence  of  any  other  cause,  it  was  quite 
natural  to  diagnose  specific  nephritis,  which  had  set  in  seven  months  after  the  chancre. 

I  put  him  on  rrulk  diet,  and  prescribed  injections  of  biniodide  of  mercury.  During 
the  next  few  days  the  situation  did  not  improve  ;  the  oedema  persisted,  the  urine  in- 
creased in  quantity,  and  the  albumin  varied  from  250  to  300  grains  in  the  twenty-four 
hours.  After  the  seventh  injection,  the  biniodide  of  mercury  was  stopped.  The 
patient,  who  was  of  a  very  optimistic  nature,  felt  neither  discomfort  nor  pain,  and  readily 
took  his  8  pints  of  nulk.  The  oedema  unfortunately  increased,  and  reached  the  loin. 
The  scrotimi  and  penis  was  as  large  as  a  foetal  head.  I  gave  iodide  of  potassium  in 
small  doses,  but  stopped  it,  because  no  benefit  resulted.  The  injections  of  bin- 
iodide were  given  again,  and  then  suspended.  On  April  4 — that  is  to  say,  twenty  days 
after  his  admission — he  passed  135  instead  of  250  grains  of  albumin.  The  anasarca, 
however,  still  increased  ;  this  seemed  a  bad  sign  to  me.  On  April  13  he  complained  of 
distress,  and  on  auscultation  I  heard  rales,  due  to  pulmonary  oedema.  He  had  gained 
11  pounds  in  weight  since  his  admission,  this  increase  being  due  to  the  oedema,  which 
was  gaining  gi-ound.  On  April  20  he  was  not  so  well,  dishking  his  milk,  and  feehng 
nausea.  The  urine  increased  in  quantity,  but  the  pulmonary  oedema  made  progress. 
On  April  24  he  felt  pain  in  the  right  side  of  the  abdomen ;  it  was  due  to  diffuse  lym- 
phangitis and  a  patch  of  erysipelas.  This  comphcation  was  most  dangerous,  in  my 
opinion,  because  in  several  cases  of  early  syphilitic  nephritis  death  has  been  due  to 
erysipelas.  During  the  evening  cyanosis  and  severe  dyspnoea  came  on.  In  spite  of  all 
the  means  taken,  he  became  rapidly  worse :  the  pain  in  the  erysipelatous  areas  was 
severe ;  the  pulse  grew  threadhke  and  irregular,  and  the  heart-beats  were  tumultuous. 
The  face  was  pale  and  mottled,  and  he  died  next  day,  after  retauiing  consciousness 
almost  to  the  last.  Results  of  the  post-mortem  examination  :  In  the  lungs  oedema  and 
congestion  were  fairly  extensive.  The  cavities  of  the  right  side  of  the  heart  were  filled 
with  a  large  clot ;  it  was  white,  sohd,  and  formed  of  pure  fibrin.  It  was  not  a  post- 
mortem clot,  but  had  certainly  formed  during  the  death-agony.  It  filled  the  entire  right 
auricle,  passed  into  the  ventricle  through  the  tricuspid  valve,  and  from  the  ventricle 
into  the  pulmonary  artery,  where  it  ended  in  a  point  a  short  distance  from  the  bifurca- 
tion. 

The  kidneys  were  enlarged.  The  right  kidney  weighed  7  ounces,  the  left  one 
6  ounces.  The  cortex  was  pale,  and  showed  a  well-marked  network  of  vessels.  The 
capsule  stripped  readily.  The  pyramidal  substance  was  congested  and  of  a  bluish 
tint. 

The  histological  examination  showed  that  the  lesions  were  most  marked  in  the 
cortex.  The  epithehal  cells  which  lined  the  convoluted  tubules,  instead  of  forming  a 
row  of  equal  cells,  with  weU-stained  nuclei,  were  irregular  in  form  and  size.  The 
protoplasm  was  rmiformly  cloudy  ;  the  nuclei  had  either  disappeared  or  were  ill-defined, 
and  unstained.  In  some  of  the  tubules  there  were  several  rows  of  these  altered 
cells.  Elsewhere  desquamated  cells  or  cellular  debris  blocked  the  tubules  ;  in  other 
places  the  cells  had  disappeared,  leaving  the  basal  membrane  in  direct  contact  with  the 
lumen  of  the  tube  at  certain  points.     The  basal  membrane  of  the  tubules  was  not 


DISEASES  OK  THE  KIDNEYS  lltV.i 

affoctod,  and  the  tissuo  botweon  the  tuhulos  showod  no  losion.  The  gluriiMruU,  with  thoir 
arterioles,  wore  heullliy.  The  tirloriul  and  venous  iinastoinosos  at  tlio  juuctiunn  of  the 
cortical  and  pyruinidal  substancos  showed  no  change.  The  pyramidal  substance  showed 
both  tubules  with  changes  similar  to  tliose  m  the  convoluted  tubules  and  narrow 
tubules  which  were  healthy.  Tiio  interstitial  tissue  of  the  pyramids  was  healthy. 
The  cajwulo  of  the  kichiey  showed  no  change. 

In  conclusion,  in  tliis  case  of  syphilitic  nephritis  the  lesion  was  purely  epithehal. 
The  glomeruli  were  intact,  the  narrow  tubules  wore  healthy,  and  the  lesion  affected  only 
certain  portions  of  the  secretory  and  e.vcrotory  systems.  These  lesions  were  marked 
in  the  convoluted  and  straight  tubules,  the  epithelial  cells  being  changed  or  destroyed. 

Case  III. — A  young  man  contracted  syphilis,  which  appeared  at  first  to  bo  mild  ; 
the  rash  was  slight,  and  from  the  outset  Siredey  gave  mercury.  Nephritis  appeared  six 
months  after  infection,  with  sjTuptoms  of  headache,  nausea,  and  weakness.  The  urine 
contained  nearly  an  oimce  of  albumin  in  35  ounces.  In  spite  of  milk  diet  and  specific 
treatment,  he  grew  rapidly  worse,  suffering  from  drowsiness  and  foetid  diarrhoea.  The 
tongue  was  dry,  and  the  pulse  rose  to  120.  The  dropsy  made  rapid  progress,  mvolving 
the  lungs  and  the  abdominal  cavity.  In  spite  of  treatment,  the  vomiting  and  diarrhoea 
were  still  severe.  The  milk  was  continued,  and  mercury  was  rubbed  in  over  the  kidneys. 
■The  situation  was  now  so  satisfactory  that  the  patient  took  6  pints  of  milk  a  day,  and 
he  passed,  on  an  average,  6  to  7  pints  of  urine.  The  albumin  diminished  from  1  ounce 
to  45  grains,  the  pulmonary  oedema  improved,  the  headache  disappeared,  the  anasarca 
grew  less,  constipation  replaced  the  diarrhcea,  and  his  nights  were  much  quieter. 
This  phase  of  relative  calm  lasted  a  fortnight,  when  the  anasarca  returned ;  the  skin 
was  much  affected,  the  legs  and  thighs  being  three  times  their  normal  size,  and  the 
scrotum  as  large  as  a  man's  head.  Pain  soon  appeared  in  the  left  side,  and  pleural 
effusion  showed  itself.  The  ascites,  which  was  very  shght  at  first,  now  became  marked. 
We  estimated  that  the  peritoneum  contained  about  15  pints  of  fluid.  The  vomiting 
was  acute  ;  the  vomited  matter  was  mucous,  blackish,  and  there  was  slight  hsematemesis. 
Dyspnoea  now  became  the  chief  sjinptom.  The  pleiu*al  effusion  on  the  left  side  in- 
creased, and  fluid  also  formed  on  the  right  side.  We  decided  to  aspirate  the  fluid  at 
several  sittings,  in  order  to  prevent  acute  oedema  of  the  lungs.  At  the  first  sitting  I 
drew  off  8  ounces.  The  patient,  who  was  much  relieved,  asked  for  a  second,  and  later 
for  a  third,  pxmcture.  Each  time  we  withdrew  some  10  ounces  of  fluid,  and  this  gave 
temporary  rehef.  The  fluid,  however,  reformed,  the  heart  grew  weaker,  and  the 
torpor  almost  merged  into  coma.  The  dyspnoea  grew  worse,  and  in  a  few  weeks  this 
early  syphilitic  nephritis  proved  fatal. 

Analysis  of  the  Symptoms. — We  may  now  consider  the  history  of  early 
svphihtic  nephritis  of  the  grave  type.  The  first  point  of  importance  is 
that  the  nephritis  is  early.  In  syphilis  it  is  customary  to  look  upon  the 
secondary  troubles  as  being  much  less  serious  than  the  tertiary  lesions. 
This  is  true  in  the  majority  of  cases.  The  grave  troubles  (cerebral,  aortic, 
laryngeal,  or  pulmonary  syphihs)  do  not  appear,  as  a  rule,  till  some  years 
after  the  infection.  Many  exceptions  to  this  rule,  however,  occur.  Amongst 
the  early  visceral  lesions  nephritis  stands  out,  even  when  the  kidneys  were 
healthy  before  the  attack  of  syphihs.  The  s}-phiUtic  poison  kills  the  epi- 
thehum  of  the  organ  or  destroys  its  functions,  and  renal  insufficiency,  with 
its  grave  sjnnptoms,  appears.  In  order  to  emphasize  this  fact,  I  give  the 
dates  when  the  nephritis  appeared  in  seventeen  cases  :  In  two  cases  eight 
months  after  infection ;  in  two,  six  months  ;  in  two,  four  months  ;  in  five, 


1170  TEXT-BOOK  OF  MEDICINE 

three  montlis  ;  in  five,  two  months.  According  to  these  statistics,  syphihtic 
nephritis  usually  appears  in  the  second  and  third  months  after  the  chancre. 
It  is  often  contemporary  with  the  roseola  and  the  first  mucous  patches.  It 
is  less  coromon  from  the  eighth  to  the  twelfth  month  after  infection,  and 
after  the  first  year  the  patient  is  practically  safe  from  this  terrible  eventu- 
ahty.  I  do  not  assert  that  acute  nephritis  cannot  appear  later,  but  this  is 
an  exception. 

The  next  point  is  the  sudden  onset  of  the  nephritis  and  its  tendency 
to  cause  general  infiltration — anasarca,  oedema  of  the  lung,  pleural  effusions, 
and  ascites.  In  my  first  case  puflfiness  of  the  face  and  considerable  oedema  of  the 
leg  appeared  suddenly.  I  estimated  the  infiltration  to  be  about  20  pints.  In 
my  second  case  the  oedema  appeared  suddenly,  and  in  a  few  days,  judging 
from  the  weight  of  the  patient,  the  infiltration  was  about  30  pints.  The 
young  man,  whom  I  saw  with  Siredey,  had  such  marked  anasarca  that  he 
resembled  a  toy  manikin  of  goldbeaters'  skin.  Furthermore,  he  had  pul-. 
monary  oedema,  double  pleural  effusion,  which  promptly  reformed  after 
thoracentesis,  and  ascites.  In  a  case  pubhshed  by  Gastou  the  anasarca 
became  general  in  a  day,  and  was  soon  followed  by  effusion  into  both  pleurse 
and  by  ascites.  The  sudden  onset  of  anasarca  and  of  pulmonary  oedema  is 
noted  by  Jaccoud.  The  above  examples  prove  that  rapid  oedema,  with 
serous  effusion,  is  one  of  the  principal  characteristics  of  early  syphilitic 
nephritis.  I  agree  with  Jaccoud  that  scarlatinal  nephritis  can  alone  be 
compared  with  it. 

The  abundance  of  the  albumin  is  another  pecuharity  of  early  syphihtic 
nephritis — Mb  graios  in  my  first  case,  in.  the  second  case  240  grains,  and 
in  the  third  case  500  grains  in  twenty-four  hours. 

This  excessive  albununuria  ia  early  syphihtic  nephritis  agrees  with  the 
extent  of  the  epithehal  lesions,  which  may  exist  to  the  exclusion  of  any 
interstitial  or  vascular  lesion  in  the  kidney.  The  lesions  in  Case  2  were 
strictly  limited  to  the  epitheha  of  the  convoluted  and  straight  tubules.  In 
another  case  (Darier  and  Hudelo)  glomeruhtis  was  associated  with  parenchy- 
matous changes.  In  a  case  reported  by  Horteloup  and  Wickham  the 
histological  examination  showed  similar  epithehal  lesions  with  interstitial 
changes.  In  two  cases  pubhshed  by  Brault  the  glomerular  and  arterial 
lesions  occupied  an  important  place.  They  differed  notably  from  the 
lesions  found  in.  my  patient.  Indeed,  here  the  epithehal  changes  were  prac- 
tically exclusive,  whilst  elsewhere  the  changes  were  especially  vasculo- 
connective.  It  is  possible  that  the  lesions  may  present  some  differences, 
according  to  the  duration  of  the  nephritis.  In  two  cases  reported  by 
Brault  the  nephritis  had  in  the  one  instance  lasted  five  or  six  weeks  and 
in  the  other  four  months. 

Description. — The  following  are,  in  general   terms,  the  most  sahent 


DISEASES  OF  THE  KIDNEYS  117 1 

featuies  of  early  svq)hilitic  nephritis  :  An  iudividiuil  has  contracted  a  chancre 
a  few  weeks  or  a  few  months  previously.  The  roseola  has  hardly  faded,  and 
mucous  patches  have  just  made  their  appearance,  when  puffiness  of  the  face, 
oedema  of  the  lower  limbs,  and  general  anasarca  suddenly  appear.  The 
urine  contains  a  quantity  of  albumin  and  perhaps  blood.  The  iniiltration 
tends  to  reach  the  organs,  and  we  find  oedema  of  the  lungs,  pleural  effusion, 
and  ascites.  During  this  phase  oedema  and  albuminuria  are  often  the  only 
appreciable  sjTiiptoms.  After  a  few  weeks  of  treatment  improvement 
and  cure  may  supervene,  \vithout  any  other  incident,  as  in  the  first  case 
quoted.  In  other  cases  the  oedema  and  the  albuminuria  are  accompanied 
by  headache,  dyspnoea,  vomiting,  and  profuse  diarrhoea.  The  urine  be- 
comes scanty,  and  if  the  disease  progress,  the  patient  succumbs  in  a  few 
weeks  or  months.  Death  may  result  fiom  general  dropsy,  dyspnoea,  and 
coma,  from  some  intercurrent  infection  (lymphangitis,  erysipelas),  or  from 
uraemia.  Uroemic  symptoms  (convulsions,  coma,  etc.)  are,  however,  not 
as  common  here  as  in  cases  of  chronic  nephritis. 

Syphilitic  nephritis  often  appears  to  be  cured.  The  oedema  and  albu- 
minuria disappear ;  the  patient,  tired  of  treatment,  and  believing  himself 
to  be  henceforth  invulnerable,  wrongly  resumes  his  ordinary  life,  without 
troubling  about  his  former  illness.  The  nephritis,  although  apparently 
cured,  sometimes  leaves  sequelae,  which  will,  at  the  first  opportunity,  result 
in  an  outbreak  of  acute  nephritis.  I  have  seen  a  young  man  with  severe 
Bright's  disease,  following  upon  acute  svphihtic  nephritis,  which  was  con- 
sidered cured,  and  which  was  too  soon  left  to  itself.  It  is  not  sufficient  to  limit 
the  nephritis.  It  must  be  closely  watched,  even  after  the  disappearance  of 
symptoms,  because  the  condition  may  end  in  chronic  nephritis.  In  this 
respect  it  does  not  differ  from  the  other  forms  of  acute  nephritis,  which  may 
become  chronic. 

The  diagnosis  is  not  difficult.  Two  symptoms  are  generally  present — 
rapid  oedema  and  abundant  albuminuria.  We  must  not  mistake  syphihtic 
nephritis  for  nephritis  a  frigore.  I  do  not  absolutely  deny  nephritis 
a  frigore,  which  is  allowed  by  the  most  eminent  writers.  I  beheve  that  I 
have  seen  undoubted  cases  of  it,  but,  on  closer  scrutiny,  we  are  forced  to 
admit  that  the  so-called  nephritis  a  frigore  has  sometimes  an  origin  other 
than  cold,  and  that  syphilis  plays  an  important  part.  If  we  look  for  the 
cicatrix  and  the  induration  which  point  to  a  recent  chancre,  and  search  for 
the  enlarged  glands  which  persist  after  the  chancre,  we  shall,  then,  find  that 
in  a  supposed  case  of  nephritis  due  to  cold  the  condition  is  really  syphihtic 
nephritis,  which  has  appeared  a  few  months  after  infection. 

Our  prognosis  must  be  guarded  in  this  event,  because  experience  shows 
that  we  may  find  cases  of  early  syphihtic  nephritis  in  which  the  oedema  and 
albuminuria  are  slight  and  treatment  is  successful,  and  also  cases  in  which 


1172  TEXT-BOOK  OF  MEDICINE 

the  oedema,  efiusion,  albuminuria,  and  uraemic  symptoms  are  severe,  and 
fraught  vnth  danger  because  treatment  fails.  This  does  not  mean  that 
grave  syphihtic  nephritis  cannot  be  cured.  It  is  curable,  even  though  the 
anasarca  is  great  and  the  albuminuria  severe,  as  we  have  seen  in  the  first 
case  quoted.  The  ameUoration  is  announced  by  diminution  of  the  oedema 
and  albuminuria.  On  the  other  hand,  persistence  of  the  albumin  and 
increase  in  the  oedema,  in  spite  of  the  treatment,  demand  reservation  as  to 
the  ultimate  issue  of  the  disease. 

The  gravity  does  not  arise  solely  from  the  uraemic  troubles,  which  are 
less  frequent  here  than  in  the  case  of  chronic  nephritis.  The  patients  die 
from  the  general  anasarca,  which  involves  the  pleurae,  the  peritoneum, 
the  lungs,  and  the  larynx.  Secondary  infection  often  shows  itself,  and 
hastens  death.  My  second  case  died  of  erysipelas,  with  oedema  of  the  lung 
and  a  clot  in  the  heart.  The  young  man  whom  I  attended  with  Siredey, 
died  from  pulmonary  oedema,  pleural  effusions,  which  thoracentesis  failed 
to  reheve,  and  coma,  probably  due  to  cerebral  oedema. 

Treatment. — In  early  syphihtic  nephritis  we  must  first  prescribe  abso- 
lute milk  diet,  which,  though  far  from  being  sufficient,  is,  nevertheless, 
indispensable.  I  question  as  to  whether,  from  the  prophylactic  point  of 
view,  milk  diet  ought  not  to  be  prescribed  for  some  months  in  every  case 
of  chancre,  just  as  it  is  in  every-  case  of  scarlatina.  When  we  see  the 
rapidity  and  intensity  with  which  the  renal  epithehum  is  affected,  by  the 
syhiHtic  toxine,  it  may  be  asked  whether  the  kidneys  would  not  benefit  by 
a  preventive  regimen  which  renders  them  more  able  to  resist  the  poison. 
Milk  diet  is  even  more  necessary  when  syphiHs  attacks  an  individual  whose 
kidneys  are  already  affected.  Many  people  have  had  their  kidneys  damaged 
by  scarlatina,  influenza,  puerperal  condition,  malaria,  plumbism,  gout, 
calculus,  etc.  And  though  every  trace  of  the  former  nephritis  has  appar- 
ently disappeared,  we  must  not  forget  that  the  kidneys  under  these  con- 
ditions present  a  locus  minoris  resistenticB  to  syphihs  for  a  long  time.  It  is, 
therefore,  a  good  rule  to  recommend  milk  in  every  case  of  syphilitic  chancre. 
This  regimen  must  be  followed  for  three  or  four  months,  because  syphihtic 
nephritis  usually  appears  some  two  or  three  months  after  infection.  Mer- 
curial preparations  are  indicated,  but  we  must  prescribe  them  in  moderation. 
As  to  the  mode  of  administration,  we  have  a  most  varied  selection  to  choose 
from :  proto-iodide  of  mercury  in  the  form  of  pills,  in  daily  doses  of  |  to 
1  grain  ;  or  biniodide  of  mercury,  in  solution  or  as  an  injection.  I  use  an 
aqueous  solution  of  biniodide  of  mercury.  Fifteen  minims  of  this  solution 
contain  y|-  grain  of  the  active  principle  ;  10  to  15  drops  of  the  solution  are 
injected  daily  for  a  week  to  a  fortnight.  The  injections  are  then  stopped, 
and  again  given  if  need  be.  Other  mercurial  preparations  may  be  recom- 
mended, with  or  without  iodide  of  potassium — Gibert's  syrup,  for  instance, 


DISEASES  OF  rill-:  Kij)M-:vs  iiv;; 

in  (losos  of  1  fo  2  (liaclims  daily;  iudide  of  potassium,  iii  diisi-s  (»f  15  to 
.'{()  i^iaiiis  |MM-  diiv.  iMercui'v  and  iodides,  whicdi  give,  siidi  miirvi-llous  nvsults 
ill  nuuiy  sy]»liiliti(;  lesi«Mis,  are  loss  certain  in  acnito  syi)liiliti(;  nepliiitis.  We 
see  both  cases  of  undoubted  and  rapid  success,  and  others  in  which  these 
drugs  do  little  good.  In  any  case,  we  must  use  care  in  f)n;s(;ribing  mercury, 
because  the  kidneys  are  weak,  and  the  filter  is  bad.  if  ra])id  impnjvement 
occur  (as  in  my  first  case),  we  may  rest  content ;  but  if,  in  spite  of  mercury 
and  milk  diet,  the  disease  remain  stationary  or  become  worse  (as  in  my 
second  case),  we  may  well  feel  alarmed  lest  we  have  exceeded  the  proper 
dose  or  have  not  reached  it.  The  drug  is  stopped,  and,  then,  given  again, 
but  the  disease  progresses.  It  would  appear  that  the  epithelial  lesions 
of  the  kidneys  caused  by  the  syphilitic  toxine  are  irreparable. 

The  cedema  and  the  effusions  demand  rehef.  This  point  requires  some 
words  of  explanation.  The  patient  who  has  pleural  effusion  on  one  or 
both  sides  has  certainly  also  cedema  of  the  lung,  which  helps  to  cause  the 
symptoms  of  dyspncea.  The  effusion  is  rightly  tapped,  but  we  must  not 
withdraw  2  or  3  pints  at  a  time,  because  a  circumscribed  oedema  of  the  lung 
may,  immediately  after  thoracentesis,  become  a  superacute  oedema  of  the 
gravest  kind.  In  such  a  case  let  us  be  satisfied  with  withdrawing  8  to 
10  ounces  of  the  liquid.  The  operation  may  be  repeated  several  times  a 
week,  as  was  done  in  my  third  case.  Thoracentesis  with  a  No.  2  needle 
is  of  no  more  consequence  than  a  puncture  made  with  a  Pravaz  syringe. 
Repeated  withdrawals  of  small  amounts  of  fluid  protect  against  every 
compUcation,  and  reheve  the  patient.  Unfortunately,  the  pleural  Uquid 
is  often  quick  to  reform. 

Wlien  the  anasarca  is  abundant,  we  should  favour  the  exit  of  the  Uquid 
by  acupuncture  of  the  legs,  thighs,  and  scrotum.  We  can,  by  this  means, 
draw  off  several  pints  of  fluid  in  the  day,  and  give  the  sufferer  great  rehef. 
The  puncture  may,  however,  in  spite  of  every  aseptic  precaution,  become 
the  starting-point  of  erythema  or  lymphangitis ;  and,  indeed,  erysipelas, 
and  lymphangitis  (apart  from  any  puncture)  often  cause  death  in  patients 
with  dropsy  due  to  early  syphihtic  nephritis.  If,  then,  lymphangitis  or 
fatal  erysipelas  supervene  in  consequence,  we  may  be  held  tesponsible  for 
a  fatal  result. 

2.  Tertiary  Syphilis  of  the  Kidneys. 

Late  renal  syphihs  is  a  variety  of  chronic  nephritis  sometimes  associated 
with  gummatous,  fibrous,  or  amyloid  lesions,  which  appear  many  years 
after  the  chancre.  It  may  be  called  "  syphihtic  Bright's  disease."  I  know 
that  under  such  circumstances  it  is  often  difficult  to  decide  the  share  of 
syphihs  as  an  setiological  factor.  If  a  sypliihtic  patient  has  Bright's  disease, 
and  at  the  same  time  we  find  from  his  history  one  or  more  causes  of  nephritis 
u.  75 


1174  TEXT-BOOK  OF  MEDICINE 

(scarlatina,  influenza,  typhoid  fever,  plumbism,  renal  calculus,  or  gout),  it 
is  difl&cult  to  decide  how  far  sypHlis  is  concerned.  If,  however,  he  has 
chronic  nephritis,  and  we  iBud  in  his  history  no  other  cause  than  syphihs, 
and  if,  a  fortiori,  the  nephritis  is  contemporaneous  with  other  tertiary 
lesions  (gummata  of  the  skin  or  tongue,  nasal  syphihs,  osteoperiostitis,  etc.). 
it  is  logical  to  set  down  the  kidney  trouble  to  syphihs. 

Pathological  Anatomy. — Pathological  anatomy  has  specified  the  various 
forms  which  tertiary  syphihs  of  the  kidneys  may  assume.  We  find  chronic 
nephritis,  with  or  without  gummatous,  fibrous  or  amyloid  changes.  They 
may  exist  alone  or  in  combination.  Let  us  first  consider  the  gummata. 
"  Syphilitic  gummata,"  says  Cornil,  "  are  not  common  in  the  kidney.  In 
1864  I  saw  a  kidney  with  about  twenty  in  the  cortex.  The  patient  was  an 
old  woman  who  had  died  from  albuminuria  and  anasarca.  The  hver  was 
riddled  with  typical  gummata.  The  kidneys  showed  amyloid  degeneration, 
and  the  gummata  presented  the  characteristic  three  zones." 

Ciifier  showed  a  case  of  syphilis  of  the  kidney  at  the  Societe  Anato- 
mique  characterized  by  a  large  grey  and  homogeneous  gumma.  Wagner  has 
published  a  case  of  gumma  in  the  right  kidney,  which  was  small,  dark,  and 
smooth,  whilst  the  left  kidney  was  enlarged  and  pale.  Piingel,  Lancereaux, 
LaiUer,  and  Key  have  found  gummata  of  the  kidney  associated  with  othei 
syphihtic  lesions.  Chronic  syphilitic  nephritis  with  interstitial  fibrosis  may 
end  in  atrophy  of  the  organ.  In  sixty-three  cases  of  syphihtic  nephritis 
Wagner  in  eight  cases  found  that  the  kidney  was  small,  granular,  and 
atrophied.  Sometimes,  on  the  other  hand,  the  kidneys  are  enlarged,  and 
show  parenchymatous  lesions.  In  some  cases  one  kidney  shows  atrophic 
nephritis,  whilst  the  other  is  enlarged  and  amyloid.  Lancereaux  has  seen 
renal  syphihs,  characterized  by  gummata,  interstitial  nephritis,  amyloid 
degeneration,  and  deep  cicatrices.  In  two  cases  of  syphilosis  of  the  kidney 
Key  noted  that  the  atrophic  fibrosis  was  hmited  to  the  lower  part  of  the 
kidney.  Weigert  has  pubhshed  six  cases  of  unilateral  atrophy  of  the 
kidney  in  syphihtic  patients.  These  various  quotations,  borrowed  from 
Mauriac's  monograph,  prove  that,  while  early  syphihtic  nephritis  is 
general  and  uniform,  tertiary  syphihs  may  not  afiect  both  organs  to 
the  same  extent.  It  may  limit  itself  to  one  kidney  or  to  a  portion 
of  the  kidney.  Amyloid  degeneration  is  a  very  common  lesion  in  renal 
syphihs,  and  often  coincides  with  simflar  degeneration  of  the  hver  and 
spleen. 

These  gummatous,  fibrous,  and  amyloid  changes  are  associated  to  an 
unequal  degree  with  chronic  nephritis.  We  often  find  chronic  nephritis 
alone,  without  any  trace  of  gummatous  or  amyloid  change.  In  other  words, 
the  kidney  in  tertiary  syphihs  may  differ  much  in  shape  and  appearance. 
It  may  be  enlarged,  or  atrophied,  nodular  and  furrowed. 


DISEASES  OF  THE  KIDNEYS  llVr, 

Description. — Tlie  following  cases  will  give  an  idea  of  I  he  cliiiioal 
featiiies  : 

Casis  I. — A  iiiJin  was  admittod  into  my  wards  for  chronic  nephritis.  Tho  diKouso 
had  appoarod  a  yuar  previously  with  tho  minor  symptoms  of  Bnghtism.  (Edoma 
supervened  later.  At  this  period  tho  patient  was  examined  by  Charrier,  who  found 
Bright's  cUseaso  and  prescribed  a  milk  diet.  Tho  symptoms  persisted,  in  spite  of 
treatment ;  the  attacks  of  headache  became  more  acute,  tho  ajdema  of  tho  legs  increa.sed, 
and  Charrior  asked  mo  to  admit  him.  I  found,  as  a  matter  of  fact,  ehronic  nephritis, 
which  m  no  wise  dilTcred  as  regards  its  course  from  common  Bright's  disease. 

Headaclio  and  dyspnoea  wore  the  chief  symptoms.  The  urine,  which  was  normal  in 
quantity,  contained  albumin.  The  patient  finally  admitted  that  sixteen  years  pre- 
viously he  had  had  sypliilis,  for  which  he  had  boon  treated  at  the  Hopital  du  MicU. 
As  he  had  had  no  other  infectious  chsease  capable  of  explaining  this  nephritis,  I  con- 
sidered that  the  trouble  was  syphilitic,  and  prescribed  accordingly :  daily  inunction  of 
mercmy  and  iodide  of  potassium  in  45-giain  doses,  which  were  soon  increased  to 
90  grains  daily.  Although  the  milk  diet  which  had  akeadj'  been  given  had  by  itself 
produced  no  improvement,  it  was  continued.  In  a  fortnight  the  situation  was  very 
different,  and  in  a  month  the  patient  was  discharged  at  his  own  request,  all  symptoras 
having  disappeared.  The  albumin  gradually  diminished,  and  after  eighteen  days 
there  was  not  a  trace  in  the  urine. 

Case  II. — A  man,  forty-six  years  of  age,  was  sent  to  mo  by  Sauvineau,  who  had 
found  retinitis.  On  his  admission  to  the  St.  Christopher  Ward,  the  strain  of  walking 
upstairs  caused  such  marked  dyspnoea  that  he  could  hardly  speak.  He  told  us  that 
his  breathing  had  been  diflficult  for  a  long  time,  and  slight  effort  caused  fits  of  suffoca- 
tion. Auscultation  immediately  revealed  the  cause  :  in  both  limgs  rales  due  to  oedema 
were  audible.  His  face  was  puffy,  especially  about  the  eyehds ;  and  the  legs  were  also 
cedematous.  This  information,  together  with  abundance  of  albumin  in  the  urine,  con- 
firmed the  diagnosis  of  Bright's  disease. 

Examination  of  the  heart  revealed  a  bruit  de  galop,  and  analysis  of  the  urine  showed 
1  drachm  of  albumin  per  pint.  He  had  chronic  nephritis,  because  the  duration  of 
the  minor  symptoms  of  Brightism  showed  that  the  disaese  had  commenced  about  a 
year  and  a  half  before.  The  visual  troubles  distm'bed  the  patient  more  than  the 
dyspnoea.  He  was  able  to  walk  about,  but  could  not  distinguish  the  features  of  persons 
nor  the  hands  of  the  ward  clock.  Sauvineau  found,  Avith  the  ophthalmoscope,  that  the 
visual  troubles  were  due  to  albuminuric  retinitis. 

As  he  had  a  history  of  syphiUs,  I  ordered  mercury,  iodide  of  potassium,  and  milk 
diet.  Anyone  not  famihar  with  the  extraordinary  results  which  at  times  follow  this 
treatment  would  certainly  have  had  reason  to  be  sm'prised  at  the  rapid  improvement. 
After  three  days,  his  condition  began  to  improve.  He  breathed  more  easily,  and  could 
walk  without  feeling  breathless  (he  had  not  done  this  for  a  year).  In  six  days  he  was 
able  to  distinguish  the  features  of  those  around  him.  He  was  a  different  man  at  the  end 
of  twenty-five  days,  during  which  time  he  had  had  twenty-five  injections  of  mercury 
and  had  taken  5  ounces  of  iodide  of  potassium.  He  was  able  to  read  a  newspaper,  and 
felt  no  distress.  During  this  same  period  the  albumin  fell  to  6  grains  per  pint,  the 
pulmonary  oedema  disappeared,  and  he  felt  so  well  that  he  left  the  hospital. 

In  the  two  preceding  cases  the  history  made  a  diagnosis  possible,  but 
there  are  cases  in  which  the  patient  who  has  well-marked  uraemia  is  in- 
capable of  giving  any  information. 

A  man  was  admitted  for  coma.  We  noted  no  distortion  of  the  face  and  no  sign 
of  hemiplegia.  As  Charrier,  on  examining  him,  foimd  marked  oedema  of  the  face  and 
legs,  he  thought  of  ursemic  coma  due  to  Bright's  disease.     He  cupped  the  loins,  and  drew 

75—2 


1176  TEXT-BOOK  OF  MEDICINE 

off  about  8  ounces  of  blood.  A  letter  from  the  doctor  who  had  attended  the  patient 
informed  me  that  he  had  found  as  much  as  12  graius  of  albumin  per  ounce,  and  that 
for  the  past  ten  days  the  man  had  been  suffering  from  violent  frontal  headache.  This 
information  was  sufficient  to  confirm  the  diagnosis  of  ursemic  coma.  I  prescribed  milk. 
I  managed  to  collect  some  urine,  which  contained  7  grains  of  albumin  per  ounce.  During 
the  next  few  days  his  somnolent  condition  did  not  change,  and  he  rephed  imperfectly  to 
questions.  I  learnt  that  he  had  had  syphilis  fifteen  years  previously,  and  was,  therefore, 
hopeful  that  his  conchtion  was  dependent  on  syphihs.  In  consequence,  I  prescribed 
mercury  and  iodide  of  potassium — the  mercury  in  the  form  of  the  oHy  solution  of  bin- 
iodide  of  mercury  by  injection,  and  the  iodide  in  doses  of  60  grains  daily. 

In  four  days  improvement  was  manifest :  he  passed  twice  as  much  m-ine,  and  the 
amount  of  albumin,  which  had  been  12  grains  per  ounce,  now  fell  to  5  grains.  In  the  next 
few  days,  progressive  improvement.  The  drowsiness  and  headache  disappeared ;  the 
patient  spoke  without  difficulty ;  the  amount  of  urine  reached  6  pints  in  twenty-four 
hours,  and  contained  only  a  trace  of  albumin.  Eighteen  days  before  he  was  comatose, 
and  his  condition  was  most  grave,  but  he  could  now  get  out  of  bed  and  talk 
like  a  normal  person.  This  result  was  due  to  eighteen  injections  and  to  3-^  ounces  of 
iodide  of  potassium.  The  specific  treatment  was  stopped  for  the  time  being,  and 
resumed  a  fortnight  later,  but  the  patient  objected  to  the  strict  diet.  He  now  considered 
himself  cured  (this  idea  was  premature,  as  he  had  still  a  trace  of  albumin),  and  asked 
to  leave  the  hospital.  Sis  months  later  he  was  in  good  health,  the  albumin  being  the 
only  evidence  of  his  nephritis.  He  was  again  put  imder  the  mercurial  and  iodide 
treatment,  but  left  without  having  the  patience  to  wait  for  a  definite  cure. 

These  cases  prove  tliat  tertiary  sypMIis  of  the  kidney  shows  all  the 
symptoirLS  of  ordinary  Bright's  disease.  It  is  a  type  of  Bright's  disease  which 
often  commences  in  a  more  or  less  insidious  manner.  In  this  type,  as  in 
the  other  types  of  chronic  nephritis,  the  minor  symptoms  of  Brightism  open 
the  scene  without  otherwise  disturbing  the  patient.  During  the  course  of 
this  "  syphilo-Brightism,"  which  is  intermediate  between  a  state  of  health 
and  of  disease,  we  find  severe  epistaxis,  attacks  of  dyspnoea  simulating 
asthma,  digestive  troubles  with  vomiting,  hke  those  seen  in  chronic  gas- 
tritis and  oedema  of  the  face  and  limbs,  which  help  us  to  clear  up  a  doubtful 
diagnosis.  The  tertiary  form  of  renal  syphihs  may  not  be  chronic  from  the 
outset,  but  may  follow  acute  syphihtic  nephritis  ;  and  yet,  whatever  its 
mode  of  onset,  it  usually  ends,  in  the  absence  of  careful  treatment,  in  grave 
comphcations — dyspnoea,  coma,  delirium,  or  convulsions. 

In  some  cases,  which  are  fairly  common  (especially  in  the  case  of  un- 
treated syphilis),  the  lesions  in  the  kidney  are  comphcated  with  syphihs 
of  the  hver  (painful  and  deformed  hver,  jaundice,  ascites,  etc.).  The  associa- 
tion of  hepatic  and  renal  syphihs,  in  which  amyloid  degeneration  plays  a 
large  part,  has  been  pointed  out  by  Mauriac.  Rayer  had  aheady  noted 
this  fact.  Naegel  and  Wagner  have  reported  cases  of  it.  Brault  has 
reported  the  following  case  : 

A  woman  of  forty.-eight  years  had  albtmiinuria  with  oedema  of  the  hmbs,  which 
gradually  reached  the  hypochondriac  region,  and  at  the  same  time  the  hver  became 
painful.  The  abundant  ascites  called  for  repeated  paracentesis.  She  was  jaundiced 
throughout  the   disease.      Post   mortem  the  liver,   which  only  weighed  30  ounces, 


DISEASES  OF  TTTE  KIDNEYS  1177 

showed  nnmorous  fiRsurofl,  dividing  it  into  sovoral  lobos.  Tlio  intrahepatic  fibrous  tlRAue 
contained  giitntnata — Boino  ahnoHt  hoalod,  othorH  largo,  conflutnt,  and  in  full  growth. 
The  cliief  ciiango  in  the  livtir  was  dilTiiBo  hepatitis  of  long  atandiiig,  with  amyloid  de- 
generation of  the  largo  blood vtvsHols.  The  kiflnoya,  which  wtrnj  of  normal  sizo,  sliowod 
amyloid  degeneration  in  almost  all  the  gloineriiii. 

In  some  instances  the  syphilitic  lesions  are  not  hmited  to  the  kidneys 
and  liver,  but  invade  several  organs.  The  following  case,  taken  from  Naegel, 
will  give  an  idea  : 

A  man,  thirty-six  years  of  age,  had  a  chancre  at  the  age  of  eighteen,  and  was  treated 
with  mercmy  and  iodide  of  potassium.  Ten  years  later  ulcerous  syphilides  appeared, 
and  seventeen  years  after  the  first  infection  nephritis  showed  itself.  The  appearance  of 
ODdoma  and  albuminuria  was  followed  by  uncontrollable  vomiting  and  most  intense 
dy8pna?a ;  the  disease  advanced  so  rapidly  that  at  the  end  of  a  year  the  patient  suc- 
cumbed from  cachexia.  At  the  post-mortem  examination  the  Icidneys  showed  inter- 
stitial nephritis  and  amyloid  degeneration  of  the  arterioles  and  of  the  glomoruh.  The 
arterioles  in  the  Uver  and  spleen  were  infiltrated  with  amyloid  matter.  The  heart  was 
enlarged,  and  the  left  ventricle,  which  was  hypertrophied,  showed  no  fibrosis,  but  simply 
amyloid  degeneration.     The  lungs  were  oedematous  and  congested. 

It  will  be  well  to  sum  up  the  question  of  tertiary  renal  syphihs  briefly. 

In  the  first  variety,  the  disease  is  attenuated.  It  does  not  cause  the 
grave  symptoms  of  Bright's  disease,  but  only  the  minor  symptoms  of 
Brightism  and  albuminuria,  with  or  without  oedema.  This  form  is  "  syphilo- 
Brightism." 

In  the  second  variety,  which  is  the  most  common,  the  course  is  that  of 
ordinary  Bright's  disease.  It  commences  more  or  less  insidiously  in  the 
form  of  Brightism,  with  albuminuria  and  moderate  oedema.  Epistaxis, 
headache,  vomiting,  dyspnoea,  visual  troubles,  cardiac  hypertrophy,  etc., 
may  supervene  at  some  later  date,  and  the  major  symptoms  of  uraemia 
only  appear  if  the  disease  is  not  suitably  treated.  Sometimes  the 
onset  and  the  progress  of  the  disease  are  more  sudden  and  rapid.  The 
oedema  is  more  general  (oedema  of  the  lung  included)  ;  the  albumin  is 
more  abundant,  and  the  dyspnoea  appears  earher.  It  is  probable  that  severe 
epithehal  lesions  are  present,  in  addition  to  the  other  changes  in  the  kidneys. 

In  the  third  variety,  the  kidneys  are  not  alone  affected.  The  syphilis 
also  attacks  the  Uver,  a  coexistence  which  must  always  cause  grave  alarm. 
Hypertrophy  or  atrophy  of  the  organ,  pain,  urobihnuria,  icterus,  and 
ascites  point  to  hepatic  lesions.  Finally,  in  the  fourth  variety,  the  infection 
is  even  more  general,  and  several  organs  are  invaded.  The  liver,  spleen, 
intestines,  and  heart  are  invaded  by  amyloid  degeneration,  and  the  patient 
succumbs  from  cachexia. 

Tertiary  syphihs  of  the  kidney  may  appear  some  few  years  after  in- 
fection or  much  later — ten,  twenty,  or  thirty  years  after  the  chancre. 
It  sometimes  shows  itself  by  repeated  outbrealts,  with  intervals  of  arrest. 
The  symptoms  are  at  first  those  of  syphilo-Brightism,  and  soon  improve. 


1178  TEXT-BOOK  OF  MEDICINE 

as  though  the  disease  were  cured  ;  yet  we  must  not  be  led  astray  by  this 
fact,  because  severe  nephritis  may  reappear  later. 

A  few  words  more  concerning  hereditary  syphiKs  of  the  kidneys.  We 
have  not  at  present  full  data  on  this  subject.  It  may  appear  during  the 
course  of  the  first  year  of  life  or  only  fifteen  to  twenty  years  later  (Fournier). 
It  reveals  itself  by  symptoms  similar  to  those  of  the  acquired  disease. 

The  diagnosis  is  a  matter  of  supposition,  because  the  onset,  course,  and 
comphcations  of  syphihtic  nephritis  do  not  differ  from  ordinary  Bright' s 
disease.  If  the  patient  has  had  syphihs,  we  may  assume  that  the  nephritis 
is  sj^hihtic.  The  simultaneous  or  previous  appearance  of  specific  lesions 
in  other  regions  (gummata  of  the  skin  and  the  mouth,  tertiary  ulcerations, 
osteoperiostitis,  etc.)  has  a  bearing  on  the  diagnosis — at  any  rate,  in  case 
of  Bright's  disease.  We  should  always  look  for  syphilis,  and  if  we  find 
evidence  in  favour  of  a  specific  origin  for  the  nephritis,  we  should  at  once 
give  specific  treatment. 

I  have  now  to  discuss  those  obscure  cases  in  which  syphihtic  albuminuria 
exists  alone,  without  other  symptoms  of  chronic  nephritis.  These  cases 
reahze  what  I  have  called  "the  dissociation  of  the  morbid  acts  of  the 
kidneys." 

In  chronic  nephritis  albuminuria  and  insuflScient  depuration  usually 
appear  together,  and  are  connected  with  renal  changes.  In  other  instances, 
which  are  more  numerous  than  we  might  at  first  think,  these  two  morbid 
conditions — albuminuria  and  symptoms  of  Bright's  disease — may  remain 
dissociated  for  a  long  time.  This  dissociation  presents  itself  in  various 
forms  :  A  person  may  have  Bright's  disease  for  a  long  time  without  passing 
albumin  ;  on  the  other  hand,  he  may  pass  albumin  for  years  without  getting 
Bright's  disease.  I  have  discussed  this  question  in  Section  VII.,  but  I 
mention  it  again  with  regard  to  chronic  syphihtic  nephritis. 

Syphilo-Brightism  may  exist  without  albuminuria,  and,  on  the  other 
hand,  syphihtic  albuminuria  may  persist  without  any  other  symptoms  of 
nephritis.     To  quote  examples  : 

In  1897  a  man  came  into  my  consulting-room  supporting  himself  on  a  stick  and 
dragging  his  legs.  He  had  paraplegia.  He  told  me  that  some  months  before  he  had 
experienced  formication,  pain,  and  heaviness,  which  made  walking  diflficult.  These 
symptoms  had  been  preceded  by  pains  in  the  loins.  His  doctor  found  much  albumin 
present  in  the  urine.  Absolute  milk  diet  was  prescribed  for  two  months.  A  second 
examination  of  the  urine  showed  that  the  albuminuria  had  increased,  in  spite  of  the 
milk  diet.  When  I  examined  the  patient,  I  fotmd  symptoms  of  slowly  progressive 
paraplegia.  As  an  infantry  officer,  he  was  accustomed  to  long  marches,  but  was  now 
unable  to  walk  fifty  steps  without  stopping.  The  patellar  reflexes  were  much  dimin- 
ished, especially  on  the  right  side.  The  bladder  was  sluggish^  and  although  true  reten- 
tion was  not  present,  micturition  was  slow  and  difficult.  As  he  had  had  syphilis  eight 
years  before,  it  was  evident  that  the  paraplegia  was  due  to  syphihtic  mischief  in  the 
cord.     And  as  the  albuminuria  and  the  paraplegia  had  come  on  together,  it  might  be 


DISEASES  OF  TIIR  KTDNRYS  II79 

presnmoil  lliat  the  kidiioys  had  Ixuni  atfacUoiI  Minmltaiicoiisly  l)y  nypliilis.  I  found 
plenty  of  albumin,  but  no  other  symptom  of  nephritis.  (Edoina,  jtollakiuria,  fi-y.-DRtliosia, 
cramp  fh  the  oalvoa  of  the  logs,  increased  arterial  tension,  bruit  dr.  (folop,  dyspncoa,  and 
any  indication  of  insviflicient  urinary  depuration,  were  all  absent.  The  kidneys,  there- 
fore, were  normal  as  regards  the  function  of  depiiration,  though  thny  allowed  the  passage 
of  albumin.     Thoro  was,  therefore,  dissociation  of  the  morbid  acts  of  the  kidnoy.>9. 

I  ordered  mercury  and  iodidi^a.  Six  weeks  later  the  improvement  was  so  marked  that 
he  could  climb  several  flights  of  stairs  or  walk  a  mile  without  any  fatigue.  Although 
I  stopped  the  milk  diet  from  the  first,  tho  albuminuria  diminished.  The  mercurial 
treatment  was  resumed,  and  six  months  later  ho  rejoined  tho  service,  marching  several 
miles  without  fatigue,  and  having  regained  his  health.  The  albuminuria  still  persists, 
without  any  other  symptom  of  Bright's  disease.  Those  are  probably  tho  cases  which 
Jaccoud  had  in  view  when  lio  wrote :  "  This  form  of  nephritis  in  which  the  symptoms 
of  the  renal  localization  are  limited  to  the  change  of  the  urine — at  least,  for  a  very 
long  time." 

Treatment. — Mercury  and  iodide  of  potassium  are  the  two  best  drags 
in  tertiary  sypliilis  of  the  Iddney.  The  mercurial  preparations  are,  however, 
to  be  preferred.  I  give  injections  of  an  aqueous  sohition  of  biniodide  of 
mercury.  Iodide  of  potassium  may  be  given  in  daily  doses  of  30  grains. 
The  action  of  these  remedies  must  be  closely  watched,  because  the  renal 
filter  is  compromised.  If  only  the  kidneys  are  attacked  by  syphihs,  the 
hver  and  other  organs  being  free,  the  treatment  gives  the  best  results.  We 
can  restore  health  to  patients  who  have  advanced  Bright's  disease  when  the 
disease  is  due  to  syphilis. 

To  bring  about  complete  cure,  however,  the  treatment  must  be  stopped 
and  resumed  several  times.  Tertiary  lesions  of  the  kidneys  or  elsewhere 
rarely  recover  at  the  first  attempt.  The  improvement  is  often  rapid,  some- 
times surprising,  but  definite  cure  is  difficult  to  obtain.  Sometimes  the 
improvement  stops  while  treatment  is  being'  taken ;  sometimes  the  disease 
reappears  at  a  shorter  or  longer  date  after  supposed  cure.  The  disease 
leaves  some  traces.  The  nephritis  must,  therefore,  be  watched,  even  when 
it  appears  to  be  cured,  and  treatment  must  be  resumed  when  necessary. 
The  cures  at  Luchon,  Uriage,  and  Aix-la-Chapelle,  where  thermal  baths  and 
mercurial  inunction  are  combined,  are  of  much  service.  Hospital  patients 
are  rarely  completely  cured,  because  they  leave  as  soon  as  they  feel  some- 
what better,  being  unwilling  or  unable  to  wait  longer.  Relapses  are  also 
frequent. 

The  milk  cure  is  not  as  important  in  syphilitic  as  in  other  forms  of 
nephritis.  One  of  my  patients  was  cured  by  specific  treatment  after  an 
absolute  milk  diet  had  given  no  result.  Milk  is,  nevertheless,  a  useful 
adjunct.  Dechlorination  (of  which  I  spoke  under  Bright's  Disease)  must 
be  employed  in  syphihtic  nephritis,  especially  when  oedema  is  present. 


1180  TEXT-BOOK  OF  MEDICINE 

XI.  CYSTS  OF  THE  KIDNEY— ENLARGED  POLYCYSTIC  KIDNEY. 

Cysts  of  the  kidney  may  be  congenital  or  acquired.  To  tlie  latter 
variety  belong  (1)  tbe  small  cysts  of  interstitial  nephritis ;  (2)  blood  cysts ; 
(3)  cystic  degeneration  in  the  adult ;  (4)  hydatid  cysts. 

1.  Congenital  Cysts. 

Cystic  degeneration  of  the  kidney  in  the  foetus  may  assume  such  dimen- 
sions as  to  cause  dystocia.  The  enlarged  kidneys  press  upon  and  push 
back  the  neighbouring  organs.  The  surface  is  nodular,  and  a  section  of  the 
kidney  shows  a  number  of  pockets  of  variable  dimensions.  These  pockets 
contain  a  clear  or  dark  hquid.  Many  theories  have  been  propounded  to 
explain  the  formation  of  these  cysts  :  atrophy  of  the  medullary  substance, 
constriction  and  obhteration  of  the  straight  tubules,  distension  of  the 
glomeruh  (Virchow),  or  faulty  development  of  the  urinary  system  (Koster). 
In  certain  cases  this  cystic  degeneration  coincides  with  other  malformations 

of  the  foetus. 

2.  Cysts  of  Interstitial  Nephritis. 

They  are  of  the  size  of  a  pin's  head  or  a  small  pea,  and  are  found  on  the 
surface  and  in  the  interior  of  the  kidney.  They  contain  a  colloid  substance, 
and  are  due  either  to  enlargement  of  the  tubules,  which  are  constricted  by 
the  fibrous  tissue,  or  to  dilatation  of  the  glomeruh. 

3.  Blood  Cysts. 

Blood  cysts  probably  have  their  origin  in  obhteration  of  a  tubule. 
They  become  fairly  large.  HEemorrhage  takes  place  from  the  vascular 
hning  membrane,  and  the  hquid,  which  is  more  or  less  clear,  contains  granules 
of  h^matosin  and  crystals  of  hsematoidin  (Lancereaux). 

4.  The  Enlarged  Polycystic  Kidney— Cystic  Degeneration. 
Pathological  Anatomy. — Cystic  degeneration  of  the  kidneys  in  the 
adult  somewhat  resembles  that  seen  in  the  foetus.  Both  kidneys  are  always 
affected,  but  to  a  different  extent  and  at  a  different  time.  Each  kidney 
may  weigh  30  or  40  ounces.  The  polycystic  kidney  often  looks  hke  a 
bunch  of  grapes.  The  single  grapes  are  not  of  the  same  shape  and  size, 
and  are  said  to  be  formed  by  the  cystic  pockets.  These  anfractuous  pockets, 
which  may  be  isolated  or  fused,  are  filled  with  opaque  or  transparent  fl'iid 
of  various  colours  and  kinds.  The  fluid  may  be  serous,  albuminous,  gelatini- 
form,  or  purulent,  and  often  contains  urea,  chlorides,  and  phosphates.  In 
a  cyst  of  average  size  fibrous  bands  divide  it  into  compartments.  The  walls 
are  thin,  and  the  renal  parenchyma  between  the  cysts  may  be  healthy  or 
may  undergo  fibrous  change.     The  renal  tissue  is  finally  replaced  by  fibrous 


DISEASES  OE  THE  KIDNEYS  llRl 

or  cystic  tissue.    TIk^  cysts  arise  in  the  cortex,  and  extend  into  the  nKMlnlbiry 
substance. 

The  polycystic  kidneys  often  contract  adhesions  with  the  liver,  dia- 
phragm, spleen,  lumbar  fascia,  or  duodenum.  They  are  sometimes  sur- 
rounded by  a  shell  of  fibro-adiposc  tissue,  sucli  as  is  seen  in  all  chronic 
affections  of  the  Icidneys,  and  arises  in  the  perirenal  fat.  A  perinephritic 
abscess  may  be  found.  When  the  organ  is  not  kept  in  place  by  adhesions, 
it  becomes  movable.  The  ureter  and  the  pelvis  are  of  normal  size  and 
patency — a  condition  opposite  to  that  found  in  hydronephrosis.  The  left 
side  of  the  heart  may  be  hypertrophied,  just  as  in  chronic  nephritis. 

The  Uver  often  shows  cystic  degeneration.  This  simultaneous  degenera- 
tion of  the  hver  and  of  the  kidneys  is  fairly  common.  Lejars  has  collected 
seventeen  cases.  The  changes  in  the  Hver  are  similar  to  those  seen  in  the 
kidney.  The  organ  becomes  enormous  and  may  weigh  8  or  10  pounds 
(Sabourin).  Its  surface  is  studded  with  reddish  or  brownish  transparent 
cysts,  from  the  size  of  a  pea  to  that  of  an  apple.  The  cysts  commence  on 
the  surface  under  the  capsule,  and  spread  into  the  deep  tissue  of  the  organ. 
On  section,  the  Hver  has  the  appearance  of  a  hive,  the  cystic  pockets  being 
more  or  less  shut  off. 

The  lesions  in  the  kidneys  and  the  Uver  may  be  successive  or  simul- 
taneous, but  have  no  tendency  to  become  general.  The  lesion  of  the 
Iddneys  remains  confined  to  that  organ.  It  invades  neither  the  glands  nor 
the  neighbouring  tissues. 

The  formation  of  the  polycystic  kidney  is  a  matter  of  supposition.  "  In 
spite  of  its  character  as  an  epitheHal  tumour  which  estabHshes  its  relation  to 
the  new  growths,  cystic  degeneration  of  th^  kidneys  does  not  tend  to  become 
general.  It  never,  therefore,  resembles  a  cystic  epithelioma  of  invading 
tendency.  It  is  a  transformation  of  the  organ  in  situ,  analogous  to  that 
wliich  may  be  found  in  the  Hver,  breast,  or  testicle  "  (Brault). 

Description. — The  symptoms  show  extraordinary  variation.  I  shall 
describe  some  of  the  various  forms.  They  will  also  give  an  idea  of  the 
extreme  diflSiculty  in  diagnosis. 

In  the  first  variety  the  disease  is  latent.  A  post-mortem  examination 
is  performed  on  a  patient  who  has  died  of  some  other  malady,  such  as  tuber- 
culosis or  pneumonia,  and  the  surprise  is  great  on  finding  two  polycystic 
kidneys.  This  latency  is  not  difficult  to  explain.  As  long  as  one  of  the 
kidneys  performs  its  functions  sufficiently  well,  or  as  long  as  there  remains 
in  the  kidneys  sufficient  renal  substance  to  assure  urinary  depuration,  the 
cystic  disease,  which  is  harmless  in  nature,  may  pass  unnoticed.  It  may 
not  cause  pain,  hsematuria,  or  urasmic  symptoms,  and  the  patient  may  die 
from  another  disease  before  the  renal  lesion  has  given  rise  to  symptoms.  1 
am  of  the  opinion  that,  while  the  renal  substance  is  completely  atrophied 


1182  TEXT-BOOK  OF  MEDICINE 

or  fibrous  in  some  cases,  it  is  hypertropliied  in  others.  CHiantreiiil  has 
published  a  case  of  this  kind.  This  compensatory  hyperplasia,  if  verified, 
would  be  analogous  with  the  compensatory  hypertrophy  of  the  hver,  described 
under  Hypertrophic  Alcohohc  Cirrhosis  and  Hydatid  Cysts  of  the  Liver. 

In  the  second  variety  hsematuria  is  the  first  and  most  important  symptom 
of  polycystic  kidney.  Shght  or  severe  haematuria,  which  comes  on  in 
attacks,  and  is  often  accompanied  by  pain,  is  a  frequent  symptom  in  poly- 
cystic kidney ;  but  there  are  other  cases  in  which  hsematuria  is  the  chief 
symptom,  and,  indeed,  causes  errors  in  diagnosis.     For  example  : 

A  •woman,  forty-two  years  of  age,  had  sharp  pains  in  the  loins  and  attacks  of  hsema- 
turia, which  lasted  for  about  a  month.  After  an  interval,  the  pains  returned,  together 
with  the  hsematuria.  A  year  later  pains  in  the  lumbar  region  and  the  right  hypochon- 
drimn,  accompanied  by  hsematuria,  lasting  a  fortnight.  Pneumonia  came  on  a  year  later ; 
it  commenced  and  ended  with  attacks  of  hsematuria,  which  lasted  from  two  to  three  days. 
An  indefinite  swelling  was  now  found  in  the  right  hypochondrium,  and  as  profuse 
hsematuria  occurred,  cancer  of  the  right  kidney  was  suspected.  Later,  the  patient  was 
taken  iU  with  fever,  vomiting,  and  coma,  which  proved  fatal.  At  the  post-mortem 
examination  polycystic  degeneration  of  the  right  kidney  and  of  the  hver  was  fornid. 
The  left  kidney  was  also  polycystic. 

In  the  third  variety  pain  is  the  initial  or  chief  symptom.  It  is  common 
in  polycystic  kidney,  and  may  be  attributed  to  various  causes — to  the  size 
of  the  tumour,  to  its  mobihty,  to  its  displacement,  to  its  adhesions,  to  cystic 
or  perirenal  suppuration  ;  but  in  other  cases  the  pain  appears  from  the  first 
without  evident  cause.     For  example  : 

A  man,  thirty-seven  years  of  age,  was  admitted,  imder  Hanot,  for  acute  pains  in  the 
left  side  and  vomiting.  As  the  pains  radiated  into  the  groin  and  testicle,  they  seemed  to 
indicate  renal  colic.  Three  days  before,  the  pain  in  the  loin  had  been  so  severe  that 
the  patient  applied  a  bhster.  On  admission,  the  pain  was  most  marked  in  the  left 
flank,  was  increased  by  pressure,  and  radiated  into  the  right  hypochondrium.  For 
some  eighteen  years  he  had  felt,  without  apparent  cause,  acute  pains  in  the  hypo- 
chondria or  the  flanks.  The  pains  lasted  for  several  days,  and  the  patient  was  com- 
pelled to  keep  his  bed.  During  the  attacli  the  pains  were  continuous.  The  urine 
contained  albumin.  Vomiting  and  diarrhoea  appeared.  In  spite  of  milk  diet,  dyspnoea, 
and  prostration,  vomiting  with  diarrhcea,  and  almost  complete  anuria  were  present, 
and  the  patient  succumbed  in  coma.  At  the  post-mortem  examination  polycystic  de- 
generation of  both  kidneys  was  discovered ;  the  left  kidney  was  most  affected,  and 
weighed  40  ounces,  while  the  right  one  weighed  25  oimces. 

In  the  fourth  variety  symptoms  of  ursemia  or  of  Bright's  disease  are  from 
the  outset  predominant.  As  a  rule,  they  supervene  at  an  advanced  stage  of 
the  disease,  when  the  glandular  substance  of  the  kidneys  is  no  longer  equal 
to  efiecting  urinary  depuration ;  but  in  other  cases  the  degeneration  of  the 
kidneys  is  latent  until  the  ordinary  symptoms  of  chronic  nephritis  appear. 
Legrand  quotes  the  following  case  : 

A  man,  forty-nine  years  of  age,  admitted  for  violent  headache,  causing  insomnia. 
He  seemed  stupefied,  and  answered  with  great  diflficulty.  He  had  never  been  ill  until 
two  years  before,  when  he  showed  signs  of  Brightism  :  buzzing  in  the  ears  and  defective 


DISEASES  OF  THE   KIDNEYS  118?. 

hearing,  violent  rramjw  in  llio  c)ilv(!a  of  tlio  Itigs,  Llio  HotiHiition  of  doail  finj<«r8, 
aculo  it^-liingM,  orviPsthosia  in  tlio  Icigs,  and  matutinal  opislaxi.s.  Tlio  moro  sorious 
RVinploins  of  ur.t'inia  tliiMi  appoarod  :  continuous  iifadaclio,  f)aroxvflma  of  dyH[)nnea, 
vomiting,  and  diarrluoa.  CKdoma  of  ti»o  faco  and  logs  had  appoarod  at  intorvalfl  during 
tlu)  past  two  yoara.  Tho  urino  Avas  doar  and  abimdant,  but  did  not  at  tho  time  contain 
any  albumin  ;  it,  howovor,  contained  about  3  grains  to  tho  pint  ten  days  lator  ;  disaocia- 
tion  of  tho  morbid  acts  of  tlio  kidney.  Those  symptoms  pointed  strongly  to  inlorstitial 
nephritis.  He  was  put  on  milk  diet,  but  tho  miscihief  made  rapid  progress,  and  ended 
in  fatal  coma.  Post-mortem  :  no  chronic  nephritis,  but  only  polycystic  degeneration 
of  both  kidnoj^s,  which  resembled  largo  bunches  of  grapes,  and  were  composed  of  cysts 
of  various  sizes  and  colours. 

Polycystic  degeneration  of  the  kidneys  not  only  gives  rise  to  symptoms 
of  uriuaiy  insufficiency,  but  also  to  all  the  sjinptoms  which  are  at  times 
seen  in  chronic  nephritis — viz.,  high  arterial  tension,  hypertrophy  of  the 
left  side  of  the  heart,  with  bruit  de  galop,  profuse  epistaxis,  and  cerebral 
hoemorrhnge,  followed  by  apoplexy  or  hemiplegia. 

The  polycystic  kidney  is  not  always  evident  on  palpation.  A  tumour 
was  noticed  but  eighteen  times  in  sixty-two  cases  collected  by  Lejars.  It 
is  ahnost  always  in  a  forward  direction  that  the  polycystic  tumour  must 
be  sought,  because  all  renal  tumours  usually  have  a  tendency  to  project 
forwards.  The  tumour,  whether  mobile  or  not,  may  be  felt  on  bimanual 
palpation  (Guyon).  While  both  kidneys  are  enlarged,  one  is,  as  a  rule,  so 
much  larger  than  the  other  that  it  is  hardly  ever  possible  to  feel  both  organs. 
The  discovery  of  a  tumour  on  each  side  simphfies  the  diagnosis. 

Course  of  the  Disease. — The  cases  above  mentioned  show  that  poly- 
cystic degeneration  of  the  kidneys  does  not  run  a  regular  course.  Hsema- 
turia  and  pain  are  generally  early  symptoms.  A  tumour  which  can  be  felt 
gradually  appears  after  some  time.  At  a  given  moment  the  signs  of 
Brightism,  albuminuria,  and  oedema  appear,  and  patients  are  carried  off 
by  ursemia,  in  the  absence  of  some  other  intercurrent  affection.  While  this 
is  the  usual  course  of  events,  the  polycystic  degeneration  is  insidious  in 
other  cases.  The  predominance  of  symptoms  of  Bright's  disease  causes  it  to 
simulate  chronic  nephritis.  The  predominance  of  pains,  with  or  without 
attacks  of  hsematuria,  causes  it  to  simulate  renal  calculus.  The  abundance 
and  obstinacy  of  the  haematuiia  (with  or  without  a  renal  tumour)  cause  it 
to  simulate  cancer  of  the  kidney.  Diagnosis,  therefore,  is  often  extremely 
difficult,  especially  as  cystic  degeneration  of  the  Hver  may  also  compUcate 
the  situation.  Rigors  and  high  fever  in  the  course  of  polycystic  degenera- 
tion indicate  purulent  infection.  Pus  may  form  in  the  cystic  cavities,  and 
give  rise  to  abscesses,  which  open  into  the  pelvis  (pyuria).  Sometimes  the 
suppuration  leads  to  a  perinephritic  abscess. 

The  course  of  polycystic  degeneration  is  very  slow,  and  its  duration 
indeterminate,  but  its  termination  is  fatal,  because  surgery  is  powerless  in 
a  disease  which  gradually  destroys  both  kidneys. 


1184  TEXT-BOOK  OF  MEDICINE 


XII.  HYDATID  CYSTS  OF  THE  KIDNEYS. 

Pathological  Anatomy. — In  order  of  frequency  hydatid  cysts  of  the 
kidney  come  next  to  those  of  the  liver  and  the  lungs.  The  proportion  is 
as  foUows  :  Liver,  166 ;  lungs,  42  ;  kidneys,  30  (Davaine).  The  disease  is 
usually  hmited  to  one  kidney — the  left  more  frequently  than  the  right. 
The  lesion  commences,  as  a  rule,  in  the  cortex.  The  cyst  may  be  multi- 
locular  or  unilocular,  and  in  the  latter  case  it  varies  in  size  from  an  egg 
to  a  child's  head.  The  structure  and  the  Hfe-history  of  the  cyst  have  been 
fuUy  described  under  Hydatid  Cysts  of  the  Liver.  The  only  pecuHarities 
to  be  noted  are  that  the  cysts  of  the  kidney  sometimes  contain  crystals  of 
uric  acid  or  phosphate  and  oxalate  of  hme,  which  have  penetrated  into  the 
cyst  by  dialysis. 

The  hydatid  cyst  of  the  kidney  sometimes  contracts  adhesions  with 
the  hver,  the  spleen,  the  stomach,  the  mesentery,  and  the  intestine ;  these 
adhesions  become  vascular,  and  interfere  with  surgical  intervention.  The 
affected  kidney  is  sometimes  reduced  to  a  fibrous  shell ;  at  other  times  some 
glandular  substance  is  preserved.  The  remnants  of  the  renal  tissue  may 
show  interstitial  or  parenchymatous  nephritis.  In  some  cases  a  few  pieces 
of  the  glandular  tissue  escape  destruction,  and  undergo  compensatory 
hypertrophy.  The  question  of  compensatory  hjrperplasia  in  the  glandular 
organs  is  very  interesting,  and  is  becoming  well  known  as  far  as  certain 
organs  are  concerned.  It  wiU  be  found  described  in  detail  under  Alcoholic 
Hypertrophic  Cirrhosis  and  Hydatid  Cysts  of  the  Liver.  I  have  seen  it  in 
hydatid  cysts  of  the  spleen,  and  it  is  also  met  with  in  cysts  of  the  kidney. 
We  might  say  that  the  organ  regenerates,  to  supplement  the  destroyed 
portions.  Regeneration  of  the  glandular  substance  sometimes  takes  place 
in  a  cystic  kidney.  Sometimes  the  healthy  kidney  is  hypertrophied.  In 
this  respect  BraiUon  quotes  a  case  of  Blackburn.  The  kidney  and  ureter 
were  absent  on  the  right  side.  The  left  kidney  became  affected  with  a 
hydatid  cyst,  and  post  mOrtem  it  was  found  that  the  glandular  substance 
not  invaded  by  the  cyst  had  increased  threefold  in  size. 

The  pathogenesis  of  hydatid  cysts  of  the  kidney  is  still  somewhat 
obscure.  Neisser  and  Boeckel  have,  nevertheless,  attempted  to  explain 
it  as  follows : 

The  eggs  of  the  tsenia  are  introduced  into  the  digestive  passages  by  the  food.  When 
they  reach  the  intestine,  they  may  follow  various  routes.  They  may  be  transported  to 
the  hver  by  the  portal  vein,  which  explains  the  presence  of  cysts  in  the  Uver.  They 
may  be  transported  to  the  mesentery  by  the  lymphatics  (cysts  of  the  mesentery).  They 
continue  their  wanderings  through  the  lymphatic  networks,  and  give  rise  to  cysts  of  the 
peritoneum  and  of  the  pleura.  They  follow  the  track  of  the  l3Tnphatic  vessels  as  far  as 
the  thoracic  canal,  which  empties  them  into  the  venous  system  and  the  right  side  of 
the  heart.     Thence  they  penetrate  into  the  limgs  (hydatid  cysts  of  the  Imigs).     They 


DT8EASES  OF  TFIK  KIDNKYS  1185 

may  oonlinuo  tlioir  path  tliroiij^h  tliu  Iiui^^h,  nsiich  tho  loft  aido  of  the  heart,  and  be 
launoliod  into  tho  genoral  oiioulatiou  (hydatid  cysta  of  tho  brain,  muscloH,  Bpluon, 
aiid  kidneys). 

Symptoms.  -The  hydatid  cyst  of  the  kidney  develops  slowly,  until  it 
has  uc.([uii('.d  a  fair  size,  and  the  patioiit  only  feels  slight  pain  and  heaviness 
in  the  lumbar  region.  Sometimes,  however,  haimaturia  appears  early  in 
the  liistory  of  the  case,  resembhng  the  haemoptysis  that  is  so  frequent  at 
any  early  stage  in  hydatid  cyst  of  the  lung.  After  a  variable  time  a  tumour 
becomes  manifest.  If  the  tumour  is  formed  at  the  upper  pole  of  the  kidney, 
it  may  be  in  such  close  relation  with  the  hver  or  the  spleen  that  the  diagnosis 
becomes  very  difficult.  If  it  develops  at  the  lower  pole,  it  projects  into  the 
ihac  fossa.  The  cyst  may  suppurate,  as  described  under  Hydatids  of  the 
Liver,  and  the  pus  then  escapes  by  various  routes. 

Rupture  is  almost  always  preceded  by  suppuration  in  the  cyst. 
Perforation  is  commonly  preceded  by  pain,  rigors,  fever,  anorexia,  and 
prostration,  which  indicate  infection  of  the  hydatid  cyst. 

Perforation  usually  takes  place  into  the  pelvis  and  ureter.  It  may  be 
spontaneous  or  brought  on  by  trauma.  At  the  moment  of  perforation  the 
patient  experiences  a  sharp  pain,  a  sensation  of  tearing  in  the  lumbar 
region.  Liquid  debris  of  membranes  and  small  hydatid  vesicles  soon 
become  engaged  in  the  ureter,  and  give  rise  to  violent  pains  along  the 
ureter,  in  the  perineum,  in  the  penis,  and  in  the  buttock,  with  retraction  of 
the  testicle,  nausea,  and  vomiting.  Nothing  is  wanting.  If  the  foreign 
body  passes  into  the  bladder,  the  coUc  ceases.  Arrest  of  the  membranes  or 
the  vesicles  in  the  ureter  may  cause  hydronephrosis  or  pyonephrosis. 
Their  retention  in  the  bladder  may  cause  -pain  and  frequent  micturition. 
Their  arrest  in  the  urethra  may  cause  retention  of  urine,  and  necessitate 
catheterization.  If  after  rupture  the  contents  pass  freely  through  the 
urinary  tract,  the  patient  passes,  according  to  circumstances,  colourless  or 
turbid  purulent  hquid  (which  may  be  offensive),  blood-stained  fluid,  bits  of 
hydatids,  vesicles,  or  phosphatic  concretions.  Examination  of  the  liquid 
shows  hooklets  and  characteristic  stratified  membranes.  The  evacuation 
of  the  cyst  by  the  urinary  passages,  however,  may  not  take  place  at  one 
time.  The  same  troubles  wiU  be  repeated  each  time  a  fresh  discharge 
occurs.  The  fluid  "will  pass  readily.  Such  is  not  the  case  with  the  hydatids, 
the  shreds  of  the  cyst  wall,  and  the  debris,  rich  in  cholesterin  and  phos- 
phates, found  in  old  cysts.  We  must  also  remember  the  possible  infection 
of  the  urinary  passages. 

In  other  cases  the  hydatid  opens  into  the  small  intestine  or  the  colon. 
The  patient  has  acute  abdominal  pains,  and  passes  foul-smelhng  hquid, 
membranes,  and  at  times  many  hydatid  vesicles.  As  the  intestine  offers 
a  free  passage  to  the  hydatids,  recovery  generally  occurs. 


1186  TEXT-BOOK  OF  MEDICINE 

Rupture  of  tlie  cyst  into  the  bronchi  is  much  less  favourable.  The 
sjrmptoms  are  in  every  respect  similar  to  those  seen  when  a  hydatid  of  the 
hver  ruptures  into  the  bronchi.  The  cyst  has  been  known  to  open  through 
the  skin  of  the  lumbar  region.  The  perforation  is,  then,  preceded  by  the 
formation  of  an  abscess,  and  is  followed  by  a  fistula. 

The  diagnosis  is  a  matter  of  supposition.  A  feehng  of  heaviness  or  pain 
and  haematuria  appear,  and  later  a  tumour  is  felt.  This  tumour  varies  in 
size,  and  may  be  mobile  or  fixed.  It  tends  to  project  either  backwards, 
towards  the  lumbar  region,  or  forwards,  into  the  abdominal  cavity.  We 
must  decide  whether  it  is  a  floating  kidney,  a  hydronephrosis,  a  cyst  of  the 
spleen,  mesentery,  or  Hver,  an  ovarian  cyst,  or  a  hpoma  of  the  mesentery. 
The  records  of  cases  show  the  difficulties  in  diagnosis,  and  mistakes  have 
often  been  corrected  by  puncture,  operation,  or  post-mortem  examination. 

Hydatid  cyst  of  the  kidney,  though  grave,  is  infinitely  less  serious  than 

polycystic  degeneration,  because  the  latter  lesion  is  always  double  and  the 

former  is  almost  always  single.     Symptoms  of  Bright's  disease  and  death 

from  uraemia,  which  are  the  rule  in  polycystic  degeneration,  are,  therefore, 

not  met  with  in  hydatid  cyst.     Such  a  condition  might,  however,  arise  if 

by  chance  the  hydatid  cyst  is  bilateral,  and  if  the  lesion  so  afiects  both 

kidneys  as  to  cause  insufficient  depuration,  as  in  a  case  I  saw  with  Berger. 

A  woman  was  suffering  from  an  enormoiis  hydatid  cyst  of  the  left  kidney.  Profuse 
hsematuria  was  the  first  sign.  The  bleeding  recurred  on  several  occasions,  and  was 
accompanied  by  a  feeling  of  weight,  sharp  pain  radiating  in  various  directions,  and  the 
appearance  of  a  tumour.  The  tumour  was  at  first  thought  to  be  malignant.  After 
a  slow  course,  it  quickly  increased  to  an  enormous  size,  and  became  fluctuating.  Berger 
drew  off  by  puncture  a  large  quantity  of  clear,  non-albuminous  hydatid  Hquid.  As  the 
liquid  reformed,  two  more  punctures  were  made,  and  injections  of  subhmate  were  given, 
without  any  better  result.  As  the  tumour  occupied  the  left  flank  and  a  part  of  the  um- 
bilical region,  and  was  therefore  difficult  to  attack  by  the  lumbar  route,  the  abdomen 
was  opened.  The  descending  colon  was  in  front  of  the  tumoiu-,  which  was  clearly 
retroperitoneal,  and  on  incision  contained  a  large  number  of  hydatid  vesicles,  but  no 
pus.  The  lining  membrane  was  removed  piecemeal,  and  recovery  was  complete  at  the 
end  of  two  months.  A  httle  later  I  noticed  symptoms  of  Brightism,  with  albuminuria, 
cardiac  hypertrophy,  and  a  hruit  de  galop.  I  should  say  that  albuminuria  had  been 
present  from  the  first.  In  any  case,  it  was  evident  that  the  opposite  kidney,  which  had 
apparently  been  healthy,  was  now  invaded  either  by  the  hydatid  or  by  concomitant 
nephritis.     Uraemia  set  in,  and  the  patient  died  in  convulsions. 

The  only  treatment  in  hydatid  cyst  of  the  kidney  is  surgical  interven- 
tion. Simple  aspiratory  puncture  without  injection  may  be  enough,  but 
in  the  case  of  failure  an  operation  must  be  performed. 

XIII.  CANCER  OF  THE  KIDNEY. 

Pathological  Anatomy. — Cancer  of  the  kidney  may  be  primary  or 
secondary.  The  secondary  form  is  consequent  on  cancer  of  the  testicle, 
uterus,  or  stomach,  and  is  made  up  of  nodules,  which  are  usually  situated 
in  the  cortex,  and  are  of  the  same  nature  as  the  primary  growth. 


DISEASES  OK    I'll  10   KIDNEYS  1187 

The  primary  form  is  almost  always  unilateral,  and  it  does  not  spare 
youth,  with  the  exception,  well  understood,  of  cases  of  sarcoma,  which 
arc  peculiar  to  childhood.  The  growth  may  be  encephaloid,  scirrhous, 
colloid,  or  melanotic,  but  the  encephaloid  form  is  the  most  common. 
"  Whether  the  cancer  of  the  kidney  is  soft  (encephaloid  cancer),  of  an  elastic 
consistency  (adenoma),  or  fairly  firm  (scirrhous  variety),  it  is  always  formed 
of  epithelial  tissue  ;  and  we  have  never  met  with  a  cancer  of  the  kidney 
which  was  not  a  well-marked  epithelioma  "  (Brault). 

The  kidney  generally  preserves  its  shape.  Its  weight  varies  from  2  to 
20  pounds.  Nodules  covered  with  vessels  are  often  seen.  On  section,  the 
consistency  of  the  organ  varies.  The  newly-formed  portions  often  have 
an  adenomatous  appearance.  The  furrows  which  separate  them  from  the 
healthy  portions  are  almost  always  festooned  (Brault).  Compensatory 
hypertrophy  has  been  noted  by  Albarran.  The  cancer  sometimes  forms  a 
mass,  encysted,  as  it  were,  in  the  distended  capsule,  and  no  trace  of  the 
pelvis  or  the  orifice  of  the  obUterated  ureter  can  be  found.  Cancerous 
vegetations  which  have  perforated  the  mucosa,  frequently  project  into  the 
pehis. 

The  growth  often  commences  in  the  upper  pole  of  the  kidney,  first 
attacking  the  cortex  and  then  spreading  into  the  medulla.  The  tumour  is 
diffuse,  or  is  composed  of  nodules,  and  the  tissue  between  them  undergoes 
fibrous  thickening.  The  capsule  of  the  kidney  may  resist  the  onset  of  the 
growth  for  some  time.  Secondary  infection  occurs  late,  as  a  rule,  and, 
therefore,  the  patient  in  some  cases  may  survive  five  or  six  years.  In  the 
statistics  compiled  by  Roberts  secondary  growths  occurred  in  thirty-one 
of  his  fifty-one  cases.  In  Ebstein's  statistics  they  were  found  in  almost 
half  the  number  of  cases. 

The  ureter  is  often  obhterated,  and  converted  into  a  rigid  mass  by  the 
growth.  The  hilum  of  the  kidney  is  often  invaded  by  the  cancer.  The 
glands  are  large  and  adherent,  and  the  arteries  resist  for  a  long  time,  but 
the  veins  of  the  hilum  are  sometimes  perforated  by  cancerous  nodules. 
A  nodule  has  been  found  to  start  in  the  renal  vein,  and,  then,  to  assume  such 
dimensions  that  it  penetrated  the  inferior  vena  cava,  and  reached  up  into 
the  right  auricle,  which  it  partly  filled  (Brault).  The  vessels  of  the  hilum, 
if  not  invaded,  may  be  compressed  by  the  cancerous  mass.  This  compres- 
sion may  give  rise  to  thrombi,  which  form  in  the  renal  vein,  and  reach  into 
the  inferior  vena  cava  and  right  auricle,  thus  causing  oedema  of  the  leaver 
hmbs  and  of  the  lower  half  of  the  trunk. 

The  growth  may  spread  by  contiguity  or  by  infection  through  the  veins 
and  lymphatics.  The  fibrous  capsule  offers  such  resistance  that  propa- 
gation by  contiguity  is  relatively  rare.  When  the  infection  takes  place 
through  the  bloodvessels  and  lymphatics,  it  affects  the  luiigs,  the  hver,  the 


1188  TEXT-BOOK  OF  MEDICINE 

lumbar  and  mesenteric  glands,  and  the  suprarenal  capsule.  The  vertebrae 
are  also  invaded  by  the  cancer.  If  cancer  of  the  kidney  rarely  invades  the 
genito-urinary  organs,  it  is  on  account  of  the  direction  of  the  lymph  flow. 
For  a  similar  reason  cancer  of  the  genito-urinary  organs  very  often  invades 
the  kidney  (Guillet).  The  heart  is  often  dilated  and  hypertrophied — a  fact 
which,  by  the  way,  is  seen  in  the  various  tumours  of  the  abdomen. 

Deseription.— Pain,  hsematuria,  the  development  of  an  abdominal 
tumour,  and,  symptomatic  varicocele  are  the  general  symptoms  of  renal 
carcinoma.  The  iirst  point  to  remember,  however,  is  that  cancer  of  the 
kidney  may  be  absolutely  latent. 

Renal  Cancer  of  the  Latent  Type. — The  kidney  at  times  shows  such 
great  toleration  that  Rayer  gave  a  special  description  of  "  latent  cancer." 
Secondary  cancer  is  no  doubt  more  often  latent  than  primary  cancer,  but 
still  latency  may  occur  in  both  cases.  Tuffier  gives  a  clear  account  of  latent 
primary  cancer : 

A  patient,  over  fifty  years  of  age,  gradually  lost  his  strength,  and  became  of  a  pale 
yeUow  colour,  although  no  viscus  appeared  to  be  diseased.  The  urine  showed  a  very 
sUght  trace  of  albumin  at  times.  The  weakness  became  extreme,  and  the  anorexia  was 
complete.  Signs  of  compression  appeared,  affecting  the  pleurge,  the  lungs,  and  the  medi- 
astinal organs,  and  the  patient  succumbed.  The  post-mortem  examination  showed  a 
primary  cancer  of  the  kidney,  which  had  destroyed  the  entire  organ,  and  had  given 
rise  to  cancerous  nodules  in  other  organs. 

Secondary  cancer  of  the  kidney  is  frequently  quite  latent.  Tuffier 
reports  the  following  case  : 

A  labourer,  twenty-six  years  of  age,  was  admitted  to  hospital  for  a  tumour  in  the 
right  ihac  fossa.  The  patient  had  been  gro^wdng  weak  for  the  past  three  months,  when 
a  painless  tumour  was  discovered  by  accident  in  the  right  flank.  He  continued  his  work, 
when  he  was  taken  iU  with  pain  and  symptoms  of  phlebitis  in  the  right  leg.  On  examin- 
ing the  patient,  a  tumour  was  found  filling  the  right  hypochondrium,  reaching  up  as  far 
as  the  umbihcus,  and  descending  into  the  ihac  fossa  as  far  as  Poupart's  Hgament.  The 
tumour  was  hard,  nodular,  adherent  to  the  deep  parts,  duU  on  percussion,  and  absolutely 
painless.  The  only  symptom  was  increasing  weakness.  He  died  without  having  shown 
any  renal  symptoms.  Post-mortem  :  primary  cancer  of  the  right  suprarenal  capsule, 
and  in  the  enlarged  right  kidney  seven  to  eight  hard  or  soft  cancerous  tumours,  which 
had  destroyed  almost  all  the  glandular  substance  of  the  kidney. 

Renal  Cancer  of  the  Painful  Type. — Cancer  of  the  Iddney  causes  pain, 
which  may  be  due  to  adhesions,  displacement  of  the  enlarged  organ,  or  com- 
pression of  the  neighbouring  nerves.  These  pains  are  more  or  less  severe, 
and  generally  paroxysmal.  They  may  be  felt  in  the  lumbar  region  or  the 
hypochondria,  and  may  radiate  towards  the  intercostal  spaces,  hke  inter- 
costal neuralgia.  The  pains  sometimes  precede  or  accompany  the  hsema- 
turia,  and  the  clots  in  their  migration  through  the  ureter  often  provoke 
renal  cohc. 

These  varieties  of  pain  in  renal  cancer  are  classical.     There  are,  however, 


DISEASES  OF  THE  KIDNEYS  1180 

cases  in  \vlii<li  |i;iiii  becomes  the  chief  syniptora  of  roiuil  itaiirer,  tlie  other 
symptoms  being  of  minor  importance.     To  ([uote  an  exiimple  : 

A  man,iigo(l  forty,  was  iwliiiittcd  luulor  IJrault  forKovero  piiins  in  tlio  hyixxlioiKiriiiiu, 
tlu!  fliuik,  and  tlio  right  sidiv  Thi'so  pains  woro  oontinuous,  and  radiated  into  tho  opi- 
gastrium,  the  buttock,  and  tlio  testicle,  rosombUng  tho  lightning-like  pains  of  tab«>s. 
Walking,  palpation,  and  iiressiue,  brought  on  pain,  which  was  so  a'ule  that  tho  patient 
was  doubled  up  in  agony.  Careful  examination  of  the  organs  reveal<;d  neither  Hli)Uiain 
nor  an  abdominal  tumour.  Fever,  however,  appeared.  The  situation  grew  worse  ; 
tho  patient  became  thin,  the  pain  was  most  intense,  and  the  patient  finally  succumbed. 
The  post-mortem  examination  revealed  cancer  of  the  right  kidney.  Tho  kidney  was 
normal  in  size.  It  was  adherent  to  the  vertebral  column,  against  which  it  was  flat- 
tened by  tho  growth  in  tho  peritoneal  tissue  ;  a  prolongation  of  tho  growth  sheathed  the 
aorta  and  vena  cava,  and  penetrated  tho  psoas.  The  pressure  on  the  lumbar  and  sacral 
nerves  by  the  perirenal  tumour  explained  the  persistence,  violence,  and  radiation  of 
the  pains. 

This  case  supports  the  idea  put  forth  by  Roberts  that,  as  far  as  renal 
lesions  are  concerned,  sharp  and  continuous  pain  in  the  area  supplied  by  a 
given  nerve  indicates  that  the  tumour  extends  beyond  the  normal  Umits 
of  the  kidney.  The.se  obstinate  cases  of  neuralgia  may  depend  upon  attacks 
of  congestion,  which  for  a  time  increase  the  size  of  the  kidney,  and  thus 
assist  in  the  compression  of  the  nerve  trunks.  In  one  of  Tuffier's  patients  the 
pains  became  terrible  \vithin  the  sphere  of  the  crural  nerve  just  before  an 
attack  of  hsematuria,  and  grew  better  as  soon  as  there  was  free  flow  of 
blood — that  is  to  say,  as  soon  as  the  congestion  ceased. 

Renal  Cancer  of  the  Hsematuric  Type. — Cancer  stands  first  among  the 
lesions  of  the  kidney,  accompanied  by  bleeding.  Hsematuria  is  frequently 
met  with.  It  sometimes  appears  suddenly  at  the  onset  of  the  affection 
in  subjects  who  are  in  good  health ;  at  other  times  it  appears  only  at  an 
advanced  stage.  It  lasts  for  a  few  days  or  weeks,  and,  then,  disappears 
completely  for  one  or  two  months.  It  may  or  may  not  reappear.  The 
colour  of  the  urine  varies  from  pale  red  to  black,  according  to  the  amount 
of  the  hgemorrhage.  Clots  which  are  moulded  in  the  ureter  may  be  present. 
They  are  very  thin,  and  measure  5  or  6  inches  in  length.  Such  clots  are 
never  seen  in  vesical  hsemorrhage  The  passage  of  the  clots  through  the 
ureter  sometimes  causes  pain  like  that  of  renal  coUc,  and,  on  the  other 
hand,  in  obstruction  of  the  ureter  by  a  clot  the  urine  may  be  quite  clear, 
because  the  bladder  only  receives  urine  from  the  healthy  kidney.  Obstruc- 
tion of  the  urethra  by  a  clot  may  cause  retention  of  urine,  caUing  for  the  use 
of  the  catheter. 

The  hsematuria  sometimes  is  so  profuse  that  it  becomes  the  chief  symp- 
tom.    As  an  example  : 

A  man  of  about  fifty  years  of  age,  who  had  alwavs  been  in  excellent  health,  had 
been  taken  ill  three  years  previously  (without  cause,  warning,  or  pain),  with  such  profuse 
haematuria  that  the  liquid  voided  filled  half  a  chamber  with  blood.     Next  day  there 

n.  76 


1190  TEXT-BOOK  OF  MEDICINE 

was  retention  of  urine,  which  yielded  on  the  passage  of  a  catheter ;  long  clots  were 
passed  for  several  days  following.  For  six  months  the  patient  was  quite  well,  and  then, 
without  the  least  warning,  he  passed  blood  and  clots  for  several  days.  Nothing  hap- 
pened for  eight  months,  and  then  the  same  trouble  occurred  :  passage  of  blood  and  clots, 
pain,  and  retention  of  urine.  Since  that  time  the  hsematuria  appeared  for  several  days 
every  month.  Hsematuria  had  been  so  far  the  only  sign.  Two  years  after  the  first 
attack  of  hsematuria  the  physicians  in  St.  Petersburg  discovered  a  tumour  of  the  right 
kidney,  which  was  confirmed  ia  Vienna  and  in  Paris.  Guyon  diagnosed  cancer  of  the 
right  kidney ;  fresh  attacks  of  hsematuria  appeared.  The  tumour  was  now  as  large 
as  a  foetal  head,  and  occupied  the  right  flank.  Above,  it  reached  up  to  the  false  ribs  ; 
below,  it  descended  to  within  an  inch  or  two  of  the  ihac  crest.  The  tumour  was  movable 
in  all  directions,  and  absolutely  painless  on  palpation.  Hsematuria  remained  the  chief 
symptom  of  this  renal  cancer.  The  fragments  of  cancer  and  the  cells  which  are  so  fre- 
quently met  with  in  the  urine  when  cancer  of  the  bladder  is  present  are  not  found  in 
cancer  of  the  kidney.  The  appearance  of  a  varicocele  is  a  fairly  frequent  symptom 
(Guyon).  It  is  especially  apparent  during  walking  or  standing.  Its  development  is 
rapid  and  is  sometimes  imknown  to  patients. 

Tumour. — The  development  of  a  tumour,  thougli  a  fairly  late  symptom, 
is  rarely  wanting.  The  tumour  is  at  first  deeply  seated  in  the  flank,  and  is 
not  easily  made  out.  It  may,  however,  be  discovered  on  bimanual  palpa- 
tion. One  hand  is  placed  behind,  in  the  costo-vertebral  angle,  and  the 
other  hand  is  placed  in  front,  on  a  level  with  the  rectus  muscle.  The 
examiner  gives  repeated  pushes  to  the  lumbar  wall  with  the  posterior 
hand,  and  the  kidney  transmits  a  feehng  of  ballottement  to  the  other  hand. 
When  the  tumour  is  somewhat  larger,  it  has  a  tendency  to  leave  the  lumbar 
region,  and  project  in  a  forward  direction.  In  this  case  the  posterior  hand 
pushes  the  tumour  against  the  anterior  hand.  The  tumour  is,  then,  felt  to 
move  with  difl&culty.  When  the  tumour  grows  very  large,  it  fills  the  ihac 
fossa,  crosses  the  median  hne,  and  invades  the  other  side  of  the  belly. 

The  cancerous  tumour  has  a  "  renal "  shape.  It  is  hard  and  resistant. 
It  pushes  the  intestine  forwards,  and  a  resonant  note  is,  therefore,  obtained 
over  its  anterior  surface.  Sometimes  the  resonance  is  replaced  by  dullness 
when  the  caecum  and  the  colon  remain  internal  to  the  kidney,  and  the 
tumour  comes  in  direct  contact  with  the  abdominal  wall,  after  having 
pushed  aside  the  resonant  intestine  (Tuffier). 

Diagnosis.— The  signs  just  enumerated  wiU  help  us  to  diagnose  a  renal 
cancer.  Nevertheless,  in  many  cases  we  meet  with  great  difficulties.  On 
what  symptom  can  we  rely  ?  Take  hsematuria,  for  instance.  If  it  appears 
before  a  tumour  is  present,  it  tells  us  nothing,  because  the  haemorrhage 
caused  bv  calcuh,  tuberculosis,  etc.,  may  simulate  the  early  haemorrhage  of 
renal  cancer.  If  it  appears  when  a  tumour  has  formed,  it  also  tells  us 
nothing,  for  the  kidney  may  be  enlarged  by  tuberculosis,  calcuh,  or  cysts, 
and  hsematuria  may  occur  in  these  conditions,  just  as  in  cancer.  These 
remarks  hold  good  in  the  case  of  the  pain  and  tumour.  It  is  sometimes 
difficult  to  know  whether  the  tumour  is  or  is  not  renal.     The  diagnosis  from 


DISKASKS  OF  THK  KIDNKYS  U'Jl 

sarcomatous  and  futty  sub]>critoneal  tumours  is  so  dilliuult  that  in  several 
cases  the  error  has  only  been  discovered  at  the  operation.  Although 
tumours  of  the  ovary  and  uterus  are  readily  distinguished  from  tumours  of 
the  kidney,  mistakes  have  been  made,  and  Billroth  wrongly  took  myxo- 
sarcoma of  the  kidney  for  fibroma  of  the  uterus.  It  is  also  hard  to  dis- 
tinguish cancer  of  the  kidney  from  tumours  of  the  spleen.  In  the  latter 
case  we  do  not  find  the  resonance  of  the  colon.  Examination  of  the  urine 
is  important  in  diagnosis,  and  in  the  absence  of  marked  hematuria,  we 
can  generally  find  histological  haematuria.  The  microscope  reveals  red 
corpuscles  in  the  centrifugalized  urea,  and  the  ingenious  segregator  of  Luys 
allows  us  to  collect  the  urine  from  each  kidney.  By  comparison  of  the 
urines  we  can  ascertain  the  side  of  the  lesion. 

Amongst  the  complications  of  renal  cancer  I  may  mention  compression 
of  the  portal  vein  (ascites),  of  the  inferior  vena  cava  (oedema  of  the  legs),  and 
of  the  common  bile-duct  (icterus),  lesions  of  the  spine  and  compression  of 
the  spinal  cord  (paraplegia),  pulmonary  embolism,  intestinal  occlusion, 
peritonitis,  and  pulmonary  tuberculosis.  Cancer  and  calculi  often  occur 
together,  just  as  in  cancer  of  the  gall-bladder,  we  frequently  find  gall- 
stones. A  new  growth  in  the  pelvis  may  lead  to  infection  of  the  kidney, 
by  causing  retention  of  urine. 

Cancer  of  the  kidney  develops  very  slowly,  and  has  the  least  tendency 
to  become  general  of  the  visceral  cancers.  Its  average  duration  is  from 
two  to  three  years,  and  may  even  extend  to  five  or  six  years.  Death  is 
caused  by  cachexia  or  by  one  of  the  compHcations  already  enumerated. 
The  treatment  consists  in  removal  of  the  kidney. 


XIV.  RENAL  CALCULI. 

Precipitation  of  the  salts  in  the  urine  leads  to  concretions  in  the  kidneys, 
which  are  termed,  according  to  size,  "infarcts,"  "gravel,"  or  "  calcuh."  The 
infarct  is  an  intracanalicular  deposit,  more  frequent  in  the  meduUa  than 
in  the  cortex.  It  is  calcareous  or  uratic,  and  is  chiefly  seen  in  new-born 
children  and  in  gouty  subjects. 

Gravel  and  calculi  very  rarely  exist  in  the  actual  substance  of  the  kidney. 
It  is  in  the  caHces  and  the  pelvis  that  they  are  found.  They  may  be  of  all 
sizes,  from  sand  to  stones  as  big  as  a  hen's  egg.  They  are  situated  in  the 
depressions  around  the  papillae,  the  calices,  the  pelvis,  in  which  tiiey  mould 
themselves,  and  even  in  the  ureters.  The  small  gravel  is  rounded,  poly- 
hedral, irregular,  raspberry-shaped,  or  faceted.  The  large  stone  is  mammil- 
lated,  of  an  hour-glass  shape,  angular,  or  branched  like  coral,  taking  the 
shape  of  the  cahces  and  of  the  pelvis.     The  large  stone  may  be  single,  but 

76—2 


1192  TEXT-BOOK  OF  MEDICINE 

more  frequently  it  is  accompanied  by  one  or  more  pieces  of  gravel.     In 
about  half  the  number  of  cases  only  one  kidney  is  affected. 

Pathogenesis. — It  is  usual  to  describe  secondary  and  primary  lithiasis. 
TJie  former  variety  supervenes  during  the  course  of  a  suppurative  lesion  of 
the  kidney.  Pyelonephritis  may  occur  in  renal  tuberculosis,  polycystic 
degeneration  of  the  kidney,  or  in  ascending  infection,  and  the  suppuration 
and  fermentation  in  the  urine,  then,  furnish  most  favourable  soil  for  the 
development  of  secondary  calcuH.  The  phosphates  impregnate  the  necrosed 
matter,  the  organic  waste  products  become  calcified,  and  a  phosphatic  con- 
cretion forms.  Litten  has  produced  these  calcuH  experimentally  by  inter- 
rupting the  circulation  in  the  kidney  of  a  dog.  The  epithehum  began  to 
calcify,  and  the  canahcuh  were  filled  with  calcareous  salts.  Secondary 
calcuH  are  almost  always  formed  of  ammonio-magnesium  carbonates  and 
phosphates.  They  are  greyish,  chalky,  and  friable.  Their  presence  ex- 
plains the  renal  cohc  sometimes  seen  in  people  suffering  from  suppurative 
lesions  of  the  kidney. 

The  primary  calculi  are  of  a  different  composition  and  origin,  being  com- 
posed of  urates  and  oxalates.  They  may  be  small  or  large,  and  are  hard  and 
resistant.  The  small  stones  are  rounded,  smooth,  and  brownish.  They  are 
mulberry-shaped  and  reddish  if  oxalic  acid  predominates.  The  large  stones 
are  branched  Uke  coral  or  moulded  in  the  shape  of  the  renal  pelvis.  Uric 
and  oxaKc  gravels  may  occur  together,  the  oxahc  acid  being  derived  from 
the  uric  acid  by  more  complete  oxidation.  The  uric  acid  gravel  is  favoured 
by  generous  Hving,  want  of  exercise,  and  inactivity  of  the  skin — ^in  a  word, 
by  circumstances  capable  of  increasing  the  quantity  of  uric  acid.  It  is 
likewise  favoured  by  all  causes  which  lead  to  imperfect  metabohsm  and 
diminished  solubihty  of  the  uric  acid  (Bouchard).  While  this  theory  is 
true,  in  practice  we  meet  people  Kving  under  the  best  hygienic  conditions 
who  suffer  from  gravel  and  renal  cohc. 

In  most  cases  the  dominant  factor  in  primary  hthiasis  is  the  gouty 
diathesis.  This  side  of  the  question  has  been  clearly  put  by  Trousseau. 
Renal  gravel  may  be  transmitted  directly,  and  a  father  suffering  from  gravel 
may  beget  children  who  suffer  from  gravel ;  but  the  factor  which  is  especially 
transmitted  is  the  special  predisposition  that  reveals  itself  in  the  descendants 
by  various  manifestations — gout,  asthma,  migraine,  obesity,  eczema,  gall- 
stones, and  intestinal  hthiasis,  and  I  would  add  appendicular  hthiasis. 

An  individual  who  during  his  youth  has  suffered  from  migraine,  haemor- 
rhoids, or  eczema,  may  later  be  troubled  with  gout,  asthma,  and  renal 
cohc.  Renal  hthiasis  is  often  related  to  the  gouty  diathesis.  "  I  have 
nephritis  and  you  have  the  gout,"  Erasmus  wrote  to  one  of  his  friends.  "  We 
have  married  two  sisters."  Gout  and  gravel  commonly  occur  in  the  same 
subject.     Renal  hthiasis  is  common  in  children. 


DISEASES  OF  THE  KIDNEYS  110:; 

Tlip  {)uerperal  state  favours  the  formation  of  calculi,  ami  I  have  quoted 
sevoral  cases  in  a  clinical  lecture  on  the  relation  of  ])r('<^niincy  and  lithiasis.* 
Renal  colic  may  supervene  during  pregnancy  or  after  accouchement.  At 
first  sight  it  simulates  the  onset  of  labour  or  peritonitis.  A  careful  study 
of  the  case  will  clear  up  the  diagnosis.  However  violent  the  pains  of  renal 
cohc  may  be,  the  prognosis  is  good,  and  the  woman  goes  to  full  term  without 
accident. 

The  greater  frequency  of  gravel  in  certain  countries  (England,  Holland) 
and  in  certain  localities  has  given  rise  to  the  view  that  local  conditions 
(drinking-water,  nature  of  the  soil)  play  some  part  in  the  pathogenesis. 

We  cannot  absolutely  separate  secondary  or  phosphatic  Uthiasis  from 
primary  or  uric-acid  lithiasis.  Many  calculi  are  both  phosphatic  and 
oxahc.  Arthritic  patients  suffering  from  so-called  primary  hthiasis  and 
renal  coHc  pass  phosphatic  and  uratic  calculi,  and  examples  are  not  wanting 
of  secondary  lithiasis  characterized  by  oxalic  and  phosphatic  stones.  Speak- 
ing generally,  in  this,  as  in  every  other  kind  of  lithiasis,  the  genesis  of  the 
calcuU  does  not  consist  only  in  a  deposit  and  an  agglomeration  of  mineral 
substances.  Two  elements  in  variable  proportions — the  one  organic  and 
the  other  inorganic — are  always  required.  In  renal  calcuU  the  organic 
substance  is  formed  of  albuminoid  matter — peptone,  mucus,  epithehal 
cells,  and  perhaps  micro-organisms.  Traces  of  aU  of  these  are  found  in 
the  nucleus  or  in  the  reticulum  of  the  calculus.  The  inorganic  element  has 
been  described  under  the  different  varieties  of  Uratic,  OxaUc,  and  Phos- 
phatic CalcuU. 

I  have  just  given  an  idea  of  lithiasis  of  the  kidneys  and  of  the  mode  of 
formation  of  the  calculi.  The  kidneys  may  tolerate  for  a  long  time  the 
presence  of  one  or  more  calcuh,  but  for  multiple  reasons,  which  I  shall 
enumerate,  certain  troubles  may  appear.     They  are  as  foUows  ; 

1.  Mobile  calculi— renal  colic. 

2.  Fixed  calculi — pain  and  haematuria. 

3.  Calculous  anuria — uraemia. 

4.  Calculous  pyelonephritis. 
6.  Calculous  perinephritis. 

6.  Calculous  fistulse. 

7.  Fibrosis  and  renal  atrophy. 

1.  Renal  Colic— Mobile  Calculi. 

Description. — Gravel  which  is  too  large  or  too  anfractuous  to  pass  freely 
through  the  ureter  may  cause  the  syndrome  of  renal  cohc.  The  attack 
may  come  on  suddenly,  without  prodromata,  or  it  may  be  preceded  by  a 

*  Clinique  Medicale  de  rHCid-DieM,  1898,  15°"  le§ou. 


1194  TEXT-BOOK  OF  MEDICINE 

prodromal  period  of  a  few  hours  or  a  few  days,  well  known  to  persons  who 
have  already  had  renal  cohc.  This  period  is  characterized  by  the  following 
symptoms  :  Dull  or  acute  pains,  simulating  lumbago  ;  a  feeling  of  weight 
in  the  kidneys  or  the  anus  ;  painful  swelling  of  the  testicle ;  burning  at  the 
tip  of  the  penis ;  frequent  desire  to  make  water ;  discharge  of  sand  and 
blood-stained  urine  ;  and  abdominal  tympanites.  In  some  cases  renal  cohc 
comes  on  during  violent  exercise,  or  after  the  use  of  diuretic  water  in  the 
course  of  a  cure. 

The  attack  commences  with  sharp  pain  on  one  side  in  the  lumbar  region. 
After  some  time  the  pain  becomes  more  severe,  and  spreads  to  the  flank. 
Marked  retraction  of  the  testicle  is  seen^from  the  first.  The  pain  is  of  a 
stabbing  character,  and  radiates  along  the  ureter  to  the  penis,  the  urethra, 
the  glands,  the  perineum,  the  rectum,  and  the  buttocks.  The  patient 
suffers  the  greatest  agony,  and  tries  by  every  possible  means  to  lessen  the 
pain,  •  The  pulse  is  small ;  the  face  is  pale  and  covered  with  sweat ;  the 
extremities  are  cold.  Nausea  and  vomiting  are  frequent,  and  the  patient, 
after  much  straining,  passes  a  few  drops  of  urine.  Fever  is  generally 
absent. 

The  attack  may  last  for  six  or  eight  hours,  or  longer,  without  inter- 
mission. The  end  of  the  attack  is  often  announced  by  a  violent  paroxysm, 
with  or  without  vomiting,  and  when  the  gravel,  after  its  difficult  passage 
through  the  ureter,  enters  the  bladder,  all  the  symptoms  at  once  cease,  and 
the  patient  experiences  an  unspeakable  feehng  of  rehef,  often  falUng  asleep. 
After  the  attack,  the  patient  passes  either  abundant  clear  urine  or  dull, 
brownish  urine.  The  lumbar  region  remains  painful.  Shght  hsematuria 
may  persist  for  several  days.  The  patient  often  passes  not  only  gravel,  but 
also  coarse  sand,  blood,  and  thin  fibrinous  clots,  which  may  be  coloured  or 
colourless,  and  which  float  in  the  urine  hke  worms. 

Gravel  is  not,  as  a  rule,  present  in  the  first  urine  discharged  after  the 
attack  of  cohc.  It  may  not  appear  for  a  day  or  two.  The  urine  must  be 
carefully  examined  in  a  specimen  glass,  and  when  we  see  the  fine  yellowish 
or  blackish  gravel,  no  larger  than  a  grain  of  rice,  we  may  well  ask  how  so 
small  a  body  can  cause  such  terrible  pain.  The  gravel  is  sometimes  large 
enough  to  obstruct  the  urethra  and  to  cause  retention  of  urine.  It  must, 
then,  be  removed.  In  a  patient  who  had  previously  suffered  from  nephritic 
cohc  I  noted  retention  of  urine  from  a  large  piece  of  gravel  which  was 
arrested  in  the  urethra,  preventing  the  flow  of  the  urine. 

In  some  cases  the  termination  of  the  attack  is  not  followed  by  the  com- 
plete rehef  already  mentioned,  and  the  pain  does  not  entirely  cease.  The 
kidneys  remain  sensitive.  The  desire  to  pass  water  is  frequent,  and  during 
the  same  day  or  the  next  one  fresh  attacks  occur,  so  that  the  cohc  may  last 
for  several  days.     One  of  my  patients,  who  was  gouty  and  subject  to  nephritis 


DISEASES  OF  TIIK   KIDNEYS  lior. 

had  an  attack  which  lasted  for  twenty  days,  and  ended  with  the  expulsion  of 
a  large  calculus. 

These  prolonged  attacks  of  renal  colic,  comprising  a  series  of  ten,  fifteen, 
or  twenty  successive  fits,  are,  fortunately,  very  rare.  In  one  of  my  gouty 
patients  renal  colic  lasted  three  weeks,  aiid  the  calculus  was  not  passed 
until  six  weeks  after  the  disappearance  of  the  acute  pain.  When  the  ex- 
pulsion of  the  calculus  occurs  as  late  as  this,  we  may  well  ask  whether  the 
patient  is  suffering  from  renal  colic  due  to  a  calculus  or  from  an  attack  of 
renal  gout,  without  a  migratory  stone.  We  may  also  ask  whether  the 
calculus  in  the  bladder  has  not  been  there  for  some  time,  forming  the  nucleus 
of  a  vesical  calculus.  In  the  case  just  mentioned,  the  pain  lasted  for  three 
weeks,  with  an  interval  of  relative  calm,  and  then  a  second  period  of  three 
weeks  supervened,  with  gouty  pains  in  the  limbs,  frequent  passage  of  uric 
acid,  abundant  night-sweats,  but  no  fever.  It  may  be  said  that  an  attack 
of  gout  and  an  attack  of  renal  coUc  were  combined. 

During  the  attack  of  coUc  the  patient  sometimes  experiences  throbbing 
pain  in  the  kidney,  in  the  flank,  or  along  the  ureter,  analogous  to  the  pain  of 
an  abscess  which  is  about  to  open.  Happily,  there  is  no  question  of  an 
abscess,  and  the  throbbing  ceases  with  the  termination  of  the  attack.  I  have 
noticed  this  important  symptom  in  several  patients.  Renal  colic  has  not 
always  the  severe  form  just  described.  It  may  be  defaced  or  reduced  to  an 
isolated  S}'mptom,  such  as  vomiting.  Some  patients  pass  fairly  large-sized 
gravel  without  any  pain.  About  twenty  years  ago  I  attended  a  patient 
who  was  suSering  from  calculous  pyehtis,  from  which  he  recovered.  He 
had  been  previously  operated  on  by  Sanson  for  stone  in  the  bladder,  and 
since  that  time  he  passed  calculi  almost  as  large  as  peas  without  the  shghtest 
cohc.     He  had  collected  a  bushel. 

Some  individuals  have  but  one  attack  of  renal  coUc  during  their  life, 
and  they  are  fortunate.  In  others  the  attacks  occur  every  year,  several 
times  a  year,  or  at  intervals  of  several  years.  A  consoling  feature  is  that  the 
first  attacks  of  colic  are  the  most  painful.  I  do  not  know  whether  this  is 
due  to  tolerance  or  to  a  greater  extensibihty  of  the  ureter,  but  it  is  certain 
that  a  patient  who  has  suffered  terribly  can  later  expel  gravel  of  the  same 
size  with  much  less  distress.  Renal  coHc  is  never  bilateral  at  first,  but  after 
attacks  of  coHc  caused  by  calculi  in  the  right  kidney  attacks  of  coUc  may  be 
caused  by  calcuh  in  the  left  kidney. 

Between  the  attacks  some  patients  experience  a  feehng  of  discomfort 
and  heaviness  in  the  lumbar  region,  and  complain  of  lumbago.  The  urine 
contains  coarse  reddish  sand.  In  other  patients,  without  warning,  the 
testicle  corresponding  to  the  affected  kidney  becomes  painful  and  swollen. 
Palpation  shows  that  the  testicle  is  painful,  hard,  and  swollen.  These 
symptoms  last  some  hours,  and  show  that  something  is  happening  in  the 


1196  TEXT-BOOK  OF  MEDICINE 

kidney.  It  does  not  always  mean  the  onset  of  renal  colic,  but  it  is  often 
the  signal  of  congestion  of  the  kidney ;  and  if  we  examine  the  urine,  we  find 
that  it  is  of  a  brownish  colour,  and  contains  a  blackish  deposit  of  blood  and 
uric  acid.  A  discharge  has  just  taken  place,  and,  then,  everything  becomes 
normal  for  the  time  being.  In  certain  gouty  persons  the  kidney 
is  nearly  always  in  trouble,  and  perhaps  the  above-mentioned  discharges  of 
uric  acid  and  blood  act  as  a  safety-valve.  In  any  case,  the  testicle  fairly 
often  gives  us  warning,  as  I  have  long  since  noticed. 

Renal  and  bihary  gravel  often  alternate  in  the  same  subject. 

Diagnosis. — Even  moderate  care  wiU  prevent  us  from  mistaking  renal 
cohc  for  hepatic  cohc,  appendicitis,  or  lumbago.  It  is  sometimes  very 
difl&cult.to  distinguish  renal  pseudo-colic  from  true  cohc  due  to  a  calculus. 
Let  me  explain. 

Maurice  Raynaud  has  shown  that  certain  sufierers  from  tabes  have  renal 
crises.  These  renal  crises  absolutely  resemble  in  symptoms  renal  cohc,  and 
careful  examination  for  the  other  signs  or  stigmata  of  tabes  is  necessary  for 
a  diagnosis.  Many  people  having  no  renal  calculus  may  nevertheless  have 
the  most  classical  symptoms  of  renal  cohc — viz.,  radiating  pains  in  the  loin, 
pain,  swelling  and  retraction  of  the  testicle,  vomiting,  ohguria  or  anuria 
sudden  onset  and  sudden  cessation  of  symptoms.  I  am  not  speaking  of 
attacks  of  cohc  due  to  the  passage  of  blood-clots  through  the  ureter  (cancer  of 
the  kidney),  but  I  have  in  view  certain  diseases  of  the  kidneys  in  which  the 
syndrome  of  renal  cohc  arises.  Such  are  tuberculosis  or  new  growths  of  the 
kidney,  polycystic  degeneration,  movable  kidney,  with  or  without  inter- 
mittent hydronephrosis  and  pyehtis.  Tuffier  has  carefully  described  these 
cases  of  pseudo-cohc,  showing  that  it  is  possible  to  suffer  from  severe  attacks 
of  renal  cohc  without  renal  hthiasis,  and  even  without  appreciable  lesions 
in  the  kidney  or  ureter.  He  groups  these  cases  into  two  categories,  according 
as  there  is  or  is  not  an  obstacle  to  the  passage  of  urine  through  the  ureter. 

The  first  category  includes  aU  lesions  capable  of  causing  sudden  and 
total  obstruction  of  the  ureter,  with  distension  of  the  pelvis.  Such  are 
pyelonephritis,  including  renal  tuberculosis  and  intermittent  hydro- 
nephrosis due  to  displaced  kidney,  kinking  of  the  ureter,  etc.  In  such  cases 
it  is  probable  that  the  sudden  obhteration  of  the  ureter  and  the  stretching 
of  the  pelvis  of  the  kidney  produce  the  sjrndrome  of  cohc. 

In  the  second  category  Tufiier  places  cases  of  pseudo-cohc  in  which  there 
is  no  sign  of  ureteral  obstruction.    He  quotes  an  absolutely  convincing  case  : 

A  young  woman  had  for  two  years  had  attacks  of  renal  colic,  without  haematuria 
or  discharge  of  gravel.  The  attacks  became  more  frequent,  and  the  paia  was  unbearable. 
She  was  looked  upon  as  a  neurasthenic  patient  suffering  from  neuralgia.  Under  chloro- 
form, the  kidney  was  felt  to  be  shghtly  displaced,  and  Tuffier  diagnosed  pseudo-cohc, 
probably  symptomatic  of  a  shghtly  m.ovable  right  kidney.  The  medical  means  employed 
(suggestion  included)  produced  no  effect.     Later,  as  the  pain  became  worse,  an  operation 


DISEASES  OF  THE  KIDNEYS  1197 

was  doiided  on.  The  kidney  was  found  to  Ikj  absolutely  healtliy,  without  any  adheflion«. 
Acupuncture  in  all  directions  failed  to  reveal  any  calculus.  The  kidney  was  fi.ved, 
and  complete  recovery  followed. 

The  pathogenesis  of  these  forms  may,  perhaps,  be  due  to  congestion  of 
the  kidney,  consequent  on  bending  of  the  renal  vein.  Experiments  seem 
to  prov-e  the  correctness  of  this  hypothesis. 

In  any  case,  the  foregoing  series  of  facts  proves  that  nothing  resembles 
renal  colic  due  to  calculus  more  than  the  attacks  of  pseudo-colic  that  have 
no  coimection  with  any  calculus.  When  an  individual  suffering  from  renal 
coUc  is  neither  arthritic  nor  of  gouty  stock,  so  that  we  fail  to  discover  any 
other  stigmata  of  the  gouty  diathesis ;  when  the  renal  coUc  is  never  accom- 
panied by  the  haematuria,  and  is  never  followed  by  the  discharge  of  gravel ; 
when  the  urine,  in  spite  of  diuretic  treatment,  never  contains  uric  acid,  it 
is  almost  certain  that  this  individual  has  only  pseudo-cohc. 

Prognosis. — The  serious  feature  is  not  the  cohc,  but  the  renal  Hthiasis, 
because  we  are  never  sure  of  our  ground  in  these  cases.  We  can  readily 
grasp  the  truth  of  this  statement  by  reading  of  the  mishaps  and  compUca- 
tions.  There  is,  however,  a  certain  inherent  gravity,  due  to  the  anuria, 
in  renal  colic  itself. 

Treatment. — The  first  object  is  to  lessen  the  pain.  Injections  of  morphia, 
syrup  of  chloral,  or  inhalations  of  chloroform,  are  used.  Tepid  baths  are 
of  service,  and  alkaUne  diuretic  drinks  (milk  with  Vichy  water)  should  be 
given.  Aspirin  gives  excellent  results.  At  the  time  of  the  attack  two  to  four 
cachets,  each  containing  7  grains,  may  be  given  daily,  and  it  is  well  to  use 
also  injections  of  morphia.  Between  the  attacks  the  treatment  is  that  of 
urinary  Hthiasis.  Diet  and  hygiene  fill  an  important  place.  Vegetables 
rich  in  oxaUc  acid  must  be  avoided  (sorrel  or  asparagus).  AlcohoHc  bever- 
ages, truffles,  and  game  must  be  forbidden.  Carbonate  of  Hthia,  in  doses 
of  10  to  20  grains  daily,  citarine  7  grains,  urotropine  15  grains,  should  be 
prescribed.  A  cure  at  Vittel  (Bouloumie),  at  Contrexeville,  Chatelguyon, 
d'Evian,  Vichy,  or  Carlsbad  is  of  benefit.  These  measures,  however,  are 
not  sufiicient.  In  urinary  litbiasis  I  place  the  greatest  reliance  upon  the 
following  prophylactic  treatment.  As  a  matter  of  fact,  a  cure  at  Vittel, 
Contrexeville  or  d'Evian  does  not  exceed  three  or  four  weeks  in  duration, 
and  is  therefore  far  from  fulfilling  all  the  therapeutic  conditions  required. 
In  many  patients  with  lithiasis,  whether  they  are  or  are  not  gouty,  sand 
continues  to  form  in  the  kidneys  ;  in  consequence  they  are  liable  to  fresh 
attacks  of  gravel.  I  would,  therefore,  insist  that  it  is  necessary  to  flush 
the  kidneys  continuously  for  a  whole  year  or  even  longer.  It  is,  of  course, 
not  necessary  to  drink  the  large  amounts  of  water  taken  at  Vichy  or  at 
d'Evian.  It  is  essential  that  the  patient  should  drink  a  bottle  and  a  half 
of  d'Evian  water,  taking  a  portion  in  the  early  morning,  and  a  portion 


1198  TEXT-BOOK  OF  MEDICINE 

during  the  rest  of  the  day ;  it  is  important  to  take  the  water  between 
meals.  I  usually  advise  the  patient  to  take  about  four  ounces  of  milk 
with  each  draught  of  water. 

At  first  the  stomach  may  exhibit  some  intolerance ;  in  this  event  the 
quantity  is  diminished,  and  tolerance  is  soon  established.  As  a  result 
of  this  simple  and  easy  method  of  treatment,  the  urine  rises  to  1800 
grammes  per  diem,  without  putting  any  strain  on  the  kidneys.  The  urine 
is  limpid.  At  times,  however,  small  quantities  of  sand  may  be  passed ; 
but  this  sand  has  neither  the  tendency  nor  the  time  to  collect  in  the  form 
of  gravel.  Moreover,  if  the  patient  is  inclined  to  be  gouty,  he  reaps  his 
reward  from  this  regime,  and  the  unpleasant  risks  of  gouty  nephritis 
diminish  in  proportion,  I  must  repeat,  however,  that  success  is  dependent 
on  prolonged  and  continuous  treatment. 


2.  Large  Fixed  Calculi— Pains— Haematuria. 

Renal  lithiasis  only  causes  colic  when  the  stones  are  sufficiently  small 
to  engage  in  the  ureter.  The  larger  stones  which  are  fixed  in  the  pelvis  may 
for  a  long  time  give  rise  to  no  symptoms.  Legueu  has  collected  several 
cases  proving  that  fixation  of  the  calculi  under  aseptic  conditions  is  favour- 
able to  renal  tolerance.  Do  we  not  find  patients  in  whom  anuria,  hydro- 
nephrosis, pyelitis,  and  perinephritic  abscess  are  the  first  indication  of  renal 
calculi  which  have  been  latent  for  years  ?  Clark  in  his  statistics  has  noted 
thirteen  cases  of  latent  calculi  in  twenty-four  cases  of  stone  in  the  kidneys. 
Legueu's  second  case  refers  to  a  patient  in  whom  several  renal  calculi  were 
present,  without  having  given  rise  to  haematuria  or  pain.  A  fix:ed  stone 
generally  gives  rise  to  two  chief  symptoms — pain  and  hsematuria. 

Pain. — A  patient  with  a  large  calculus  experiences  a  sensation  of  heavi- 
ness in  the  lumbar  region.  The  pain  is  increased  by  pressure,  palpation, 
or  percussion,  and  reappears  as  the  result  of  exercise.  The  pain  is  not,  as 
a  rule,  continuous,  and  there  is  sometimes  a  truce  lasting  for  weeks  or  months. 
In  some  cases  the  pain  lasts  without  cessation  for  years.  I  had  a  patient  in 
hospital  who  had  had  practically  continuous  pain  for  eleven  years.  Lentz 
speaks  of  a  young  man,  eighteen  years  of  age,  who  had  suffered  for  ten  years 
from  pain  in  the  left  renal  region  without  other  symptoms.  The  kidney 
was  resected  and  a  large  calculus  was  removed. 

The  pain  caused  by  a  fixed  calculus  is  generally  much  less  severe  than 
the  pain  of  renal  cohc.  It  may,  however,  be  very  acute,  and  as  it  radiates 
it  may  simulate  the  pain  of  renal  cohc.  Pain  is  not  hmited  to  cases  of  large 
calculi.  In  Le  Dentu's  case  small  fixed  gravel  in  the  kidneys  gave  rise  to 
acute  pains  that  rendered  an  operation  necessary.  In  Moty's  case,  quoted 
by  Legueu,  the  pain  was  almost  unbearable  for  ten  years,  and  yet  only 


DISEASES  OF  THE  KIDNEYS  1199 

one  small  coral-like  calculu.s  was  found  in  the  ulcerated  kidney.  The  in- 
tensity of  tlie  ]);uii  is  not,  thcu'efore,  always  in  proportion  to  tlie  number  or 
the  size  of  the  calcuh.  It  is  also  due  to  the  hyperaesthesia  of  thf;  kidney,  the 
renal  infection  appearing  to  make  the  kidney  less  tolerant. 

In  many  cases  the  pain  due  to  large  calculi  is  not  limited  to  the  lumbar 
region,  but  radiates  to  the  testicle,  and  simulates  renal  colic.  It  may  radiate 
towards  the  abdominal  wall,  in  the  form  of  lumbo-abdominal  neuralgia,  to 
the  opposite  kidney  (reno-renal  reflex),  or  to  the  bladder  (vesico-renal  reflex). 
The  pain  in  the  bladder  may,  indeed,  be  so  severe  that  the  diagnosis  of 
vesical,  and  not  of  renal,  calculus  may  be  made.  The  pain,  radiating  into 
the  right  ihac  fossa,  may  lead  to  a  diagnosis  of  appendicitis. 

Haematuria. — Hematuria  is  the  important  Symptom  of  calculus.  I 
have  already  spoken  of  the  sHght  bleeding  which  supervenes  at  the  onset 
of  renal  coHc,  and  after  or  between  the  crises.  In  such  a  case  haematuria 
forms,  so  to  say,  a  part  of  the  renal  coHc,  announcing  or  surviving  it.  In 
other  cases  haematuria  appears  as  an  isolated  symptom  of  calcuh  of  the 
Iddney,  but  here  again  it  supervenes  in  an  individual  who  has  previously 
had  renal  colic.  In  such  circumstances  the  pathogenic  diagnosis  is  clear, 
because  haematuria  is  evidently  due  to  the  calculi  fixed  in  the  kidney.  In 
other  cases  calculous  haematuria  supervenes  in  persons  who  have  never  had 
nephritic  colic,  and  the  pathogenic  diagnosis  is,  then,  more  difficult. 
Pousson's  case  proves  this  point : 

A  farmer,  thirty-four  years  of  age,  without  personal  or  hereditary  disease,  having 
never  had  renal  coUc  or  gravel,  complained  for  several  years  of  pain  in  the  region  of  the 
right  kidney.  These  pains  did  not  radiate  along  the  ureter  or  to  the  testicle  ;  they  dis- 
appeared when  the  patient  rested,  and  came  on  when  he  worked.  The  urine,  which 
was  limpid  when  the  patient  did  not  exert  himself,  became  bloody  in  consequence  of 
work.  These  attacks  of  hsematuria  weakened  the  patient,  and  had  none  of  the 
characteristics  of  vesical  hsematuria.  Palpation  of  both  kidneys  revealed  no  enlarge- 
ment, but  the  right  kidney  was  painful  on  pressure.  An  operation  was  performed. 
Exploratory  incision  of  the  kidney  revealed  a  rounded  calculus  of  the,  size  of  a  hazel- 
nut. The  patient  recovered  completely.  "  Since  that  time,"  says  Pousson,  "  I  have 
repeatedly  heard  that  he  has  had  no  more  haematuria." 

Sydenham,  who  was  gouty,  writes  thus  of  his  own  case  : 

A  Dissertation  on  the  Discharge  of  Blood  caused  by  a  Stone  in  the  Kidney. — 
In  the  year  1660  I  had  an  attack  of  gout  in  the  feet,  the  most  severe  and 
longest  attack  I  have  ever  had.  The  attack  terminated  in  a  dull  pain,  which  I  com- 
menced to  feel  in  the  left  kidney.  The  gout  disappeared,  but  the  pain  in  the  kidney 
remained.  It  increased  at  intervals,  but  was  by  no  means  unbearable,  because  I  never 
had  a  single  attack  of  renal  colic — a  disease  always  accompanied  by  vomiting  and  by 
acute  pain  along  the  ureter  towards  the  bladder.  I  was,  however,  quite  convinced 
that  I  had  in  the  pelvis  of  one  of  my  kidneys  a  stone  of  considerable  size,  which  did  not 
cause  symptoms  of  renal  colic,  because  it  was  too  large  to  pass  through  the  ureter. 
What  happened  at  the  end  of  several  years  proved  to. me  that  I  was  not  mistaken, 
because  during  the  winter  of  1666  after  a  long  walk  during  a  great  thaw,  I  passed 
urine  mixed  with  blood.     The  same  thing  happened  every  time  I  took  long  walks  or 


1200  TEXT-BOOK  OF  MEDICmE 

drove  in  a  carriage  over  a  paved  road,  but  it  did  not  hapjien  wlien  tlie  road  was  not 
paved.  Tlie  nrine  passed  was  alarming,  because  it  seemed  to  be  notliing  but  pui-e  blood, 
and  in  tlie  deposit  tke  blood  was  collected  in  clots  at  tbe  bottom  of  tbe  chamber. 

This  case  is  typical  of  lisematuria,  due  to  a  large  calculus,  and  it  is  marvel- 
lous to  see  with  what  accuracy  Sydenham  states  the  important  features  of 
the  case — the  remarks  on  the  association  of  gout  and  renal  hthiasis ;  the 
distinction  between  large  and  small  calcuh ;  the  calculus  being  unable  to 
pass  through  the  ureter,  and  not  producing  cohc  ;  hsematuria  brought  on  by 
the  jolting  of  the  carriage.  Nothing  is  wanting  in  this  description  that  is 
nearly  two  centuries  and  a  half  old.  In  my  lectures  at  the  Faculte  I  have 
given  the  name  of  "  Sydenham's  haematuria  "  to  haemorrhage  caused  by 
large  calcuh  in  the  kidney. 

In  conclusion,  large  calcuh  of  the  kidney  may  give  rise  to  no  symptoms. 
In  most  instances,  however,  they  provoke  pain  and  haematuria.  Pain  may 
exist  without  hsematuria,  but  hsematuria  is  always  preceded  or  accompanied 
by  pain.  The  pain  is  felt  chiefly  in  the  lumbar  region  ;  it  is  brought  on  by 
pressure,  and  is  made  worse  by  violent  exercise.  The  bleeding  rarely  occurs 
during  rest,  but  is  readily  brought  on  by  running,  strains,  or  riding. 

Radioscopy  is  of  service,  especially  in  the  diagnosis  of  large  calculi.  Ringel 
has  made  the  following  experiments  on  the  cadaver  :  Three  varieties  of 
calculi  were  placed  in  the  pelvis  of  the  kidney,  and  photographed  under 
identical  conditions.  The  result  showed  the  degree  of  permeability.  The 
oxalate  stone  gave  as  clear  an  image  as  a  bullet ;  the  image  of  the  uric-acid 
stone  was  not  so  clear ;  the  phosphatic  stone  gave  no  image.  Wagner  has 
employed  radiography  in  the  following  case  :  A  girl  was  sufiering  from  a  fistula 
in  the  left  lumbar  region.  The  X  rays  showed  four  calculi — one  large,  and 
three  as  big  as  split-peas.  Wagner  does  not  share  Ringel's  opinion  as  to  the 
permeability  of  calculi  to  the  X  rays  ;  he  considers  that  uric- acid  calculi  are 
very  permeable.  Leonhard  considers  that  the  phosphatic  calculi  are  most 
permeable  ;  next  come  the  uric-acid  stones,  and  last  the  oxalate  calculi. 
Hermann  and  Alsberg  report  cases  of  calculi  diagnosed  by  the  X  rays,  the 
diagnosis  being  verified  at  the  operation.  Lauenstein  diagnosed  a  calculus 
by  means  of  radioscopy ;  the  stone  was  composed  of  carbonate  of  lime. 
This  case  is  of  much  interest  because  this  variety  of  calculus  is  not  considered 
favourable  for  X-ray  diagnosis.  Beclere's  opinion  is  as  follows  :  In  radio- 
graphic examination  for  urinary  calculi,  success  is  the  rule,  failure  the 
exception.  Calculi  of  pure  acid  are  the  only  form  likely  to  escape  recog- 
nition. Every  stone  which  contains  phosphates  or  salts  of  calcium  in 
sufficient  quantity  can  be  made  out  by  radiography.  Such  is  the  case  in 
the  majority  of  urinary  calculi. 

The  treatment  of  large  renal  calculi  is  purely  surgical;  many  persons, 
after  suffering  for  several  years,  have  been  cured  by  operation.     There  is 


1)Isi-:asks  of  tiM';  kidnkys  1201 

uo  iiud'o  jiistilicatiun  tor  leaving;  a  stuiiu  in  the  kidiiuy  than  llicru  is  tor 
loaviug  one  in  the  bhuldur. 

3.  Calculous  Anuria. 

Description.-— Let  us  first  uonaider  caicidous  anuria,  which  supervenes 
during  an  attack  of  renal  colic. 

A  lady,  forty-tlireo  years  of  age,  had  for  some  years  suffered  from  attacks  of  renal 
colic  ;  in  evorv  attack  she  had  passcnl  gravel  and  bloody  urine.  In  the  last  attack  she 
had  been  suffering  for  two  daj's  from  acute  pain  in  the  left  loin.  The  pain  radiated 
to  tiio  thiglis  and  to  the  bladder,  and  was  increased  by  the  least  movement.  The  attack 
was  similar  to  the  preceding  ones,  except  that  she  had  passed  no  urine  for  two  days. 
On  the  third  day  she  passed  half  a  wineglassful  of  urine  ;  on  the  fourth  day  the  pain 
was  as  bad  as  ever :  the  patient  was  anxious,  her  face  was  pale  and  bathed  in  sweat, 
the  extremities  were  cold,  and  she  vomited  bihous  fluid.  On  the  fifth  day  the  lumbar 
pain  was  very  acute,  but  no  tumour  was  present ;  the  headache  was  severe,  the  vomiting 
continued.  The  patient  passed  some  urine  which  was  not  blood-stained.  On  the 
ninth  day  the  situation  became  worse,  dyspnoea  setting  in,  and  the  patient  died  coma- 
tose on  the  tenth  day. 

A  man  who  had  in  five  days  passed  only  a  few  drops  of  bloody  urine  was  admitted 
to  the  Neckor  Hospital.  As  the  bladder  was  empty,  it  was  a  case  of  anuria.  The 
patient  had  suffered  three  years  before  from  renal  coUc,  the  secretion  of  urine  being 
totally  suppressed  for  four  days.  He  had  had  two  subsequent  attacks  of  cohc,  due  to 
the  passage  of  a  stone.  In  the  present  instance  he  had  suffered  for  some  days  from 
hematuria,  but  he  had  had  no  pain.  Acute  pain  in  the  left  fiank  suddenly  came  on, 
and  the  flow  of  urine  was  arrested.  The  ureter  was  evidently  blocked  by  a  calculus. 
Ura^mic  vomiting  soon  appeared,  mental  dullness  and  loss  of  strength  being  also  present. 
The  kidneys  did  not  appear  to  be  enlarged,  but  the  left  fiank  was  painful,  and  the 
muscles  were  contracted  on  this  side.  As  the  ursemic  symptoms  were  threatening, 
Legueu  operated.  The  kidney  was  exposed  and  incised  along  the  convex  edge  ;  several 
friable  stones  were  extracted  from  the  pelvis.  A  calculus  was  felt  in  the  ureter,  about 
an  inch  from  the  pelvis.  It  was  pushed  back  into  the  pelvis  and  extracted.  The 
excretion  of  the  urine  was  re-established,  and  rapid  recovery  followed. 

Calculous  anuria  may  also  occur  in  persons  who  have  never  had  an  attack 
of  renal  colic. 

A  healthy  man,  fifty-six  years  of  age,  was  surprised  to  find  that  he  could  not  pass 
water.  As  the  bladder  yielded  no  urine  on  the  passage  of  a  catheter,  it  was  a  case 
of  anuria.  The  anima  went  on  for  some  days  without  pain  or  other  incidents,  and  the 
patient  was  then  admitted  imder  Tennesson.  The  anuria  had  then  existed  for  ten  days, 
and  the  bladder  was  empty.  Calculous  anuria  was  at  first  suspected,  but  the  patient's 
answers  were  negative  as  to  previous  cohc  or  haematuria.  On  palpation  of  the  abdomen, 
no  tumour,  and  no  tenderness  on  pressure.  Symptoms  of  uremia,  then,  appeared,  and 
the  patient  died  on  the  fourth  day.  At  the  autopsy  the  bladder  was  empty  ;  the  right 
ureter  was  blocked  by  a  calculus  as  large  as  a  pea.  Hydronephrosis  was  absent,  except 
that  one  of  the  caUces  was  dilated.  The  left  ureter  was  quite  patent.  A  stone  was 
foxmd  in  one  of  the  cahces.  The  anuria  had,  therefore,  supervened  during  latent  renal 
hthiasis. 

From  these  cases  we  see  that  calculous  anuria  does  not  always  supervene 
in  renal  colic,  as  we  are  too  ready  to  suppose ;  in  most  cases  it  forms  a  part 


1202  TEXT-BOOK  OF  MEDICINE 

of  renal  colic,  but  in  other  cases  it  occurs  in  persons  who  have  never  had 
any  sign  of  renal  colic. 

Two  periods  are  seen  in  the  evolution  of  calculous  anuria  :  the  one  of 
tolerance,  the  other  of  uraemia.  During  the  period  of  tolerance,  the  suppres- 
sion of  the  urinary  secretion  is  not  revealed  by  any  symptoms  ;  the  patient 
feels  well,  and  has  no  pain  ;  he  either  passes  no  urine,  or  only  a  little  urine  of 
low  specific  gravity,  poor  in  urea,  and  sometimes  blood-stained.  This 
period  lasts  from  three  days  to  a  week  ;  the  passage  of  a  few  ounces  of  urine 
and  the  absence  of  ursemic  symptoms  induce  hope  of  recovery.  After  a 
variable  period  the  first  symptoms  of  uraemia  appear — vomiting,  torpor,  and 
cramps  in  the  calves  ;  at  the  same  time,  or  shortly  afterwards,  we  find  epis- 
taxis,  headache,  visual  troubles,  dyspnoea,  diarrhoea,  and,  in.  rare  cases, 
oedema,  and  the  patient  dies  in  convulsions  or  in  coma  from  two  to  six 
days  after  the  onset  of  uraemia. 

Pathogenesis. — Legueu  has  collected  some  thirty  cases,  which  show  the 
courses  of  events  both  in  the  affected  and  in  the  healthy  kidney.  In  thirty 
cases  of  calculous  anuria,  the  obliteration  was  situated  twenty-three  times  in 
the  ureter  and  seven  times  in  the  pelvis  ;  m  the  latter  case  the  obliteration 
was  due  to  large  calculi,  fitting  into  the  orifice  of  the  ureter.  The  kidney 
showed  various  changes — pyelitis,  hydronephrosis,  fibrosis,  etc. 

As  regards  the  opposite  kidney  the  findings  were  : 


Congenital  absence   . . 

. .     3  cases. 

Calculous  changes     . . 

..   14      „ 

Atrophy  and  fibrosis 

..     6      „ 

Obliteration  of  the  ureter 

..     6      „ 

Kidney  quite  healthy 

..     1      » 

These  cases  show  that  calculous  obhteration  does  not  always  occur  in 
the  ureter  ;  small  calculi  cause  blocking  of  the  ureter,  because  their  small  size 
allows  them  to  enter  it,  whUe  large  calculi  obstruct  the  orifice  of  the  ureter 
in  the  pelvis.  Accordingly  anuria,  accompanied  or  preceded  by  renal  colic, 
is  usually  due  to  blocking  of  the  ureter,  while  anuria,  which  is  only  associated 
with  signs  of  a  large  calculus,  or  which  is  not  accompanied  by  signs  of 
renal  colic,  is  usually  due  to  intrarenal  obliteration ;  exceptions,  however, 
occur,  as  Tennesson's  case,  already  quoted,  shows. 

How  does  obliteration  of  one  ureter  bring  about  total  suppression  of 
urine  ?  The  anuria  has  been  explained  by  lesions  of  the  other  kidney,  and  it 
has  been  argued  :  It  is  not  surprising  to  find  anuria  ;  one  kidney  is  obstructed, 
and  the  other  is  diseased.  This  is  true,  but  yet  the  kidney  was  secreting 
before  the  obliteration  of  its  fellow- organ ;  for  a  kidney  may  be  calculous, 
and  still  the  secretion  of  urine  is  not  quite  suppressed ;  and  how  ,.can  we 
explain  complete  anuria  when  the  opposite  kidney  has  no  lesions,  or  when  the 
lesions  are  slight  ?     We  are  driven  to  admit  a  functional  paralysis  of  both 


JJ18KASES  OK  TIIK  KiUNEVS  120o 

kiduoys,  which  causes  total  abolitiou  of  the  Hecu-i-tury  function.  This 
secretory  paralysis  may  affect  the  opposite  kidney,  altiiou<^h  it  is  practically 
healthy.  The  proof  of  this  functional  paralysis  is  that  the  kidney  on  the 
side  of  the  obliteration  practically  never  shows  hydronephrosis ;  the  urine, 
therefore,  is  not  so(;reted  by  the  kidney,  because  its  function  is  suspended, 
and  the  suppression  of  function  spreads  retlexly  to  the  other  kidney.  That 
the  suppression  is  functional  and  due  to  reflex  action  is  proved  by  Broca's 
case,  in  which  anuria  was  present :  although  the  obliteration  was  due  to  a 
small  cancer  of  the  bladder  affecting  only  the  left  ureter,  the  flow  of  urine 
reappeared  half  an  hour  after  nephrotomy. 

Diagnosis. — The  diagnosis  of  anuria  is  obvious,  but  it  is  sometimes 
difiicidt  to  say  whether  the  anuria  is  calculous.  There  is  no  room  for  doubt 
when  anuria  accompanies  or  follows  an  attack  of  colic  or  of  hsematuria. 
We  have,  however,  to  remember  cases  in  which  anuria  supervenes  in  persons 
with  calculi  that  have  given  no  warning ;  in  this  event  we  must  attempt  to 
provoke  lumbar  pain,  and  we  must  inquire  carefully  into  the  pathological 
history  of  the  case.  Hysterical  anuria  is  revealed  by  the  discovery  of  the 
symptoms  and  stigmata  of  hysteria.  Anuria  due  to  compression  of  the 
ureter  by  an  abdominal  or  pelvic  tumour  is  characterized  by  gradual 
diminution  of  the  urine  passed,  and  by  the  presence  of  hydronephrosis. 

It  is  not  always  easy  to  say  on  which  side  the  obstruction  exists,  and 
it  is  even  more  difficult  to  recognize  its  exact  seat.  "  As  regards  the  exact 
seat  of  the  obstruction,  aside  from  cases  in  which  the  foreign  body  can  be 
felt  by  rectal  or  vaginal  examination,  the  most  skilled  observer  has  to  rely 
on  the  fact  that  most  stones  are  arrested  in  the  upper  part  of  the  ureter  " 
(Demons  and  Pousson).  Catheterization,  of  the  ureter  may  be  of  great  help 
in  making  a  diagnosis  (Albarran). 

It  is  j)ossible  that  in  certain  cases  radiography  may  be  of  material 
assistance  by  indicating  the  presence  of  a  renal  calculus  and  also  the  side  on 
which  the  stone  occurs.  In  this  respect  it  is  of  interest  to  recall  Beclere's 
opinion  (p.  1200)  :  "  In  radiographic  examinations  for  urinary  calculi  suc- 
cess is  the  rule,  and  failure  the  exception.  Calculi  of  pure  acid  are  the  only 
form  likely  to  escape  recognition.  Every  stone  which  contains  phosphates 
or  salts  of  calcium  in  sufficient  quantity  can  be  made  out  by  radiography." 

To  recapitulate  the  points  of  importance  in  making  a  diagnosis  (Hurry 
Fen  wick) :  "  History  of  previous  attacks  of  renal  colic ;  passage  of  calculi ; 
sudden  onset  of  pain  in  one  kidney,  or  prolonged  colic  with  suppression 
and  constant  desire  to  micturate ;  presence  of  a  renal  tumour ;  tenderness 
in  the  renal  area  or  along  the  course  of  the  ureter;  rectal  or  vaginal 
examination  to  determine  the  condition  of  the  lower  part  of  the  ureter." 

Prognosis. — The  prognosis  of  calculous  anuria  is  always  most  grave, 
as   the  following  figures   show;    the   percentage   of  recoveries  in   cases 


1204  TEXT-BOOK    OF    MEDICINE 

operated  upon  is  51,  as  compared  vrith  a  total  of  28 '5  in  cases  of  spon- 
taneous recovery. 

The  condition  will  ahvays  be  one  of  extreme  gravity,  because  the  other 
kidney  is  so  often  diseased  or  absent,  as  Legueu's  statistics  on  p.  1202  so 
clearly  shovr.  Out  of  thirty  cases,  in  one  alone  was  the  opposite  kidney 
quite  healthy.  It  is,  ho\yever,  somewhat  difficult  to  say  exactly  when  the 
prognosis  becomes  grave.  Many  persons  suffering  from  renal  colic  have 
transient  suppression  of  urine  lasting  for  some  hours ;  we  cannot  reason- 
ably class  them  as  recovering  from  calculous  anuria.  Anuria  which  lasts 
for  twenty-four  hours  after  an  attack  of  renal  colic  should  cause  alarm ; 
if  it  lasts  forty-eight  hours,  the  situation  is  dangerous  ;  after  a  duration  of 
three  or  four  days  immediate  surgical  intervention  is  absolutely  indicated. 

Treatment. — When  we  call  to  mind  the  fact  that  calculous  anuria, 
even  imder  the  most  favourable  circumstances,  shows  a  mortality  of  some 
50  per  cent.,  it  is  obvious  that  this  condition  is  the  most  grave  and  the 
most  lethal  of  all  the  many  serious  complications  of  renal  calculi.  It  is 
only  in  rare  instances  that  the  anuria,  once  it  is  estabKshed,  yields  to  our 
therapeutic  efforts.  In  these  cases,  then,  our  duty  is  clear  and  imperative ; 
we  must  ever  bear  in  mind  the  question  of  operative  interference. 

The  therapeutic  measures  at  our  command  are  either  medical  or 
surgical.  Medical  measures  are  of  some  service.  In  the  first  place,  many 
observations  in  cases  of  nephrotomy  for  calculous  anuria  show  that  the 
kidney  is  extremely  congested  and  vascular.  The  natural  inference  to  be 
drawn  from  this  pathological  fact  is  that  we  should  employ  dry  cupping  or 
bleeding  over  the  renal  area  in  order  to  lessen  this  congestion  of  the  kidney. 
In  the  second  place,  drastic  purgation,  especially  by  means  of  calomel,  is 
indicated.  In  the  third  place,  we  must  carefully  avoid  the  use  of  opium. 
Diuretics,  as  might  be  expected,  are  of  no  service. 

If  these  measures  do  not  succeed  in  re-establishing  the  flow  of  urine  in 
from  seventy -two  to  ninety-six  hours,  we  must  promptly  resort  to  surgical 
measures.  To  wait  until  urcemia  has  set  in  before  deciding  on  surgical 
intervention  is  to  deprive  the  patient  of  any  reasonable  chance  of  recovery. 

It  is  to  be  noted  that  pain  is  the  best  indication  as  to  the  side  to  be 
operated  upon,  and  as  to  the  appropriate  time  for  surgical  interference. 
The  tender  kidney,  which  has  been  the  site  of  the  pain,  is  the  one  to  be 
explored.  As  long  as  pain  is  experienced,  the  stone  may  be  shifting, 
directly  the  pain  ceases  and  suppression  continues,  the  renal  vitality  is 
endangered  and  operation  should  be  considered  (Fenwick). 

"We  must  not  forget  that  even  if  spontaneous  recovery  should  occur,  the 
fon^  et  origo  mo.li  is  still  in  the  kidney  (unless  it  has  passed  into  the 
bladder),  and  that  even  after  a  period  of  apparent  recovery,  a  relapse  with 
fatal  consequences  may  take  place. 


DISEASES   OF   THE   KIDNEYS  120.J 

The  happy  results  of  a  well-tiuictl  operation  are  shown  in  the  second 
case  quoted  on  p.  1201.  The  secretion  of  urine  was  promptly  and 
spontaneously  re-establishod  after  the  removal  of  the  stone,  the  amounts 
of  Urino  passed  being  as  follows  : — 

First  day  after  tlio  oporatiun  patient  passed  1500  grammus  in  2-i  Loura. 
Second  .lay        ..  „  „  2300 

Third  day  .,  „  „  2000 

Foui-thday       „  „  „  1609 

In  the  case  of  a  young  woman  suffering  from  calculous  anuria,  the 
secretion  of  urine  was  re-established  by  reflex  action  after  the  passage  of  a 
ureteral  catheter  by  Alburran. 

4.  Calculous  Pyelonephritis. 

Pathogenesis. — Pyelitis  is  usually  due  to  calculus.  Suppuration  does  not 
occur  as  long  as  the  medium  in  which  the  calculi  develop  remains  aseptic. 
Renal  calculi  may  exist  for  years  without  causing  pyelitis,  just  as  gall-stones 
may  be  present  in  the  gall-bladder  without  causing  cholecystitis.  Persons 
have  ten  or  twenty  attacks  of  renal  colic  without  suppuration  occurring  in 
the  urinary  tract ;  a  large  stone  may  remain  for  years  in  the  kidney  without 
causing  infection  of  that  organ.  Calcuh,  then,  may  remain  for  a  long  while 
in  the  pelvis  or  in  the  calices,  and  give  rise  to  fibrous  changes  ;  but  as  they 
are  aseptic,  they  do  not  per  se  provoke  suppuration.  Furthermore,  this 
tolerance  of  the  kidneys  for  aseptic  calculi  has  been  experimentally  demon- 
strated. Legueu,  repeating  the  experiments  of  Tuffier,  has  introduced 
aseptic  gravel  into  the  pelvis  of  a  dog's  kidney ;  after  two  months  the  pelvis 
showed  no  trace  of  suppuration,  and  the  bacteriological  examination  was 
negative.  If  pyelitis  is  to  occur,  the  infection  must  be  carried  from  outside. 
In  1886  Gado  found  that  the  pathogenic  organism  of  urinary  infection  was 
a  bacterium  which  he  called  the  Bacillm  septicus.  At  the  present  day  this 
organism  is  called  the  Bacillus  coli,  which  is  often  associated  with  other 
species — streptococci,  staphylococci,  etc.  These  organisms  enter  the  urinary 
tract  through  lesions  of  the  urethra  (stricture,  gonorrhcEa,  diseases  of  the 
prostate,  use  of  septic  catheters),  lesions  of  the  bladder,  and  lesions  of  the 
ureter.  The  infection  is  an  ascending  one,  and  the  micro-organisms  reach 
the  kidney,  which  is  in  a  condition  of  morbid  receptivity  on  account  of  the 
traumatism  produced  by  the  calculi ;  pyelitis  then  results. 

Pathological  Anatomy. — In  mild  cases  of  calculous  pyelitis  we  find 
congestion  of  the  calices  and  of  the  pelvis,  with  hypersecretion  and  desqua- 
mation of  the  epithelium.  In  more  severe  cases  and  in  the  chronic  form,  the 
mucous  membrane  is  thickened,  ulcerated,  and  covered  with  muco-pus. 
The  diphtheritic  form  is  characterized  by  a  pseudo-membranous  or  fibrinous 
deposit  spread  over  the  mucosa.  The  calices  and  the  pelvis  at  times  form 
n.        •  77 


1206  TEXT-BOOK  OF  MEDICINE 

an  anfractuous,  multilocular  pocket,  containing  branching  calculi,  purulent 
fluid  and  caseous  debris.  This  pocket  may  be  of  large  size,  especially  if  the 
ureter  is  blocked ;  the  kidney  substance  is,  then,  reduced  to  an  atrophied 
fibrous  shell.  The  ureter  often  shares  in  the  inflammation  and  dilatation  of 
the  pelvis  ;  it  becomes  tortuous.  If  the  lesion  is  unilateral,  the  healthy 
kidney  hypertrophies,  and  is  thus  able  to  carry  on  the  secretion  of  urine  ;  if 
the  lesion  is  double,  anuria  and  uraemia  soon  appear.  The  contents  of  the 
pocket  may  undergo  calcareous  change,  the  walls  becoming  thickened  and 
forming  a  fibrous  shell,  while  the  ureter  is  converted  into  a  fibrous  cord. 

The  kidney  may  be  enlarged  and  cystic,  or  atrophied,  wrinkled,  and 
fibrous.  If  suppuration  has  invaded  the  kidney,  we  find  in  the  medulla 
abscesses  of  the  straight  tubules,  which  under  the  lens  are  characterized  by 
greyish  strise,  and  in  the  cortex  resemble  miliary  abscesses.  The  kidney, 
which  at  first  sight  appears  to  be  large,  sometimes  owes  its  enlargement  to 
hypertrophy  of  the  perirenal  tissue.  In  some  cases  we  find  at  the  autopsy 
perforation  of  the  pelvis,  perinephritic  abscess,  urinary  infiltration  and 
fistulse,  communicating  with  the  adjacent  organs  or  with  the  skin. 

Description. — Pyelitis  generally  occurs  late  in  renal  lithiasis  supervening 
in  persons  who  have  suffered  for  a  long  time  from  renal  coHc,  hsematuria,  or 
symptoms  of  large  calculi.  In  some  instances,  however,  intrarenal  or  peri- 
renal suppuration  may  occur  in  persons  with  calculi  which  have  been  latent. 

Pyelitis  usually  sets  in  insidiously,  without  fever  or  pain ;  after  a  while 
the  patient  finds  that  the  urine  is  slightly  turbid,  and  feels  pain  in  the  loin, 
while  the  region  corresponding  to  the  kidney  is  tender  on  pressure.  He 
suffers  from  dyspepsia,  loss  of  appetite  and  dryness  of  the  mouth,  but  fever 
is  absent  or  moderate.  This  condition  may  be  interrupted  by  attacks  of 
hsematuria  or  of  colic.  The  disease  may  not  grow  worse.  The  patient  takes 
a  cure  at  Vittel,  Evian,  or  Gapvern,  and  for  many  years  the  pyelitis  does  not 
become  worse  ;  recovery  may  even  follow.     This  is  the  mild  form. 

In  other  cases  the  symptoms  are  severe.  The  urine  contains  abundance 
of  muco-pus  ;  the  quantity  of  urine  passed  in  the  twenty-four  hours  varies, 
being  in  most  cases  above  the  normal.  The  passage  of  much  turbid  urine 
is  the  cardinal  symptom  of  pyelitis. ,  The  mucus  and  pus  give  to  the  urine 
a  milky  look.  The  urine  clears  slowly,  but  never  completely,  the  purulent 
matter  gradually  falling  to  the  bottom  of  the  glass,  though  never  completely 
so,  as  in  the  case  of  the  mineral  sediments.  The  pyuria  is  not  fortuitous ; 
the  admixture  of  pus  and  urine  is  constant  and  occurs  daily.  The  urine  in 
pyelitis  is  nearly  always  alkaline  ;  it  sometimes  contains  imbricated  plaques 
of  epithelium  from  the  pelvis. 

Severe  pyelitis  is  usually  accompanied  by  fever ;  in  some  cases  rigors 
occur,  and  the  temperature  rises  to  104°  F.,  these  symptoms  indicating 
retention   and   infection.     These   complications   may   supervene   in   every 


DTSKASKS  OF  T[1E  KIDNKYS  il>U7 

variety  of  pyelitis.  I  liave  already  montioned  them  under  Tubercular 
Pvelitis,  and  they  are  even  more  common  in  calculous  pyelitis.  As  long  as 
the  pus  can  pass  through  the  ureter,  retention  of  the  septic  products  does  not 
occur,  and  the  fever,  if  present,  is  moderate.  If,  however,  the  ureter  or  a 
suppurating  pocket  becomes  blocked,  we  have  the  formation  of  a  closed 
cavity,  with  retention  of  the  infective  products,  and  we  find  as  the  result 
renal  pain,  rigors,  and  attacks  of  intermittent  fever,  followed  by  sweating  and 
rapid  wasting.  An  apparent  improvement  in  the  urine  often  coincides  with 
this  aggravation  of  the  symptoms.  Urine,  which  was  purulent  and  am- 
moniacal  on  the  previous  day,  is  now  clear,  the  reason  being  that  the  cleai 
urine  comes  from  the  healthy  kidney,  while  the  purulent  urine  from  the 
diseased  kidney  cannot  pass  through  the  obliterated  ureter.  If  the  ureter 
regains  its  permeability,  so  that  the  pus  can  pass  freely,  the  complications 
may  disappear.     I  saw  a  typical  case  some  years  ago  : 

A  lady,  fifty  years  of  age,  had  suffered  for  nine  years  from  renal  calculi,  colic,  and 
hajmaturia  ;  for  the  last  year  pyeUtis  had  also  been  present.  The  urine  contained  some 
pus,  but  fever  was  absent,  and  the  patient's  health  was  fair.  One  day  the  urine 
diminished  in  quantity,  and  became  clear  instead  of  turbid  ;  severe  attacks  of  fever 
set  in,  with  rigors,  rise  of  temperature  to  104°  F.,  ajid  profuse  sweating.  I  foimd  the 
left  kidney  enlarged  and  painful.  I  expressed  the  opinion  that  the  kidney  was  the  seat 
of  obstructive  infection,  and  advised  prompt  surgical  intervention.  Pozzi  operated, 
and  the  fever  at  once  disappeared  after  the  nephrotomy. 

When  the  pyelitis  is  secondary  to  ureteritis  we  may  be  able,  by  rectal  or 
vaginal  examination,  to  feel  the  dilated  or  indurated  ureter.  If  the  oblitera- 
tion of  the  ureter  is  progressive  and  final,  fresh  symptoms  appear  :  the 
secreted  products  accumulate  and  form  a  renal  tumour,  which  may  contain 
several  pints  of  fluid,  and  project  into  the  abdominal  cavity  or  into  the  loin. 
In  order  to  ascertain  the  nature  of  this  tumour,  we  must  inquire  into  the 
patient's  history,  and  find  out  whether  he  has  passed  pus  and  blood  in  the 
urine,  or  whether  he  has  been  subject  to  renal  colic. 

The  prognosis  of  calculous  pyelitis  is  benign  in  mild  cases,  but  in  other 
instances  the  pyuria  grows  worse,  the  suppuration  invades  the  parenchyma 
of  the  kidney,  the  fever  becomes  hectic,  and  the  patient  dies  from  cachexia. 

Medical  treatment  consists  in  milk  diet,  cures  at  Vittel,  Contrexeville, 
Evian,  or  Capvern,  and  balsamic  remedies  ;  surgical  intervention  is  often 
necessary,  and  must  not  be  too  long  delayed.  The  ureteral  catheter  or  Luys' 
segregator  will  indicate  the  condition  of  the  kidneys.  Nephrotomy  or 
nephrectomy  is  necessary,  according  to  the  condition  found. 

5.  Calculous  Perinephritis. 

The  kidneys  are  surrounded  by  cellular  tissue,  which  may  be  called  the  renal  fascia, 
and  which  is  an  offshoot  of  the  fascia  propria.  This  sac,  which  surrounds  the  entire 
organ,  is  composed  of  connective  tissue  in  the  foetus.     Later,  an  invasion  of  fatty  tissue 


1208  TEXT-BOOK  OF  MEDICINE 

occurs,  aad  in  the  adult  the  cellulo-fatty  layer  acquires  a  considerable  thickness.  The 
fatty  capsule  of  the  kidney  is  especially  abundant  over  the  posterior  surface  of  the 
organ.  Below  it  is  continuous  with  the  cellular  tissue  of  the  iUac  fossa  and  of  the 
pelvis. 

The  perirenal  tissue  rarely  remains  perfectly  normal  in  long-standing  pyelonephritis. 
In  some  cases  its  lesions  are  of  more  import  than  those  of  the  kidney.  Rayer  coined 
the  term  "  perinephritis  "  to  designate  inflammation  of  the  perirenal  tissue  ;  but  peri- 
nephritis does  not  always  show  itself  by  suppuration,  and  we  also  see  chronic  lesions 
which  are  fibrous  or  fatty. 

Fibro-Fatty  Perinephritis. — This  form  runs  a  chronic  course ;  the  process 
ends  in  induration  of  the  connective  tissue  and  in  overgrowth  of  the  fatty 
tissue.  These  two  lesions  vary  in  degree  according  to  the  particular  case. 
At  first  the  ceEular  tissue  is  thickened,  indurated,  and  adherent  to  the 
capsule  of  the  kidney  and  to  the  ureter.  At  a  later  stage  the  lesions 
are  more  marked  and  more  extensive. 

When  the  fibrous  tissue  predominates,  the  envelope  of  the  kidney  is 
thickened  and  creaks  under  the  knife.  In  a  case  quoted  by  Tuffier  the 
fibrous  induration  invaded  the  muscles  and  the  abdominal  wall  as  far  as  the 
skin.  When  the  fatty  tissue  predominates,  we  find  masses  of  fat,  forming 
tumours,  separated  by  thick  fibrinous  septa. .  Hartmann  has  described  fatty 
tumours  situated  around  the  pelvis ;  they  may  compress  the  vessels  in  the 
hilum,  producing  thrombosis  in  the  veins,  whUe  the  arteries  are  atrophied. 
The  fatty  tissue  may  invade  the  kidney,  which  is  converted  into  a  sclero- 
lipomatous  mass,  the  kidney  substance  being  represented  by  some  remnants 
of  glandular  tissue  around  the  pelvis,  which  contains  one  large  or  several 
small  stones. 

The  sclero-lipomatous  form  of  perinephritis  is  important ;  it  is  met  with 
in  several  diseases  of  the  kidney  (tuberculosis,  pyelitis),  but  it  is  most  common 
and  most  marked  in  renal  lithiasis.  This  form  sometimes  causes  a  calculous 
kidney  to  have  the  appearance  of  a  very  large  tumour ;  examination  of  the 
patient  reveals  a  large  tumour,  and  when  we  examine  the  specimen  we  find 
that  sclero-lipomatous  degeneration  makes  up  the  major  part  of  it.  I  had 
a  remarkable  case  in  hospital : 

A  yoimg  woman  had  suffered  from  abdominal  pain  for  eleven  years.  The  left 
kidney  was  enlarged  and  painful,  and  pain  was  also  felt  in  the  lumbar  region.  The 
urine  had  contained  pus  for  eight  months,  but  the  patient  had  not  had  either  renal  coUo 
or  heematuria.  A  diagnosis  was  necessary.  Cancer  was  eUminated,  because  the  patient 
had  suffered  for  eleven  years,  and  had  not  had  hsematuria.  It  was  not  a  polycystic 
Jddney,  because  polycystic  degeneration  would  certainly  have  affected  the  other  kidney 
hi  eleven  years.  As  the  centrifugahzed  urine  did  not  contain  Koch's  bacillus,  and  as 
the  disease  was  of  many  years'  standing,  tuberculosis  could  be  eUminated.  I,  therefore, 
made  the  following  diagnosis :  calculous  kidney,  with  pyehtis  and  sclero-hpomatous 
perinephritis.  As  the  patient  had  never  had  renal  coHc,  I  concluded  that  the  calculus 
was  a  large  one,  giving  rise  to  but  moderate  pain  for  several  years,  the  pain  being 
increased  for  some  months  by  the  pyehtis.  The  operation  proved  the  correctness  of 
my  diagnosis. 


DISEASES  OF  THE  KIDNEYS  1200 

Suppurative  Perinephritis. — Calculous  pyelonephritis  may  at  any  time 
cause  perireuul  suppuration.  The  abscess  may,  indeed,  bo  the  first  sign  of  a 
latent  pyelitis  due  to  stoue. 

Pathogenesis. — Perirenal  suppuration  is  due  to  tlie  invasion  of  the 
perirenal  tissiie  by  pyogenic  organisms.  Alharran,  in  his  bacteriologir-al 
researches,  has  given  the  following  results  :  In  seven  cases  of  perinephritic 
abscess  the  Bacillus  coli  was  in  pure  culture  in  four,  and  in  the  other  three 
cases  it  was  associated  with  other  organisms. 

We  can  show  experimentally  the  invasion  of  the  perirenal  tissue  by 
injecting  micro-organisms  into  the  ureter.  They  pass  through  the  lymphatics. 
Albarran  has  caused  suppurative  nephritis  and  perinephritis  by  injecting 
pyogenic  organisms  into  the  blood  of  the  rabbit,  after  bruising  the  kidney 
and  the  perirenal  tissue. 

Pathological  Anatomy. — Perinephritis  is  nearly  always  unilateral,  and 
more  common  on  the  right  side.  The  abscess  wall  is  thickened,  anfractuous, 
and  covered  by  organized  false  membranes.  In  some  cases  the  abscess  sends 
prolongations  into  the  psoas,  latissimus  dorsi,  and  external  oblique  muscles. 
The  pus  contained  in  the  cavity  may  be  laudable,  or  mixed  with  gravel  and 
sloughy  shreds.  The  abscess  gives  off  a  fsecal  odour,  even  when  it  does  not 
communicate  with  the  bowel.  The  invaded  muscles  are  reduced  to  a  greyish 
pulp.  The  kidney  shows  calculous  pyelonephritis.  If  the  abscess  is 
confined  beneath  the  capsule  of  the  kidney,  the  purulent  collections  may  be 
small  and  multiple,  or  may  completely  surround  the  kidney,  which  is  bathed 
in  pus  (subcapsular  abscess) ;  in  this  case  the  pelvis  is  external  to  the  abscess, 
because  the  capsule  ceases  at  the  hilum. 

Symptoms. — ^Pain  and  fever  are  usually  the  first  symptoms.  The  pain, 
situated  in  the  lumbar  region,  is  spontaneous,  and  is  always  increased  by 
pressure,  especially  if  the  painful  region  is  compressed  between  the  two  hands. 
It  is  important,  because  it  may  be  for  days  or  weeks  the  only  local  sign.  The 
fever  is  continuous,  with  periodical  paroxysms  ;  at  night  the  patient  has  a 
rigor,  followed  by  a  hot  stage  and  sweating  ;  vomiting  sometimes  occurs. 
Wasting  and  loss  of  appetite  follow  ;  the  constipation  is  absolute. 

Other  signs  appear  after  a  week  to  a  fortnight  when  the  course  of  the 
disease  is  acute,  and  after  several  weeks  if  the  course  is  chronic.  "  More  or 
less  brawny  induration  appears  in  the  lumbar  region,  which  becomes  more 
and  more  tender  on  pressure  ;  the  ilio-costal  hollow  fills  up,  and  when  the 
patient  lies  on  his  back,  the  examiner,  by  pushing  his  hand  into  the  loin,  can 
feel  a  more  or  less  marked  prominence.  The  induration  in  the  loin  is  often 
accompanied  by  oedema,  which  may  extend  to  the  dorsal  and  gluteal  regions  ; 
slight  redness  of  the  skin  is  also  present  "  (Trousseau). 

Diagnosis. — The  diagnosis  presents  no  difficulty  when  the  abscess  has 
been  preceded  by  renal  colic,  pyelitis,  haematuria,  or  the  passage  of  muco- 


1210  TEXT-BOOK  OF  MEDICINE 

purulent  urine.  When  we  have  this  history,  and  when  the  patient  suffers 
from  sharp  pain  in  the  loin,  with  daily  attacks  of  fever,  and  when  we  find 
induration  and  cedema  in  the  lumbar  region,  we  can  say  that  a  perinephritic 
abscess  is  forming. 

The  diagnosis  is  not,  however,  always  so  easy ;  in  some  cases  the  prime 
cause  of  the  abscess  passes  unnoticed,  and  for  several  days  the  only  symptom 
is  more  or  less  acute  lumbar  pain,  accompanied  by  remittent  or  intermittent 
fever.  Calculous  pyelitis  may  present  the  same  symptoms,  and  even  end 
in  the  formation  of  a  tumour  (pyonephrosis) ;  the  diagnosis  is,  then,  most 
difficult.  In  pyonephrosis,  however,  the  tumour  is  mainly  abdominal;  in 
perinephritis  the  tumour  is  mainly  lumbar.  In  pyonephrosis  the  tumour  is 
more  rounded  and  more  clearly  limited,  while  the  perirenal  abscess  is  more 
diffuse,  and  blends  with  the  oedematous  abdominal  wall.  The  prognosis  is 
more  serious  in  the  acute  and  septic  forms  than  in  the  phlegmonous  forms. 

The  treatment  is  purely  surgical. 

6.  Renal  and  Perirenal  Fistulse. 

We  have  seen  that  a  perinephritic  abscess  may  open  in  the  loin,  at  the 
navel,  into  the  intestine,  or  into  the  bronchi ;  when  the  opening  does  not 
close,  a  fistula  results. 

When  the  fistula  originates  in  the  kidney,  it  is  called  renal ;  when  it 
originates  in  the  perirenal  tissue,  it  is  called  perirenal.  The  fistula  is  called 
purulent  or  urinary,  according  as  the  discharge  is  pus  or  urine.  If  the 
fistula  opens  on  the  skin,  it  is  called  reno- cutaneous ;  if  it  discharges  into  an 
organ,  it  is  called  reno-intestinal,  reno-bronchial,  etc. 

Reno-Cutaneous  FistUlae. — These  fistulas  usually  open  in  the  loin,  the 
discharge  being  purulent  or  urinary ;  the  external  opening  is  funnel-shaped, 
with  f ungating  edges,  and  the  canal,  which  has  thick  fibrous  waUs,  ends  in  a 
deep  renal  or  perirenal  focus.  The  ureter  is  nearly  always  constricted  or 
obliterated,  and  the  discharge,  then,  contains  urine  and  pus  ;  the  flow  is 
continuous,  and  has  a  characteristic  odour  ;  the  edges  of  the  wound  are  raw, 
erythematous,  and  painful,  so  that  frequent  dressing  is  required. 

Intestinal  Fistulse. — These  fistulae  are  fairly  common,  especially  those 
which  open  into  the  colon.  They  are  preceded  by  symptoms  of  enteritis ;  the 
dejecta  are  purulent  and  foetid  ;  the  patient  wastes  and  finally  succumbs. 

7.  Fibrosis  and  Atrophy. 

Fibrous  atrophy  may  or  may  not  be  accompanied  by  hydronephrosis. 
While  pyonephrosis  due  to  calculus  is  common,  hydronephrosis  is  rare. 
Brault  and  Cornil  have  studied  the  changes  in  the  kidney  consecutive  to 
compression,  ligature  and  obstruction  of  the  ureters  ;  the  changes  end  in 
atrophy  of  the  kidney.     When  the  ureters  and  the  pelvis  are  dilated  and 


DISEASES  OF  THE  KIDNEYS  1211 

contain  fluid,  the  kidney  appears  to  be  enlarged  ;  it  is  f edematous,  and  the 
limit  of  the  cortex  and  of  the  medulla  is  no  longer  dear  ;  the  calices,  pushed 
back  by  the  pressure  of  the  lluid,  in  their  turn  push  back  the  cortex.  On 
making  a  section  of  the  kidney  we  find  calculi  which  often  betray  their 
presence  by  bosses  on  the  surface.  The  cortex  is  hollowed  out.  Some  of  the 
cavities  communicate  with  the  dilated  calicos  and  pelvis,  while  others  are 
isolated  in  the  form  of  independent  cysts. 

On  histological  examination  the  kidney  presents  lesions,  divided  by 
Jardet  into  three  stages.  At  first  the  renal  lesion  is  characterized  by  stasis 
of  the  urine,  with  dilatation  of  the  tubules  from  the  glomerulus  to  the  papilla. 
The  arteries  are  thickened  from  arteritis.  At  a  more  advanced  stage  the 
fibrosis  invades  the  medulla  and  the  cortex  in  an  irregular  fashion  ;  the 
lumen  of  the  tubules  is  sometimes  enlarged,  sometimes  constricted,  and  the 
glomeruli  are  fibrous  and  atrophied.  In  the  final  stage  the  fibrosis  ends  in 
atrophy ;  the  kidney  tissue  may  be  atrophied,  although  the  organ  as  a 
whole  is  enlarged  by  reason  of  the  distension  of  the  calices  and  of  the  pehas. 
In  the  opposite  case  the  atrophic  fibrosis  causes  diminution  in  the  size  of  the 
organ.  Jardet  has  pointed  out  that  these  atrophic  lesions  are  not  always 
consecutive  to  mechanical  obliteration  of  the  ureter  ;  it  is  probable,  on  the 
contrary,  that  the  fibrous  lesions  precede  the  obliteration. 

"  When  the  kidney  has  been  destroyed  by  atrophic  nephritis,  the  other 
kidney  is  usually  hypertrophied,  but  the  hypertrophy  is  less  marked  and  less 
regular  than  it  is  after  nephrectomy.  The  kidney  as  a  whole  appears  to  be 
larger,  but  we  can  nearly  always  see  with  the  naked  eye  traces  of  partial 
fibrosis.  The  microscope  shows  fibrosis  at  some  spots,  and  at  others  en- 
largement of  the  canaliculi  and  of  the  glomeruli ;  in  short,  compensatory 
hypertrophy  exists,  but  only  at  certain  parts  of  the  Icidney.  This  peculiarity 
appears  to  be  due  to  the  fact  that  the  nephritis  is  frequently  bilateral  in  the 
case  of  a  calculous  kidney  ;  the  fibrous  lesions  so  common  in  these  cases  are 
due  not  only  to  the  presence  of  calculi  in  the  pelvis,  but  also  to  the  irritant 
action  of  the  urine,  the  composition  of  which  is  altered  by  the  special  mode 
of  nutrition  of  the  patient  "  (Albarran). 

As  long  as  the  fibrosis  is  limited  to  the  diseased  kidney,  the  secretion  of 
urine  is  assured  by  the  opposite  kidney ;  but  when  both  are  the  seat  of 
lithiasis  or  of  fibrosis,  the  minor  symptoms  of  Brightism  appear,  and,  later,  the 
major  symptoms  of  uraemia.  Raymond  has  published  a  case  in  point. 
An  elderly  man  who  had  never  suffered  from  renal  colic  or  from  symptoms 
of  calculus  died  from  ursemia.  The  autopsy  revealed  large  calculi  in  both 
kidneys  and  atrophy  of  the  cortex,  with  interstitial  nephritis. 


1212  TEXT-BOOK  OF  MEDICINE 

XV.  PYELITIS— PYELONEPHRITIS. 

Pyelitis  is  inflammation  of  the  mucous  membrane  of  tlie  calices  and 
pelvis  ;  it  may  be  acute  or  chronic,  and  nephritis  may  or  may  not  be  present. 
The  word  "  pyelitis  "  has  been  preserved,  although  its  etymology  (Tri^eXo?, 
pelvis)  bears  no  relation  to  the  morbid  localization.  Pyehtis  may  supervene 
as  a  secondary  infection  in  such  diseases  as  typhus,  scarlatina,  measles, 
smallpox,  or  cholera.  In  some  cases  it  follows  poisoning  by  turpentine, 
cubebs,  and  especially  cantharides. 

Affections  of  the  genital  organs  in  women,  cancer  of  the  uterus,  infections 
of  the  urethra,  bladder,  and  ureter  (gonorrhoea),  often  cause  pyelitis  ;  the 
micro-organisms  take  the  urine  for  a  culture  medium,  and  the  infection  nearly 
always  spreads  by  the  ascending  path. 

Tubercular  pyelitis  has  been  described  (p.  1158  et  seq.).  The  most 
frequent  cause  of  pyelonephritis  is  renal  calculus.  The  question  has  already 
been  fully  discussed. 

XVI.  SUPPURATIVE  NEPHRITIS. 

Pathological  Anatomy. — I  shall  here  describe  suppurative  nephritis 
properly  so  called  and  metastatic  abscesses  of  the  kidney.  The  history  of 
suppurative  nephritis  is  often  associated  with  that  of  pyelitis,  the  two 
lesions  being  successive  stages  of  the  same  infection. 

The  nephritis  may  be  unilateral  or  bilateral.  It  is  due  to  many  causes. 
Some  are  exceptional,  such  as  contusions,  wounds,  and  adjacent  abscesses; 
others  are  more  common,  and  include  infection  by  the  ascending  path  and 
by  the  blood-stream.  Cystitis,  enlarged  prostate,  strictures  of  the  urethra, 
and  operations  on  the  urethra  or  on  the  bladder,  may  cause  nephritis  by 
ascending  infection. 

In  nephritis  due  to  blood  infection  the  course  of  events  is  as  follows :  The 
primary  affection  of  the  urinary  tract  induces  general  infection,  and  the 
organisms  carried  by  the  blood  form  emboli  in  the  renal  vessels.  Albarran, 
by  injecting  the  colon  bacillus  into  the  ureter  of  the  rabbit,  has  produced 
ascending  nephritis.  Furthermore,  any  blood  infection  (staphylococcus, 
pneumococcus,  streptococcus,  etc.)  may  cause  abscesses  in  the  kidney. 
The  suppuration  may  be  diffuse  or  collected  in  the  form  of  an  abscess  ; 
these  two  forms  at  times  occur  together.  Diffuse  nephritis  commences  with 
congestion  of  the  organ ;  the  kidney  is  swollen,  red  on  section,  and  studded 
with  ecchymoses,  caused  by  parenchjonatous  and  interstitial  haemorrhages. 
Pus  then  forms,  and  infiltrates  the  cortex  and  pyramids  of  the  kidney.  The 
organ  is  yellowish  and  opaque  on  section,  and  homogeneous  pus  can  be 
squeezed  out  on  pressure. 


DISEASES  OF  THE  KIDNEYS  121  r. 

The  nephritis  may  be  infiltrating  or  radiating.  In  the  clifTuse  infiltrating 
form  the  parenohvnia  is  a  mottled  red  and  grey  ;  ahsfcsses  of  different  sizes 
are  found  in  the  cortex  or  at  the  base  of  the  pyramids.  In  the  radiating  form 
the  pyramids  are  marked  with  perpendicular  stria?  of  a  greyish  colour, 
standing  out  against  the  dark  red  background.  Some  of  the  stria?  are  larger, 
forming  a  cone  with  a  peripheral  base,  and  containing  a  drop  of  pus.  The 
centre  of  the  foci  is  usually  a  tubule  dilated  by  the  microbes  which  are  found 
in  the  glomerulus  between  the  tuft  and  the  capsule. 

The  recent  abscesses  contain  homogeneous  pus,  and  their  walls  are  formed 
by  the  kidney  tissue.  The  old  abscesses  contain  pus  mixed  with  lime  salts, 
and  their  walls  are  formed  by  a  membrane  of  connective  tissue.  When  the 
lesion  is  old,  the  kidney  is  more  or  less  deformed  and  nodular.  These 
abscesses  are  rarely  larger  than  a  hazel-nut ;  the  large  abscesses  are  chiefly 
seen  in  suppuration  of  the  pelvis.  The  abscesses  may  open  into  the  pelvis ; 
into  the  duodenum  ;  in  the  lumbar  region ;  into  the  peritoneum,  where  they 
cause  acute  peritonitis;  or  into  the  bronchi,  after  perforating  the  diaphragm. 
In  case  of  cure  cicatrization  and  atrophy  of  the  kidney  follow.  The  meta- 
static abscesses  occur  in  the  form  of  isolated  or  agglomerated  miliary 
abscesses.  The  latter  are  found  both  in  the  cortex  and  in  the  medulla; 
their  shape  is  conical,  the  base  being  peripheral ;  the  topography  depends 
on  the  distribution  of  the  renal  arteries. 

Description. — Acute  suppurative  nephritis  is  ushered  in  by  rigors  and 
fever,  which  is  sometimes  of  an  intermittent  type  ;  nausea  and  vomiting  are 
frequent.  The  patient  complains  of  sharp  pain,  situated  in  the  loin  and 
radiating  along  the  ureter  to  the  bladder  and  to  the  testicle.  The  desire  to 
micturate  is  urgent,  and  the  patient  usually  passes  but  a  small  quantity  of 
high-coloured  acid  urine,  containing  albumin  and  blood.  In  some  cases  the 
onset  is  insidious,  and  the  disease  is  of  a  typhoid  type,  with  adynamia,  dry 
tongue,  and  sweating.  In  old  people  suppurative  nephritis,  like  suppurative 
pneumonia,  may  be  apyretic.  The  gravity  of  the  disease  depends  on  the  age 
of  the  patient,  on  the  cause  and  extent  of  the  suppuration,  on  the  duration 
of  the  disease,  and  on  the  condition  of  the  other  kidney.  If  both  kidneys 
are  affected,  death  may  result  from  urgemia. 

Diagnosis. — Suppurative  nephritis  rarely  has  a  sudden  onset.  The  seat 
and  the  radiation  of  the  pain,  as  well  as  the  urinary  troubles,  are  in  favour 
of  nephritis.  "We  can  ascertain  by  means  of  Luys'  segregator  whether  the 
nephritis  is  unilateral  or  bilateral.  The  pain  of  nephritis  may  simulate 
that  of  renal  colic,  but  as  the  latter  is  ap}Tetic,  this  fact  decides  the  point. 
In  pyelitis  the  urine  is  purulent  from  the  first,  and  remains  so.  In  nephritis 
the  pus  appears  late,  and  is  not  constantly  present. 

Acute  nephritis  demands  antiphlogistic  measures.  Leeches  over  the 
kidneys  are  indicated ;  soothing  and  diuretic  drinks  are  to  be  given ;  the 


1214  TEXT-BOOK  OF  MEDICINE 

pain"  is    to    be  relieved    with    morpMa,    and   the    vomiting   with   iced 

beverages.      We  must   be   ready  to   employ   surgical    intervention    (see 
Section  VI.). 


XVII.  PRIMARY  AND  SECONDARY  PERINEPHRITIC  ABSCESS. 

A  perinephritic  abscess  is  an  abscess  in  the  fatty  tissue  around  the 
kidney.  This  tissue  is  most  abundant  behind  and  at  the  extremities  of  the 
kidney.  It  is  continuous  with  the  subperitoneal  tissues,  and  with  the 
cellular  tissue  in  the  iliac  fossa  and  in  the  pelvis.  On  the  other  hand,  it  is 
continuous  with  the  cellular  tissue  in  the  lumbar  region,  external  to  the 
quadratus  lumborum,  between  the  borders  of  the  latissimus  dorsi  and 
external  oblique  muscles.  The  pus  may  remain  limited  to  the  perirenal 
focus,  but  in  some  cases  it  extends  to  the  cellular  tissue  of  the  lumbar,  dorsal, 
or  gluteal  regions,  to  the  tissue  in  the  iliac  fossa,  and  even  into  the  vesical 
and  rectal  cellular  tissue. 

Secondary  Abscess. — This  form  occurs  in  lesions  of  the  neighbouring 
organs,  and  especially  in  certain  affections  of  the  kidney.  In  the  first  place 
stands  renal  lithiasis,  with  or  without  pyelo-nephritis ;  the  infection  extends 
by  propagation  or  by  perforation.  Tuberculosis  of  the  kidney  also  favours 
the  occurrence  of  perirenal  suppuration.  Other  causes  are :  pyelonephritis 
of  various  origins,  including  ascending  infection  by  the  gonococcus ;  hydatid 
cysts  and  cancer  of  the  kidney ;  suppuration  in  the  liver,  the  gall-bladder, 
the  psoas,  and  the  cellular  tissue  of  the  pelvis  ;  perforation  of  the  colon, 
appendicitis,  and  pancreatitis.  Perinephritis  may  be  associated  with  other 
diseases,  such  as  typhoid  fever,  typhus,  and  puerperal  conditions. 

When  the  kidneys  are  at  fault  and  pyelonephritis  is  already  present,  we 
can  readily  understand  the  occurrence  of  suppuration,  on  account  of  the 
proximity  of  th«  lesions.  In  other  cases,  however,  the  original  focus  of 
infection  is  far  more  remote  ;  this  fact  leads  me  to  mention  the  relations 
between  perirenal  infection  and  pleuro-pulmonary  infection.  This  side  of 
the  question  was  recognized  by  Rayer  and  Trousseau.  The  following  case 
is  taken  from  Rayer's  work  : 

A  woman,  sixty-five  years  of  age,  who  had  suffered  from  renal  colic,  had  been  ill 
for  some  months,  with  pain  in  the  right  kidney,  fever,  and  malaise.  The  right  loin  was 
very  tender  on  pressure,  and  palpation  revealed  an  iho-lumbar  tumour.  The  diagnosis 
of  extrarenal  abscess  was  made.  An  incision  gave  exit  to  a  pint  of  foul-smeUing  pus. 
Digital  examination  showed  that  the  focus  was  behind  the  kidney,  and  the  abscess  was 
therefore  perinephritic.  Much  relief  followed.  On  the  thirteenth  day,  however,  the 
patient  was  taken  ill  with  pneumonia  of  the  right  lung.  The  attack  subsided  in  a  few 
days ;  the  lumbar  wound  still  discharged  some  pus.     The  patient  finally  recovered. 

Trousseau  has  repeatedly  insisted  on  the  relations  between  perirenal 
suppuration  and  pleuro-pneumonia.     "  Perinephritic  abscesses  may  cause 


DISEASES^  OF  TFTE  KTDXEYS  1215 

pleurisy  and  pneumonia.  I  would  have  you  remember  that  in  cases 
where  a  perinephritic  abscess  is  complicated  by  pleuro-pneumonia,  the 
latter  is  always  on  the  same  side  as  the  abscess.  Desruelles  found  a 
perinephritic  abscess  in  an  old  woman  convalescent  from  gangrenous 
pneumonia." 

Recent  researches  have  explained  the  pathogenesis  of  these  reciprocal 
infections.  Tuffier  and  Lejars  have  described  a  costo-lumbar  hiatus,  through 
which  the  subpleural  fat  communicates  with  the  perirenal  fatty  tissue. 
The  hiatus  is  traversed  by  veins  and  lymphatics,  which  establish  com- 
munication between  the  perirenal  tissue  and  the  thoracic  cavity ;  in  this 
way  pleuro-pulmonary  infections  may  become  perirenal,  and  vice  versa. 
Tuffier  has  published  a  case  of  pneumococcal  perinephritic  abscess  secondary 
to  pneumonia. 

Injury  plays  an  important  part  in  the  causation  of  diseases.  The  occur- 
rence of  pneumonia  and  the  appearance  of  tuberculosis  after  injury  are  well 
known,  although  it  is  not  always  easy  to  explain  the  pathogenesLs.  A 
similar  aetiology  obtains  in  the  history  of  perinephritic  abscess.  The 
following  example  is  from  De  Mussy's  lectures  : 

A  woman,  forty  years  of  age,  who  had  been  kicked  in  the  loin  by  a  horse,  was  taken 
ill  six  months  later  with  acute  pain,  fever,  and  rigors.  The  pain  spread  from  the  loin 
to  the  ihac  region.  The  symptoms  improved  mider  sedative  measures,  but  reappeared 
a  week  later.  In  the  space  between  the  last  rib  and  the  iliac  crest  a  swelling,  with 
induration  of  the  cellular  tissue,  could  be  made  out.  Pressure  in  the  liunbar  region 
caused  unbearable  pain.  The  fever  was  continuous,  with  an  evening  rise  and  rigors. 
The  diagnosis  was  perinephritic  abscess.  Xelaton  made  a  puncture,  giving  exit  to  a 
quantity  of  pus.  After  a  transient  improvement,  the  rigors  and  the  fever  reappeared, 
because  the  pus  did  not  find  a  free  exit.     The  patient  finally  succumbed. 

Bergounhioux  speaks  of  a  peasant  who  fell  from  a  tree,  sustaining  a  severe  bruise 
in  the  right  lumbar  region.  The  urine  contained  blood  for  several  days.  The  patient 
felt  deep-seated  pain  in  the  loin,  and  fever  set  in.  The  passing  of  blood  then  ceased, 
but  the  bruised  region  swelled  up,  and  fluctuation  became  evident.  An  incision  was 
made,  giving  exit  to  pus.     Recovery  followed. 

x^ppendicitis  is  fairly  often  a  cause  of  perinephritic  abscess,  either  by 
continuity  or  by  remote  infection  ;  the  Bacillus  coli  is  the  organism  usually 
present.     I  have  named  this  variety  "  appendicular  perinephritic  abscess." 

Suppurative  pancreatitis  has  been  noted  as  a  cause  of  perinephritic 
abscess. 

Primary  Perinephritic  Abscess. — I  shall  now  quote  two  cases  from  one 
of  my  clinical  lectures  :* 

I  saw  a  yoimg  girl  who  at  first  sight  appeared  to  be  suffering  from  typhoid  fever, 
the  temperature  being  104°  F.  The  chief  symptom  was  pain  in  the  left  lumbar 
region.  The  illness  had  commenced  a  month  before  with  lumbar  pain,  so  that  lumbago 
was  at  first  suspected.     The  suffering  soon  became  so  great  that  the  patient  could  only 

*  Clinique  Medicale  de  P Hotel- Dim,  1899,  8"«  lejon. 


1216  TEXT-BOOK  OF  MEDICINE 

walk  Tvitli  her  body  bent.  About  the  eighteenth  day  the  patient  felt  shooting  pains  in 
the  left  lumbar  region,  the  fever  became  severe,  and  vomiting  set  in  ;  this  condition 
persisted  until  her  admission  to'  hospital. 

Inspection  revealed  some  induration  in  the  lumbar  region,  which  was  evidently 
the  seat  of  the  mischief.  The  evolution  of  the  symptoms  led  to  the  diagnosis  of 
perinephritic  suppiiration.  The  abscess  was  primary,  since  no  cause  for  a  secondary 
abscess  was  present.  There  was  no  history  of  calculus,  tuberculosis,  pyelonephritis, 
appendicitis,  injury,  pleuro -pulmonary  infection,  or  furunculosis.  Accordingly  the 
most  Ukely  lesion  was  a  primary  perinephritic  abscess.  The  diagnosis  was  confirmed 
next  day.  The  urine  suddenly  became  turbid,  with  a  marked  deposit.  The  urinalysis 
showed  the  presence  of  pus,  and  the  exclusive  existence  of  the  Staphylococcus  aureus. 
The  abscess  had  opened  into  the  urinary  passages. 

Marion  operated.  In  front  of  the  quadratus  he  opened  an  abscess  cavity,  passing 
down  into  the  iUac  fossa,  and  upwards  into  a  long  track.  The  kidney  appeared  to  be 
of  normal  size.     The  pus  contained  the  Staphylococcus  aureus. 

After  transient  improvement,  pneumonia  appeared  on  the  left  side,  the  infection 
being  secondary  to  the  perirenal  mischief.  Shooting  pains  were  felt  in  the  hypogastrium, 
and  a  swelling  was  found  above  the  pubes.  This  abscess  was  opened,  the  pus  containing 
the  Staphylococcus  aureus.  The  fever  persisted  for  some  days ;  the  two  incisions  dis- 
charged some  pus,  and  showed  a  tendency  to  close  ;  but  the  pyuria  persisted.  Recovery 
finally  followed. 

A  man,  thirty-five  years  of  age,  was  admitted  for  pain  in  the  left  lumbar  region. 
It  had  come  on  suddenly  ten  days  before,  without  appreciable  cause,  and  was  so  acute 
that  the  patient  was  confined  to  bed.  On  admission  the  temperature  was  102^  F., 
the  tongue  dry,  and  the  lu'ine  scanty.  There  was  marked  tenderness  on  pressure  in 
the  loin  and  in  the  iHac  fossa.  The  muscular  resistance  rendered  abdominal  palpation 
difficult.  Within  the  next  few  days  the  loin  became  indurated,  and  som.e  swelling 
appeared.  I  diagnosed  primary  perinephritic  abscess,  because  there  was  no  history 
of  any  cause  for  a  secondary  abscess. 

An  operation  was  decided  upon,  when  a  new  incident  supervened.  The  urine 
suddenly  became  purulent.  At  the  same  time  the  temperature  fell  to  98°  F.,  the  pain 
diminished,  and  the  patient  felt  much  rehef.  The  abscess  had  evidently  opened  into 
the  urinary  tract.  It  was  impossible  to  say  whether  this  incident  meant  a  favourable 
ending  to  the  disease,  or  whether  the  suppuration  might  not  continue. 

The  patient  was  given  fluids  in  abundance.  The  pus  diminished  progressively, 
the  swelling  in  the  loin  disappeared,  and  the  pain  yielded.  The  patient  left  the  hospital 
cured. 

Description. — The  same  description  holds  good  for  primary  and  secondary 
abscesses.  The  initial  symptom  is  pain  in  the  loin  ;  its  situation  sunulates 
lumbago.  This  mistake  has  often  been  made.  The  patient  complains  of 
lumbar  pain.  Fever  rarely  appears  at  the  same  time  as  the  pain  ;  at  an 
advanced  period  it  is  acute,  and  accompanied  by  rigors.  Pain  and  fever, 
and  at  times  vomiting,  are  the  only  symptoms  at  the  onset  of  perine- 
phritic abscess.  Rigors,  swelling,  and  oedema  of  the  lumbar  region  appear 
later. 

The  course  of  the  abscess  has  been  well  described  by  Trousseau.  The 
patient  suddenly  feels  deep-seated  and  diffuse  lumbar  pain,  which  may  be 
acute  or  duU.  The  pain,  though  spontaneous,  is  always  made  worse  by 
pressure,  especially  bimanual  pressure.     The  pain  may  disappear  for  some 


DISEASES  OF  THE  KIDNEYS  1217 

weeks  or  months,  until  a  fresh  cause  brings  on  another  attack.  As  a  rule, 
however,  the  suft'ering  is  persistent,  and  increases  until  the  pus  is  let  out. 
This  pain  is  of  the  highest  importance,  because  for  a  considerable  period  it 
is  the  only  local  sign ;  certain  general  troubles  show  that  the  suffering 
depends  on  an  organic  cause  ;  the  fever  is  continuous,  and  an  evening  rigor 
often  occurs.  The  patient  loses  appetite  and  wastes  rapidly  ;  vomiting 
sometimes  occurs  at  the  onset  of  the  febrile  paroxysm,  and  obstinate  con- 
stipation is  nearly  always  present. 

"  For  a  week  or  a  fortnight  the  only  symptoms  are  local  pain,  general 
weakness,  and  fever,  with  a  daily  paroxysm.  Other  local  signs  of  deep 
inflammation  then  appear :  the  region  becomes  more  and  more  tender  on 
pressure,  and  more  or  less  extensive  induration  develops ;  at  the  same  time 
the  ilio-costal  hollow  is  effaced,  and  bimanual  palpation — the  patient  being 
in  the  dorsal  decubitus — reveals  a  deep  swelling  continuous  with  the  sub- 
cutaneous cellular  tissue.  The  tumour  does  not  move  with  respiration,  thus 
proving  that  it  is  independent  of  the  liver,  which  moves  up  and  down  on 
respiration.  The  induration  of  the  lumbar  region  is  often  accompanied  by 
oedema,  which  may  extend  to  the  dorsal  and  gluteal  regions  ;  the  skin 
may  be  slightly  reddened.  The  redness  is  erysipelatous  when  the  inflam- 
mation extends  to  the  cellular  tissue  "  (Trousseau). 

The  above  description  portrays  in  a  striking  way  the  onset  and  the 
evolution  of  the  perinephritic  abscess.  In  the  absence  of  surgical  inter- 
vention the  following  varieties  may  be  seen  :  (a)  The  suppuration  reaches 
the  subdiaphragmatic  cellular  tissue,  and  pleurisy  or  pneumonia  follows,  or 
the  pus  opens  into  the  bronchi.  Rupture  into  the  pericardium  has  been 
noted,  (b)  More  often  the  suppuration 'extends  into  the  iliac  fossa,  which 
becomes  painful,  and  a  swelling  appears  either  above  or  below  Poupart's 
ligament ;  in  the  latter  case,  the  pus  follows  the  sheath  of  the  vessels  and 
points  in  Scarpa's  triangle.  In  some  cases  the  pus  follows  the  sheath  of  the 
psoas  down  to  the  lesser  trochanter,  and  may  invade  the  hip-joint,  (c)  The 
suppuration  spreads  into  the  pelvis,  and  the  abscess  opens  into  the  bladder 
or  the  vagina.  (6)  Rupture  into  the  colon  is  followed  by  the  expulsion  of 
muco-purulent  or  bloody,  foul-smeUing  stools,  while  the  gas  from  the 
intestine,  entering  the  abscess  cavity,  may  produce  emphysema  of  the 
dorsal  region,  (e)  Rupture  into  peritoneum  is  exceptional,  a  fact  ex- 
plained by  the  distance  between  the  peritoneum  and  the  abscess,  which 
is  usually  behind  the  kidney.  (/)  Rupture  at  the  umbilicus  is  fairly 
common. 

Perinephritic  abscess,  then,  may  terminate  in  the  foregoing  ways.  The 
course  of  events  may,  however,  be  different.  The  invasion  may  be  marked 
by  repeated  attacks  of  pain  and  fever,  occurring  weeks  or  months  apart,  as 
though  the  first  attacks  were  followed  by  resolution.     In  other  cases  the 


1218  TEXT-BOOK  OF  MEDICINE 

symptoms  are  sudden  and  severe,  resembling  acute  septicaemia :  tlie  rigors 
are  violent,  tlie  temperature  is  mucli  raised,  the  sweating  is  profuse,  the 
diarrhoea  is  foetid,  the  abdomen  is  tjonpanitic,  the  pulse  is  bad,  delirium  is 
present ;  the  general  condition  becomes  alarming  in  a  few  days,  and  death 
may  result  unless  intervention  is  most  prompt. 

Diagnosis.— The  diagnosis  is  at  first  very  difficult,  especially  in  the 
primary  form.  The  secondary  form  is  not  so  difficult,  because  the  provoking 
cause  gives  valuable  information.  Let  us  suppose  an  injury  to  the  renal 
region.  Some  days  or  weeks  later  we  are  told  of  pain  at  the  injured  spot,  with 
rigors  and  fever ;  the  lumbar  region  becomes  very  tender  on  pressure,  and 
is  indurated  and  ^?rollen,  whUe  the  fever  increases.  Our  attention  being 
aroused  by  the  injury,  we  diagnose  an  abscess  in  process  of  formation.  Let 
us  suppose  that  a  patient  has  suffered  from  calculus,  with  renal  colic, 
hsematuria  and  pyuria,  pointing  to  pyelitis.  We  can  readily  diagnose  perine- 
phritic  abscess,  if  lumbar  pain,  rigors,  and  fever  appear,  and  are  followed  by 
tenderness  on  pressure  and  by  induration  in  the  loin.  The  same  remark 
applies  to  cases  of  perinephritic  abscess  secondary  to  appendicitis,  or  to 
other  well-known  causes. 

If,  however,  the  abscess  is  primary,  and  appears  when  the  patient  is  in 
good  health,  the  diagnosis  remains  obscure.  Our  only  guide  is  pain  :  as  the 
movements  of  the  trunk  are  painful,  the  muscles  are  hard  and  contracted ; 
we  suspect  lumbago,  and  order  rest,  massage,  cupping,  morphia,  and  anti- 
pyrin.  The  condition  remains  unchanged  for  several  days.  The  lumbar 
pain  is  the  chief  symptom,  and  examination  is  rendered  difficult  by  the 
muscular  contraction.  The  patient  complains  of  malaise,  insomnia,  and  loss 
of  appetite,  and  feels  that  there  is  something  more  than  lumbago  ;  he  suffers 
from  rigors  and  sweats,  vomiting  comes  on,  the  temperature  rises  to  102°  F., 
and  the  diagnosis  commences  to  be  obvious. 

The  situation  is  at  times  rendered  obscure  by  the  fact  that  the  patient 
is  prostrated  with  diarrhoea  and  epistaxis,  as  in  enteric  fever.  In  this  event 
the  lumbar  pain  and  the  fever  are  our  best  guide.  Bimanual  palpation  of  the 
loin  causes  intense  suffering.  The  fever  points  to  suppuration.  Blood 
examination  shows  marked  polynucleosis  :  20,000  to  30,000  polynuclear 
cells  in  place  of  6,000.  Sooner  or  later  the  painful  region  becomes  brawny 
and  oedematous,  and  the  diagnosis  of  perirenal  abscess  is  clear.  Immediate 
intervention  is  necessary,  and,  though  in  some  cases  recovery  may  follow 
spontaneous  evacuation  of  the  pus  by  the  urinary  tract,  we  must  not  trust 
to  this  event,  because  many  complications  may  occur. 


DISEASES  OF  TliK  KIDNEYS  1219 


XVIII.  HYDRONEPHROSIS. 

The  torrii  "  liydrouephrosis  "  is  applied  to  dilatation  of  the  caliccs  and 
of  the  pelvis  caused  by  accumulation  of  urine.  If  the  urine  becomes  purulent, 
the  term  "  pyoneplirosis  "  is  employed.  When  the  obstruction  to  the  flow 
of  urine  is  low  down  in  the  urinary  passages,  the  ureter  becomes  dilated. 
Hydronephrosis  in  the  footus  is  usually  double,  and  obstructs  delivery; 
it  is  dependent  on  a  congenital  malformation.  In  the  adult  hydronephrosis 
is  due  to  compression  of  the  ureter  by  a  tumour  of  the  bladder,  of  the  uterus, 
or  of  the  ovary. 

Cancer  of  the  uterus,  by  spreading  to  the  trigone  or  to  the  ureters,  pro- 
duces more  or  less  complete  obstruction  of  these  ducts  ;  the  obstruction  and 
the  resulting  anuria  are  sometimes  intermittent ;  hydronephrosis  may  result. 
Obliteration  of  the  ureter  due  to  the  migration  of  gravel  is  rarely  followed 
by  hydronephrosis. 

Pregnancy  is  a  cause  of  hydronephrosis.  The  enlarged  uterus  may  press 
upon  the  ureter,  especially  on  the  right  side,  bringing  on  dilatation  of  the 
ureter  and  of  the  pelvis.  Cruveilhier  found  marked  dilatation  of  the  ureters 
in  women  who  had  died  at  the  end  of  pregnancy  or  after  delivery.  If 
infection  occurs  during  delivery,  the  micro-organisms  carried  by  the  circula- 
tion infect  the  kidney,  which  is  in  a  state  of  receptivity  by  reason  of  the 
retention. 

Hydronephrosis  is  generally  unilateral.  Although  the  dilatation  may  be 
limited  to  one  of  the  calices,  it  is  usually  general,  the  kidney  being  flattened 
and  converted  into  a  pouch  containing  several  pints  of  fluid,  while  the 
remnants  of  the  kidney  tissue  have  undergone  fibrous  atrophy.  AVhen  the 
ureter  takes  part  in  the  dilatation,  it  may  be  as  large  as  a  coil  of  gut.  The 
fluid  in  hydronephrosis  contains  scarcely  any  of  the  elements  of  the  urine, 
but  it  is  often  albuminous,  and  in  some  cases  purulent,  the  infection  taking 
place  either  by  the  ascending  path,  or  by  the  blood-stream. 

Hydronephrosis  is  not  appreciable  until  the  tumour  reaches  a  certain 
size  ;  we  then  find  an  abdominal  tumour  that  can  also  be  felt  in  the  loin. 
The  tumour  may  be  fluctuating,  and  may  invade  the  neighbouring  regions 
in  every  direction.  The  diagnosis  is  difficult,  but  the  patient's  history  may 
be  of  value ;  thus  previous  renal  coKc  would  point  to  obstruction  by  a  calculus. 
Radioscopy  may  help  in  making  a  diagnosis.  The  prognosis  is  very  grave 
in  double  hydronephrosis,  on  account  of  the  risk  of  uraemia  ;  it  is  not  so 
serious  in  unilateral  hydronephrosis  as  long  as  the  other  kidney  is  healthy. 
The  treatment  is  surgical. 


1220  TEXT-BOOK  OF  MEDICINE 


XIX.  H^MATUEIA— CHYLUEIA. 

Haematuria  denotes  the  passage  of  blood  in  tlie  urine  ;  we  speak  of 
vesical  or  renal  haematuria,  according  as  the  lesion  is  situated  in  the  bladder 
or  in  the  kidney.  The  colour  of  the  fluid  passed  is  rosy,  reddish,  brownish, 
or  blackish,  according  to  the  amount  of  the  blood  passed  and  of  the  urine 
with  which  the  blood  is  mixed.  More  or  less  elongated  clots  float  in.  the 
liquid.  These  clots  may  form  a  mould  of  the  ureter,  being  8  or  10  inches 
in  length ;  in  their  passage  through  the  ureter  they  may  cause  renal  colic 
and  temporary  retention  of  urine.  I  shall  describe  secondary  haematuria  and 
essential  haematuria. 

1.  Secondary  Haematuria. 

Secondary  haematuria  may  be  associated  with  some  general  disease  or 
with  a  local  lesion  of  the  kidney. 

Hgematuria  in  General  Diseases. — Many  general  infections  may  cause 
the  kidney  to  bleed,  the  most  common  being  scarlet  fever.  In  some  cases 
variola,  measles,  purpura,  erysipelas,  and  er}i;hema,  assume  the  haemor- 
rhagic  form,  and  the  haematuria  is  simply  an  episode  in  the  general 
haemorrhagic  process.     Acute  rheumatism  may  cause  haematuria. 

This  form  of  haematuria  is  due  to  micro-organisms,  or  to  their  toxines. 
They  may  lead  to  haemorrhages  in  the  skin  and  the  mucous  membranes,  or 
from  the  kidneys.  The  renal  haemorrhage  is  nearly  always  associated  with 
nephritis. 

Haematuria  associated  with  Renal  Lesions.— In  the  preceding  sections 
on  tuberculosis,  cystSj  cancer,  and  Hthiasis  we  have  seen  that  any  one  of  these 
affections  may  give  rise  to  haematuria. 

Tuberculosis  of  the  kidneys  often  causes  haematuria,  the  blood  appearing 
at  the  onset  or  at  a  more  advanced  stage  of  the  lesion.  The  bleeding  is 
usually  slight,  of  short  duration,  and  independent  of  external  causes  (riding, 
driving,  or  exercise).  In  other  instances  it  is  so  severe  and  so  obstinate  as 
to  constitute  a  haemorrhagic  form  of  renal  tuberculosis. 

Cysts  of  the  kidney,  especially  polycystic  degeneration,  are  often  accom- 
panied by  haematuria.  The  bleeding,  though  usually  shght,  may  be  serious 
in  amount.  Of  aU  the  renal  affections  cancer  causes  the  most  copious 
bleeding  ;  the  haemorrhage  may  appear  early  or  late.  It  is  generally  profuse 
and  obstinate,  whether  the  kidney  is  or  is  not  enlarged. 

Renal  lithiasis  very  frequently  causes  haematuria.  The  stones  may  be  so 
small  as  to  produce  renal  colic,  or  so  large  that  they  remain  fixed  in  the 
kidney.  The  bleeding,  though  moderate  as  a  rule,  is  readily  brought  on  by 
shocks  or  exercise,  and  is  at  times  so  profuse  and  continuous  as  to  constitute 
a  haemorrhagic  form  of  renal  lithiasis. 


DISEASES  OF  THE  KIDNEYS  1221 

This  enumeration,  and  the  details  already  given  in  the  preceding  sections 
on  the  diseases  of  the  kidneys,  show  that  luematuria  is  a  symptom  of  but  little 
value  in  distinguishing  between  the  lesions  of  the  kidneys.  Profuse  and 
obstinate  haematuria  is  not  solely  the  appanage  of  cantsr,  because  it  is  also 
met  with  in  tuberculosis  and  in  lithiasis  of  the  kidney.  Haematuria,  with 
enlargement  of  the  kidney,  is  not  always  the  result  of  cancer,  since  we  also 
find  it  in  enlargements  of  the  kidney  due  to  perinephritis  or  to  cysts. 

Hematuria,  in  spite  of  its  abundance  and  its  obstinacy,  in  spite  of  the 
long  clots  which  accompany  it,  and  in  spite  of  the  size  of  the  kidney,  whether 
enlarged  or  normal,  may  give  no  hint  as  to  the  nature  of  the  renal  lesion 
producing  the  bleeding.  It  may  also  happen  that  the  haematuria  is  not 
associated  with  any  of  the  lesions  above  mentioned.  A  patient  may  have 
profuse  and  repeated  haematuria,  so  that  we  suspect  tuberculosis,  cancer, 
cyst,  or  calculus  of  the  kidney,  and  yet  the  patient  has  not  any  one  of  these 
diseases. 

Acute  and  chronic  nephritis  may  be  accompanied  by  haematuria,  but  it 
is  not  a  case  of  pure  haematuria  ;  the  urine  (apart  from  the  haematuria) 
contains  albumin,  and  the  usual  signs  of  nephritis  are  present. 

I  believe  that  the  haematuria  of  interstitial  nephritis  has  not  always 
been  correctly  interpreted.  According  to  my  observations,  haematuria 
considered  as  dependent  on  interstitial  nephritis  is  frequently  dependent 
on  tubercular  mischief.  The  nephritis  is  often  unilateral  and  amenable  to 
surgical  intervention. 

Pregnancy  is  sometimes  accompanied  by  haematuria,  due  to  congestion ; 
in  some  cases  nephritis  gravidarum  may  be  the  cause. 

Parasitic  haematuria  is  endemic  in  Brazil,  Cape  Colony,  India,  and  the 
islands  of  Maurice  and  Reunion.  It  occurs  chiefly  in  young  persons  under 
the  following  conditions  :  Sometimes  the  urine  becomes  bloody  without 
prodromata  being  present,  and  this  symptom  recurs  for  months  and  years 
without  afEecting  the  health  ;  at  other  times  the  haematuria  is  accompanied 
by  lumbar  pain,  fatigue,  and  anaemia.  In  many  instances  the  patient,  after 
passing  bloody  urine  for  some  days  or  weeks,  begins  to  pass  milky,  rose- 
coloured  urine  ;  this  is  called  chylous  haematuria.  The  urine  forms  three 
layers  in  the  test-glass  :  a  bottom  layer,  composed  of  blood  ;  a  middle  layer 
of  urine  ;  and  a  top  layer  of  the  chylous  matter.  The  urine  becomes  clear 
on  shaking  with  ether.  The  fat  is  present  in  the  form  of  an  emulsion,  and 
examination  of  the  blood  shows  that  it  does  not  contain  any  excess  of  fat. 
The  prognosis  is  fairly  good,  and  the  haematuria  may  disappear  if  the  patient 
emigrates  to  a  temperate  cUme. 

The  pathogenesis  of  chylous  haematuria  is  obscure.  BUharz,  Griesinger, 
and  other  writers,  have  shown  that  the  endemic  haematuria  of  hot  countries 
depends  on  the  presence  of  various  parasites  in  the  blood.     The  parasite 

n.  78 


1222  TEXT-BOOK  OF  MEDICINE 

in  Northern  and  Sonthem  Africa  is  a  distoma ;  in  Gruadeloupe  and  in  Brazil 
it  is  usually  a  strongylus.  The  parasites  are  said  to  cause  the  hsematuria  by 
producing  changes  in  the  mucous  membrane  of  the  urinary  passages.  In 
some  cases  the  parasite  has  been  found  in  the  blood  passed  fer  urethram. 

How  can  we  explain  the  chyluria  so  often  associated  with  the  hsematuria  ? 
Some  authorities  say  that  the  presence  of  the  chyle  is  due  to  changes  in  the 
red  corpuscles,  which  break  up,  and  allow  the  fat  to  escape  in  the  form  of 
granules.  Gubler  holds  that  the  chyluria  is  due  to  lymphatic  varices 
which  open  into  the  urinary  tract. 

The  distinction  between  vesical  and  renal  hsematuria  is  not  always  easy. 
In  case  of  doubt  cystoscopy  will  indicate  the  exact  origin  of  the  hsemorrhage. 

2.  Essential  Hsematuria. 

Essential  hsematuria  resembles  congestive  epistaxis,  which  supervenes 
without  appreciable  lesions  of  the  nasal  mucosa.  Essential  hsematuria, 
though  very  rare,  certainly  occurs,  as  the  following  example  shows  : 

A  patient,  twenty-eight  years  of  age,  who  had  no  previous  history  of  hsemophiUa  or 
of  tuberculosis,  was  taken  Ul  with  pain  in  the  right  lumbar  and  hjrpochondriac  regions 
during  an  attack  of  hsematuria,  which  had  lasted  for  six  months.  The  urine  had  always 
been  more  or  less  blood-stained ;  the  blood  was  intimately  mixed  with  the  urine,  and 
from  the  first  the  hsematuria,  instead  of  diminishing,  became  more  profuse.  The  renal 
pain  was  bilateral,  sUght,  and  transitory  on  the  left,  but  continuous  on  the  right  side. 
It  never  had  the  character  of  renal  cohc,  being  rather  a  feeling  of  heaviness  and 
painfulness  in  this  region.  No  ohguria,  no  gravel,  no  deposit  of  uric  acid  in  the  chamber. 
These  symptoms  were  quite  consistent  with  an  organic  lesion,  such  as  tuberculosis  or 
cancer.  Broca  found  that  the  right  kidney  was  neither  hypertrophied  nor  pushed 
down  ;  it  was  painful  on  pressure  in  the  costo- vertebral  angle.  Micturition  was  painless, 
frequent,  and  the  urine  always  contained  blood.  The  hsematuria  was  not  affected  by 
walking  or  by  jolting  in  a  carriage.  The  patient  looked  well,  and  had  not  lost  flesh. 
Rest  in  bed,  instead  of  improving  the  situation,  caused  a  reappearance  of  the  pain  and 
hgematuria.  The  urine  did  not  contain  Koch's  baciUi.  Broca  decided  to  operate. 
The  kidney  was  found  to  be  quite  normal ;  the  pelvis  and  ureter  were  normal.  Terrier 
and  Hartmann  examined  this  kidney  with  the  same  result ;  they  could  not  discover  any 
lesion.  It  was  considered  unnecessary  to  carry  the  operation  further ;  the  result  was 
most  satisfactory,  though  most  unexpected.  The  hsematuria  ceased,  and  the  patient 
when  seen  three  years  later  was  in  perfect  health. 

Broca,  in  his  work,  has  collected  seven  cases  which  in  various  ways 
resemble  his  own  case,  and  whether  we  speak  of  hsemophiha,  or  of  con- 
gestive vasomotor  troubles,  matters  very  httle.  The  interesting  and 
undeniable  fact  remains  that  persistent  and  copious  hsematuria,  with  or 
without  pains,  may  appear  independently  of  any  known  lesion,  and  may  be 
cured  by  surgical  intervention.  The  following  case  may  be  included  under 
this  variety  of  hsematuria  : 

Some  years  ago  a  boy  of  fifteen  years  of  age  came  into  the  Necker  Hospital  for 
hsematuria  of  two  years'  duration.     The  hsematuria,  of  renal  origin,  was  not  continuous  ; 


DISEASES  OF  THE  KIDNEYS  12i';i 

it  RoraotlmoB  oamo  on  without  apparent  cauao,  at  other  timos  aH  the  n^Hult  of  the  loaat 
o.vortion.  Ho  tdid  mo  that  ho  cuuld  not  stand  for  two  hours  without  his  urino  becoming 
blood-stainotl.  If  ho  took  a  short  walk,  tho  IjliMiding  appeared  ;  it  often  lasted  for 
Bbvoral  days  in  spito  of  rest.  Tho  persistent  hiemorrhago  had  made  the  patient  so  weak 
and  ana)uiic  that  ho  was  quite  prepared  to  undergo  any  operation.  Tho  kidneys  wore 
not  especially  tender,  and  I  found  it  impossible  to  formulate  any  pathogenic  diagnosis  ; 
Uthiaais,  tuberculosis,  and  cancer  wore  all  possible.  There  were  no  renal  colio  and  no 
tubercle  bacilh  ;  the  general  condition  was  not  such  as  a  cancer  of  long  standing  would 
have  caused. 

I  put  the  patient  on  turpentine  in  increasing  doses ;  tho  hseraaturia  disappearefl 
completely.  In  five  years  it  has  only  recurred  once.  After  two  years  and  a  half  of 
illness  the  cui'e  was  definite.  The  patient  can  now  take  long  walks,  and  work  standing 
throughout  the  day,  sometimes  doing  overtime  at  night.  His  health  is  excellent  in 
every  way,  and  there  has  not  been  the  slightest  reappearance  of  hsematuria.  He 
continues  to  take  turpentine.  These  oxami)le3  and  this  discussion  with  regard  to 
hasmaturia  prove  that  the  pathogenic  diagnosis  of  renal  haematuria  is  often  dilficult,  and 
at  times  impossible. 

XX.  HiEMOGLOBINUKIA. 

Description. — Hsemoglobinuria  is  a  false  hsematuria.  The  urine  in 
hscmoglobinuria  owes  its  colour  to  hsemoglobin,  and  never  contains  red 
corpuscles,  or  only  in  quite  an  insignificant  quantity — a  condition  very 
different  from  hsBmaturia,  where  the  blood  is  passed  in  its  natural  state. 

Hsemoglobinuria  is  only  a  sjTnptom,  but  it  shows  itself  in  such  various 
conditions  that  three  varieties  may  be  considered  :  (1)  Paroxysmal  or 
essential  hsemoglobinuria  ;  (2)  hsemoglobinuria  symptomatic  of  infectious 
diseases  ;    (3)  hsemoglobinuria  symptomatic  of  poisoning. 

Essential  hsemoglobinuria  (also  called  "  primary "  or  a  frigore)  was 
first  described  by  Harley  in  1864,  and  seems  to  constitute  a  definite  morbid 
entity.  In  consequence  of  a  chill,  an  individual,  otherwise  in  good  health, 
is  taken  ill  with  rigors,  malaise,  and  pain  in  the  loins  and  the  epigastrium. 
These  more  or  less  pronounced  phenomena  are  accompanied  by  a  rise  in 
temperature,  which  may  reach  to  102°  F.  During  these  attacks,  which  last 
from  six  to  eight  hours,  the  urine  gradually  becomes  darker.  The  urine  first 
passed  is  of  a  pale  red  ;  the  subsequent  discharges  are  the  colour  of  Bordeaux 
or  of  Malaga  wine.  After  the  attack  the  urine  gradually  loses  its  colour, 
and  some  hours  later  it  is  quite  normal. 

The  urine  is  albuminous.  The  microscope  reveals  no  red  corpuscles 
and  no  debris  of  corpuscles ;  the  spectroscope  reveals  the  two  fines  of  oxy- 
hsemoglobin.  The  transformation  of  these  two  bands  into  the  single  band 
of  reduced  hsemoglobin  may  be  observed.  In  some  cases  a  third  fine — the 
line  of  methsemoglobin — is  seen.  This  methsemoglobinuria  is  not  constant 
(Henocque).  The  urinary  deposit  is  formed  by  a  reddish  sediment,  com- 
posed of  granules  of  hsemoglobin,  of  casts,  and  of  epithehal  cells.  The 
examination  of  the  blood  made  during  the  attack  shows  a  delay  in  tho 

78—2 


1224  TEXT-BOOK  OF  MEDICINE 

formation  of  the  fibrinous  coagulum,  and  a  feeble  tendency  of  the  corpuscles 
to  form  rouleaux  (Hayem). 

At  the  moment  of  the  crisis  there  is  a  shght  increase  in  the  number  of 
white  corpuscles  and  a  notable  diminution  in  the  red  corpuscles.  Two 
days  later  haematoblasts  and  dwarf  corpuscles  appear.  The  study  of  the 
serum  will  be  discussed  under  Pathogenesis. 

Paroxysmal  hsemoglobinuria  is  especially  frequent  in  male  adults.  The 
attacks  may  occur  at  intervals  of  several  days,  or  even  of  several  months. 
Cold  favours  its  appearance,  whence  the  name  "  winter  hsemoglobinuria.," 
and  I  have  often  seen  Mesnet  bring  on  an  attack  in  his  patient  by  making 
him  go  into  the  hospital  garden  when  the  thermometer  stood  at  0°  G.  In 
addition  to  these  symptoms,  which  are  constant  during  the  attacks,  there 
are  others  which,  though  not  constant,  are  of  much  value  from  the  patho- 
genic point  of  view.  These  are  :  (1)  urticaria  and  purpura  ;  (2)  acute, 
painful,  and  temporary  swelUng  of  the  spleen  and  of  the  hver ;  (3)  a  sub- 
icteric  tint,  that  lasts  for  several  days  after  the  disappearance  of  the  other 
symptoms. 

The  attack  is  not  always  so  severe.  It  is  sometimes  characterized  by 
a  few  rigors,  lassitude,  and  sHght  albuminuria.  Side  by  side  with  these 
abortive  attacks  we  find,  on  the  contrary,  others  which  are  very  severe, 
and  it  is  especally  in  these  cases  that  we  see  the  foregoing  inconstant  symp- 
toms. After  the  attack  the  urine  is  normal ;  the  patient  is  more  or  less 
anaemic,  but  he  soon  regains  his  health,  and  never  becomes  cachectic.  Widal 
and  myself  have  seen  a  case  in  which  death  supervened  during  an  attack 
of  hsemoglobinuria. 

The  most  typical  form  of  hsemoglobinuria  due  to  infection  is  seen  in 
malaria,  when  it  is  known  as  "  hsemoglobinuric  fever."  It  appears  only 
in  those  who  have  lived  for  a  long  while  in  fever-stricken  countries.  The 
attack  is  most  frequently  preceded  by  a  shght  attack  of  simple  or  of  biUous 
fever.  The  duration  is  generally  twelve  to  thirty-six  hours.  Hsemo- 
globinuria  generally  appears  with  the  rigor  and  diminishes  with  the  de- 
fervescence. At  the  same  time  as  hsemoglobinuria  appears  we  find 
bihous  symptoms  of  much  severity,  characterized  by  vomiting,  bihous  stools, 
lumbar  pain,  jaundice,  and  bile  in  the  urine.  The  attack  may  be  shght  or 
severe,  and  it  may  end  in  collapse,  anuria,  or  uraemia.  In  the  opinion  of 
Kelsch  and  Kiener,  haemoglobinuria  in  this  case  always  indicates  rapid  destruc- 
tion of  the  red  corpuscles.  Jaundice  is  a  contingent  phenomenon,  resulting 
from  the  direct  action  of  the  malarial  organism  on  the  bihary  secretion. 

Haemoglobinuria  may  occur  in  the  ox  as  an  infectious  disease,  due  to 
a  bacterium,  described  by  Babes.     It  can  also  be  reproduced  by  experi 
mental  infections  in  the  laboratory.    It  has  been  noted  in  typhus,  scarlatina, 
and  perhaps  it  would  be  found  more  frequently  if  it  were  looked  for  in 


DISEASES  OF  THE  KIDNEYS  1225 

the  infectious  diseases  of  man.  The  introduction  into  the  system  of  certain 
vegetable  or  minoral  substances,  such  as  mushrooms,  carboUc  acid,  arseniu- 
retted  hydrogen,  chlorate  of  potash,  pyrogaUic  acid,  iodine,  and  glycerine, 
may  cause  so-called  toxic  hfomoglobinuria.  The  simple  injection  of  water, 
the  injection  of  dissolved  haemoglobin  or  of  bile  acids,  into  the  blood  of 
animals  also  causes  experimental  hajmoglobinuria.  Under  the  influence  of 
the  toxic  agent  the  haemoglobin  leaves  the  red  corpuscles  and  dissolves  in 
the  senim.  The  researches  of  Ponfick,  and  also  those  of  Marchand,  Lebe- 
deff,  and  Litten,  have  revealed  three  varieties  in  the  preliminary  hsemoglo- 
binaemia.  In  the  first  one,  the  haemoglobin  dissolved  in  the  blood  is  in  such 
small  quantity  that  it  is  destroyed,  and  does  not  appear  in  the  urine.  In 
the  second,  the  spleen  and  the  marrow  of  the  bones  contril)ute  to  change 
the  corpuscular  detritus  into  pigments.  In  the  third,  the  destroying  organs 
are  insufficient,  and  we  see  hoemoglobinuria,  with  jaundice,  and  oliguria,  or 
anuria  from  obliteration  of  the  tubules  of  the  kidney. 

Pathogenesis. — The  pathogenesis  of  malarial  and  toxic  hsemoglobinuria 
has  been  cleared  up  within  recent  year-s  by  means  of  anatomical  and  experi- 
mental research.  We  shall  see  how,  in  a  certain  degree,  it  may  help  us  to 
understand  the  disputed  mechanism  of  paroxysmal  hsemoglobinuria  a  frigore. 
In  malarial,  as  in  experimental,  hsemoglobinuria  we  find  a  phase  of  hsemo- 
globinuria followed  by  a  phase  of  renal  change. 

In  order  that  hsemoglobinuria  may  occur,  the  destruction  of  corpuscles 
must  correspond  to  about  a  sixth  of  the  total  mass  of  the  red  blood- corpuscles. 
It  must  be  rapid,  and  take  place  in  less  than  twenty-four  hours  at  the  most. 
The  renal  changes  are  due  to  the  excretion  of  the  pigment  by  the  tubuli 
contorti.  The  pigment  is  not  seen  in  Henle's  descending  loop,  in  the  straight 
tubules,  in  the  collecting  tubules,  or  in  the  glomeruli.  It  is  only  found  in 
the  epitheHum  of  the  convoluted  tubules  and  in  Henle's  ascending  loop. 
The  localization  simulates  that  of  colouring  substances  injected  into  the 
circulation,  as  in  Heidenhain's  well-known  experiment  with  indigo.  The 
cells,  infiltrated  by  the  indigo,  become  opaque ;  the  nuclei  and  the  divisions 
of  the  cells  are  no  longer  visible.  ,The  pigmentary  inundation  may  be 
such  that  in  the  interior  of  the  tubes  we  find  a  fine  granular  dust  of  the 
same  aspect  as  the  pigment,  sometimes  forming  large  masses  that  may  block 
the  canalicuh  and  cause  anuria. 

Two  theories  have  been  propounded  as  to  the  pathogenesis  of  paroxysmal 
hsemoglobinuria :  renal  congestion  and  primary  hsemoglobinsemia.  The 
renal  theory,  supported  in  France  by  Hayem  and  Robin,  rests  on  pure 
theory.  According  to  Robin,  it  is  due  to  local  congestion  in  the  kidney, 
assisted  by  disordered  nutrition,  consequent  on  rheumatism,  syphilis,  or 
malaria. 

The  partisans  of  the  second  theory  say  that  the  process  is  that  of  experi- 


1226  TEXT-BOOK  OF  MEDICINE 

mental  toxic  hsemoglobinuria.  Hsemoglobinsemia  is  said  to  be  tbe  initial 
phenomenon,  while  the  renal  change  is  secondary.  The  question  to  be  solved 
is,  then,  whether  in  an  attack  of  paroxysmal  haemoglobinuria  there  is  previous 
hsemoglobinsemia,  and  consequent  renal  lesion,  characterized  by  pigmentary 
infiltration  of  the  cells  of  the  convoluted  tubules.  If,  as  certain  writers  have 
maintained,  there  are  cases  in  which  the  serum  of  the  blood  presents  no 
changes,  there  are  other  authors,  such  as  Lepine,  Rodet  and  Salle,  Ehrhch, 
de  Cazal,  Boas,  and  Lichteim,  who  have  proved  hsemoglobinsemia  beyond  a 
doubt  by  collecting  blood  during  the  attack. 

The  often  quoted  experiment  of  Ehrlich  is  most  significant.  He  was 
able  to  reproduce,  apart  from  a  crisis,  alteration  of  the  blood  in  a  hmited 
zone.  He  plunged  a  finger  into  iced  water,  after  having  appUed  an  elastic 
hgature,  and  produced  a  circumscribed  hsemoglobinsemia  in  the  superficial 
capillaries, 

Hayem,  though  a  partisan  of  the  renal  theory,  admits  that  the  conges- 
tion of  the  kidney  must  be  assisted  by  a  change  in  the  blood.  In  his  opinion, 
the  cherry-red  colour  of  the  serum,  stated  to  be  characteristic  of  hsemoglo- 
binsemia, is  only  produced  after  the  blood  has  remained  some  time  in  vitro. 
It  is  said  to  indicate  that  the  blood  is  certainly  changed,  because  this  colora- 
tion of  the  serum  does  not  take  place  in  normal  blood.  If,  on  the  other 
hand,  we  shake  a  tube  four  hours  after  having  poured  some  blood  into  it, 
the  central  clot  is  completely  dissolved,  and  gives  a  red  colour  to  the  mixture 
■ — a  phenomenon,  says  Hayem,  not  observed  in  any  other  disease. 

The  previous  change  in  the  blood  (hsemoglobinsemia)  is  not  a  matter  of 
doubt,  but  in  order  to  know  whether,  during  an  attack  of  paroxysmal 
hsemoglobinuria,  the  renal  lesions  are  similar  to  those  seen  in  other  varieties 
of  hsemoglobinuria,  we  needed  a  post-mortem  examination,  where,  death 
having  occurred  during  the  attack,  we  could  observe  the  renal  lesion  at  the 
moment  when  the  hsemoglobinuria  began.  The  lacuna  has  been  filled  by 
a  unique  case  which  Widal  and  myself  were  fortunate  enough  to  observe  : 

A  woman  died  during  an  attack  in  the  Necker  Hospital.  At  the  autopsy  we  found  the 
entire  renal  cortex  of  a  marked  sepia  colour.  Under  the  microscope  the  glomeruU  were 
healthy  ;  the  cells  of  the  convoluted  tubules  and  of  Henle's  ascending  loop  alone  showed 
hsemoglobinic  infiltration ;  large  granules  of  haemoglobin  were  met  with  even  in  the 
lumen  of  the  tubules.  The  localization  corresponded  to  that  of  the  pigments,  previously 
dissolved  in  the  general  circulation,  and  eUminated  by  the  kidney,  in  the  well-known 
experiment  of  Heidenhain.  This  post-mortem  examination,  then,  furnishes  one  of 
the  proofs  which  the  hsemoglobinsemic  theory  lacked. 

What  is  the  cause  of  this  instabihty  of  the  blood  ?  Cold  or  fatigue 
seems  to  be  the  most  common  determining  cause,  but,  furthermore,  patients 
with  hsemoglobinuria  have  nearly  all  had  malaria  or  syphiHs.  One  of  my 
patients  had  suffered  from  both  these  diseases.  He  improved  on  the  mer- 
curial treatment  which  I  ordered. 


DISEASES  OF  THE  KIDNEYS  1227 

Donath  and  Landateiner  have  aliown  that  "  EhrUch'fl  experiment  of 
the  cold  finger  "  may  be  reproduced  in  vitro  with  the  plasma  from  a  case  of 
ha3moglobiiiiiria.  These  authors  mix  hunum  red  coquisclos  with  the 
serum  or  oxalate  plasma  collected  from  a  case  of  hsemoglobinuria  in  the 
interval  of  the  attacks.  They  subject  the  mixture  for  half  an  hour  to  a 
temperature  of  0°  C,  and  then  place  it  in  the  oven  at  'iV  C.  for  two  hours. 
They  find  after  this  treatment  marked  heBmatolysis,  but  when  the  mixture 
is  submitted  to  a  temperature  of  37°  C.  without  previous  cooUng,  the 
hcematolysis  does  not  occur. 

This  experiment  of  coohng  in  vitro  closely  reproduces  an  attack  of 
hoemoglobinuria  resulting  from  cold.  Widal  and  Rostaine  have  shown  that 
this  phenomenon  is  due  to  a  lack  of  the  anti-immune  body  which  the  blood 
normally  contains  in  order  to  protect  its  corpuscles  by  neutrahzing  the 
action  of  the  immune  body  which  it  constantly  carries.  If  the  red  cells 
remain  whole  in  their  own  proper  serum,  or  in  serum  from  an  animal  of 
the  same  species,  it  is  because  of  this  anti-immune  body,  which  is  powerless 
to  protect  them  against  a  strange  serum. 

Bordet  has  proved  the  existence  of  an  anti-immune  body  specific  for  the 
corpuscle  of  a  given  species  in  serum  from  animals  of  a  different  species, 
treated  with  injections  of  red  cells  or  serum  from  the  first  species.  Widal 
and  Rostaine  have  injected  horses  with  massive  doses  of  human  serum, 
obtained  by  bleeding  for  therapeutic  purposes.  In  the  serum  of  animals 
thus  treated  there  developed  an  anti-immune  body  specific  for  the  ambo- 
ceptor of  human  red  corpuscles.  These  authorities  have  shown  that  a  very 
minute  quantity  of  this  serum  heated  to  55°  C,  in  order  to  remove  its  cytose, 
and  added  to  the  plasma  of  a  patient  with  haemoglobinuria,  sufficed  to 
remove  its  power  of  affecting  human  red  corpuscles  after  exposure  to  cold. 
The  anti-immune  body,  by  uniting  with  the  immune  body,  which  was 
attached  to  the  corpuscles  by  the  action  of  cold,  has  thus  neutraUzed  this 
action. 

As  it  is  sufficient  to  add  to  the  plasma  of  a  patient  \vith  haemoglobinuria 
a  relatively  small  amount  of  the  anti-immune  body  in  order  to  prevent  the 
solvent  action  on  the  red  corpuscles  that  cold  produces,  it  was  natural  to 
see  whether  injection  of  the  anti-immune  body  would  not  prevent  an  attack 
a  frigore  in  man.  Widal  and  Rostaine  have  been  able,  by  means  of  large 
injections  of  their  horse  serum,  to  prevent  the  attack  a  frigore  in  haemo- 
globinuric  patients. 

The  protection  of  the  organism  varied  directly  with  the  dose  injected, 
and  for  a  given  dose  the  resistance  to  haemoglobinsemia  was  the  greater,  the 
less  severe  the  cold  and  the  less  prolonged  its  action.  So  far  in  human 
pathology,  serotherapy  has  only  furnished  results  in  diseases  due  to  micro- 
organisms and  toxines.     It  is  therefore  interesting  to  note  the  action  of 


1228  TEXT-BOOK  OF  MEDICINE 

serum  upon  a  humoral  trouble  such  as  hsemoglobinsemia.     We  can  in  this 

way  confer  but  a  transient  immunity,  lasting  some  three  weeks.  After  this 
period  it  is  necessary  to  inject  large  doses  of  serum  when  the  patient  is 
very  sensitiye  to  cold. 

Another  variety  of  hasmoglobinuria  occurs.  It  is  due  to  the  elimination, 
of  the  muscular  haemoglobin.  There  exists  in  muscle  a  special  haemoglobin, 
which  gives  it  its  red  colour.  In  these  cases  there  is  no  hagmoglobin- 
semia,  as  may  be  proved  by  examination  of  the  blood-serum.  This  is 
because  the  muscular  haemoglobin  passes  through  the  kidneys  far  more 
readily  than  the  corpuscular  haemoglobin  does.  Furthermore,  it  is  eliminated 
as  soon  as  it  is  set  at  hberty,  and  does  not  accumulate  in  the  blood.  As  with 
the  haemoglobin  of  the  red  blood- corpuscles,  the  freeing  of  the  haemoglobin 
in  muscle  is  caused  by  cold.  The  attack  is  accompanied  by  pain  in  the 
muscles,  which  may  cause  paresis  (Camus  and  Pagniez). 

Finally,  false  haemoglobinuria  may  follow  on  nephrorrhagia  or  cystor- 
rhagia.  The  red  corpuscles  are  dissolved  in  the  contents  of  the  bladder, 
and  the  proper  character  of  the  haematuria  then  disappears.  This  occurs 
in  certain  kinds  of  urine,  which  dissolve  the  red  corpuscles  with  great 
facihty.  We  then  speak  of  "  cythaemolytic  urine."  This  property  is 
especially  marked  in  watery  urine.  It  is  remedied  by  administering  chloride 
of  sodium  to  the  patient,  the  ehmination  of  which  increases  the  density  of 
the  urine,  and  transforms  false  haemoglobinuria  into  haematuria  (Camus). 

Patients  with  haemoglobinuria  must  avoid  cold  or  sudden  changes  of 
temperature,  and  hve  as  far  as  possible  in  temperate  climates.  These 
measures  will  at  least  prevent  the  attacks. 

If  the  patient  has  had  malaria,  we  should  give  quinine  and  arsenic. 
The  mercurial  preparations  should  be  reserved  for  syphilitic  patients. 


XXI.  MOVABLE  KIDNEY— COEXISTENT  UNILATERAL 
NEPHRITIS. 

Pathogenesis. — In  order  to  gain  a  clear  idea  of  displacements  of  the 
kidneys  we  must  first  consider  how  the  organ  is  fixed.  The  kidney  is  held  in 
its  normal  position  by  a  ceUulo-fibrous  envelope,  rich  in  adipose  tissue.  The 
kidney  is  buried  in  this  envelope,  to  which  it  adheres  by  fine  threads.  Accord- 
ing to  certain  writers,  the  fibrous  element  is  said  to  form  a  sort  of  trans- 
verse sheK,  ensheathing  the  kidney  in  front  and  behind,  and  uniting  below 
the  organ,  but  absent  inside  and  below.  It  is,  in  fact,  in  these  directions 
that  the  kidney  escapes.  In  its  migration  it  covers  itself  with  the  peri- 
toneum, which  it  pushes  in  front  of  it.  It  may  even  descend  very  low 
between  the  intestinal  coils. 

According  to  Trocart,  it  is  not  the  cellulo-fatty  envelope,  but  the  peri- 


DISEASES  ()¥  THE  KIDNEYS  1229 

toneum,  which  is  the  principal  obstacle  to  displacement  of  the  kidney. 
This  writer  lias  found  that,  in  order  to  draw  a  kidney  covered  by  its  peri- 
toneum downwards  or  forwards,  a  force  of  20  to  25  pounds  is  reciuired, 
whilst  the  resistance  of  the  cellulo-fatty  capsule  does  not  exceed  5  pounds. 

Renal  ectopia  (floating  kidney,  nephroptosis)  is  much  more  frequent 
in  women  than  in  men.  It  affects  the  right  kidney  more  often  than 
the  left,  and  rarely  both  kidneys.  Repeated  pregnancies,  tight  corsets, 
relaxation  of  the  abdominal  walls,  contusions,  strains,  and  absorption  of 
the  cellulo-fatty  layer  around  the  kidney,  have  been  assigned  as  causes. 
The  influence  of  sex  is  undoubted,  because  we  find  that  in  100  cases  of 
renal  ectopia  about  86  cases  occur  in  women.  The  right  kidney  is  displaced 
four  times  as  often  as  the  left  one.  As  to  pregnancy,  its  influence  has  been 
singularly  exaggerated,  since  in  94  cases  (Kiittner)  the  kidneys  were  dis- 
placed in  40  women  who  had  never  borne  a  child.  Glenard,  who  included 
nephroptosis  under  the  more  general  theory  of  enteroptosis,  supposes  that 
the  movable  kidney  is  a  digestive  syndrome.  Potain  thinks  that  the 
mobiUty  of  the  kidney  is  due  to  inflammatory  phenomena.  He  says  that 
displacements  of  the  kidney  by  sliding  are  the  most  common ;  they  are 
often  associated  with  muco-membranous  cohtis.  The  displacements  by 
anteversion  are  often  associated  with  bihary  Uthiasis. 

Pathological  Anatomy. — As  people  do  not  die  of  renal  ectopia,  the 
pathological  anatomy  is  based  upon  the  operation  findings.  In  a  thousand 
post-mortem  examinations,  made  in  different  diseases,  we  may  not  find  one 
case  of  movable  kidney  (Schultze).  When  the  kidney  is  much  displaced,  it 
may  be  found  in  the  iliac  fossa,  epigastrium,  or  hypochondria,  but  the  supra- 
renal capsule  never  accompanies  the-  kidney  in  its  displacement.  The 
kidney  is  sometimes  fixed  in  its  new  position  by  adhesions.  The  kidney 
may  be  cystic  or  cancerous.     It  is  sometimes  afiected  by  chronic  nephritis. 

Description. — Many  patients  have  a  displaced  kidney  without  being 
aware  of  the  fact ;  this  is  the  latent  form.  An  individual  complains  of 
dyspeptic  troubles,  belching,  or  abdominal  tympanites.  On  examination  we 
find  dilatation  of  the  stomach  and  of  the  colon,  and  also  a  movable  kidney. 
Another  individual  is  neurasthenic,  and  complains  of  vertigo,  hot  flushes, 
headaches,  loss  of  appetite,  weakness,  and  loss  of  flesh.  Examination 
reveals  a  displaced  kidney.  A  third  subject  has  discovered  a  tumour  in 
the  belly,  but  experiences  no  symptoms.  Examination  reveals  a  floating 
kidney.  In  these  various  cases  the  displaced  kidney  is  associated  with 
diverse  morbid  conditions,  without  causing  its  own  symptoms. 

The  floating  kidney  has  two  chief  symptoms — pain  and  abdominal 
tumour,  with  more  or  less  pronounced  general  troubles.  Renal  ectopia 
is  sometimes  sudden  in  its  onset.  In  consequence  of  fatigue  or  strain,  or 
even  without  appreciable  cause,  the  patient  is  taken  iU  with  acute  paiQ  in 


1230  TEXT-BOOK  OF  MEDICINE 

the  abdomen.  Tlie  usual  story  is  :  "I  fancy  that  something  has  got  loose 
in  my  inside."  The  kidney  may  be  replaced,  and  the  patient  is  cured.  This 
sudden  displacement  of  the  kidney,  sometimes  accompanied  by  a  tendency 
to  syncope,  may  be  of  traumatic  origin. 

In  other  cases  the  symptoms  come  on  gradually.  The  pain,  limited  to 
the  hypochondrium  or  to  the  lumbar  region  of  the  afiected  side,  is  often 
accompanied  by  a  feehng  of  weight  or  dragging.  The  pain  is  duU,  or  pulsa- 
ting like  an  abscess,  and  is  brought  on  by  walking,  riding,  or  exercise,  and 
reheved  by  the  horizontal  position.  Very  painful  attacks  may  supervene 
as  the  result  of  strain  or  of  menstruation.  They  are  accompanied  by 
rigors,  vomiting,  and  syncope  (Lancereaux).  Rest  in  bed  generally  puts  an 
end  to  these  attacks.  In  some  people  the  pains  simulate  hepatic  or  renal 
colic  ;  in  the  latter  event  they  radiate  to  the  ureter,  bladder,  loins,  or  thighs. 
Anorexia,  gastralgia,  gastro-intestinal  distension,  pyrosis,  eructations, 
nausea,  and  vomiting,  are  frequent  in  patients  with  movable  kidney.  The 
same  remark  appHes  to  the  neurasthenic,  hysterical,  and  hjrpochondriacal 
symptoms. 

The  displaced  kidney  forms  a  tumour,  which  can  be  felt  deep  under  the 
costal  margin  and  toward  the  lateral  part  of  the  abdomen.  This  tumour  is 
reniform,  painful  on  pressure,  and  generally  so  mobile  that  it  can  be  dis- 
placed in  aU  directions.  In  some  cases,  however,  the  kidney  is  fixed  by 
adhesions. 

Strangulation  of  the  Kidney. — I  must  now  refer  to  an  acute  compHca- 
tion  which  appears  in  the  following  manner  :  An  individual  with  a  displaced 
kidney  is  taken  suddenly  iU,  without  appreciable  cause,  with  symptoms 
resembling  acute  peritonitis.  Sharp  pains  in  the  beUy,  nausea,  vomiting, 
feeble  pulse,  cold  sweats,  abdominal  tympanism,  pinched  face,  and  syncope 
occur,  closely  simulating  the  picture  of  acute  peritonitis  caused  by  perfora- 
tion. The  first  thought  is  perforation  of  the  stomach  or  duodenum  by  an 
ulcer,  or  appendicular  peritonitis ;  but  a  more  careful  examination  reveals 
in  the  abdomen  a  mobile,  reducible,  and  painful  tumour,  which  is  the  dis- 
placed kidney.  The  organ  is  for  the  time  being  enlarged  by  hydronephrosis, 
which  is  a  compHcation  of  renal  strangulation.  The  attack  may  last  for 
several  hours  or  days,  with  intervals  of  cahn,  and  then  everything  again 
becomes  normal  if  the  patient  has  been  ordered  to  rest  in  the  horizontal 
position.  The  attack  ceases  suddenly  with  the  passage  of  abundant  urine 
and  the  disappearance  of  the  fluid  tumour  in  the  beUy.  Although  the  name 
"  renal  strangulation,"  invented  by  Dietl,  is  not  absolutely  true,  it  sums 
up  fairly  well  the  pathogenesis  of  the  troubles  due  to  torsion  of  the  ureter, 
with  intermittent  hydronephrosis  and  venous  stasis,  caused  by  temporary 
arrest  of  the  circulation  in  the  renal  vein.  These  attacks,  which  are  ex- 
tremely painful,  may  occur  frequently.     They  were  wcU  known  to  Trousseau, 


DISEASES  OF  THE  KIDNEYS 


12P.1 


wlio,  at  the  commencement  of  his  lecture  on  "  Movable  Kidney,"  gives  a 
description  to  which  nothing  remains  to  be  added. 

Tlie  diagnosis  of  renal  ectopia,  though  easy  in  some  cases,  may  present 
"much  difficulty.  Many  abdominal,  renal,  mesenteric,  hepatic,  and  ovarian 
tumours  may  simulate  a  displaced  kidney.  The  diagnosis  of  renal  strangula- 
tion  is  simplified  by  the  recognition  of  the  displaced  kidney  ;  we  must  always 
think  of  it  in  these  cases  of  pseudo-peritonitis,  which  simulate  appendicitis, 
internal  strangulation,  and  gastro-intestinal  perforations. 

The  prognosis  is  not  grave,  and  yet  its  indefinite  duration,  its  serious 
effect  on  the  system,  and  the  compUcations  that  it  may  cause  (nephritis), 
deserve  careful  consideration. 

Renal  Lesions  —  Albuminuria  —  Nephritis. — It  was  for  a  long  time 
beheved  that  the  composition  of  the  urine  was  not  affected  in  movable 
kidney.  A  floating  kidney  was  said  to  be  exempt  from  lesions.  These  ideas 
must  be  modified,  as  Tuffier  has  already  shown.  In  a  patient  with  movable 
kidney  albuminuria  is  fairly  common  (according  to  Schilhng,  in  14  per  cent, 
of.  the  cases).  The  presence  of  casts  is  sometimes  noticed,  in  addition  to 
albuminuria. 

I  had  a  woman  in  my  wards  with  symptoms  of  movable  kidney  at  the  fourth  month 
of  pregnancy.  After  her  confinement  she  was  attacked  by  puerperal  infection,  with 
phlebitis,  cystitis,  and  ascending  nephritis,  which  grafted  itself  on  to  the  movable  kidney 
{locus  minoris  resistentioe).  Three  months  later  the  patient  resumed  duty  as  infirmary 
nurse,  but  she  had  still  pains  in  the  right  loin  and  sUght  pyaemia.  It  was  interesting 
to  ascertain  the  composition  of  the  urine  from  each  kidney  ;  this  was  readily  done  with 
the  segregator.  The  analysis  of  the  quantity  of  urine  passed  in  twenty  minutes  was 
made  by  Gouraud : 

Right  Movable  Kidney.        Left  Kidney. 
180  minims      . .         360  minims 
1-0  grains         . .         4  grains 
I'O  grains  . .         5  grains 

abimdant  . .         notable 

absent  . .         absent 

absent  . .         absent 

numerous  . .         numerous 

numerous  . .         numerous 

numerous  . .         numerous 

abundant  . .         absent 


Quantity 

Urea  . . 

Chlorides 

Albumin 

Cells  from  the  kidney 

Casta . . 

Cells  from  the  bladder 

Red  corpuscles 

White  corpuscles 

Streptococci 


This  table  shows  that  the  activity  of  the  movable  kidney  is  diminished 
by  one-half,  and  that  it  is  from  this  kidney,  infected  by  the  streptococcus, 
that  nearly  aU  the  albumin  comes. 

The  researches  of  recent  years  have  shown  that  movable  kidneys  fairly 
often  show  shght  or  severe  lesions,  amounting  even  to  chronic  nephritis.  I 
have  discussed  this  unilateral  nephritis  in  Section  VI.  It  has  often  been 
noticed  by  surgeons,  particularly  by  Edebohls. 

The  medical  treatment  of  movable  kidney  has  as  its  object  the  main- 


1232 


TEXT-BOOK  OF  MEDICINE 


tenance  of  the  organ  in  position  by  appropriate  bandages.     Massage  may 
give  good  results.     Nephropexy  is  often  necessary.     This  operation  consists 
in  provoking  adhesions  between  the  kidney  and  the  abdominal  wall. 
Tuffier's  figures  read  : 


'Perfect  cure     . . 

. .     86 

Lasting  improvement    . . 

. .     25 

In  163  eases  - 

Satisfactory  results 

. .     24 

Temporary  improvement 

..       8 

Failures 

. .     20 

If  the  reader  wiU  refer  to  Section  VI.,  he  will  see  the  results  obtained 
by  Edebohls  in  cases  of  movable  kidney,  comphcated  with  nephritis.  In 
several  cases  the  ectopia  and  the  coexistent  nephritis  have  been  cured 
simultaneously. 


CHAPTER  II 
DISEASES  OF  THE  SUPRARENAL  CAPSULES 

ADDISON'S  DISEASE— DEFACED  TYPE  OF  ADDISON'S 

DISEASE 

Description. — Addison's  disease  is  characterized,  in  a  typical  case,  by 
marked  asthenia,  bronzed  colouring  of  the  skin,  pain,  and  gastro-intestinal 
troubles. 

Asthenia  is  generally  the  first  symptom,  and  has  a  special  character. 
It  is  characterized  by  muscular  weakness,  which  makes  every  efEort  im- 
possible, and  which  at  its  commencement  presents  the  pecuhar  feature  "  that, 
when  the  disease  is  primary  and  isolated,  it  is  not  accompanied  by  albu- 
minuria, hsemorrhage,  leucocytosis,  or  even  by  the  customary  diarrhoea  " 
(Jaccoud).  This  land  of  asthenia,  then,  is  very  different  to  cachectic 
asthenia. 

One  of  my  patients  repeated  incessantly  :  "  I  am  done  for ;  my  strength 
is  gone  ;  I  am  incapable  of  any  effort."  It  is  certain  that  the  patient 
reahzes  the  weakening  of  his  muscular  strength.  As  far  as  he  is  concerned, 
there  can  be  no  question  of  walking  or  riding.  At  a  more  advanced  period 
of  the  disease  any  movement  causes  absolute  horror.  Speaking  and  eating 
cause  fatigue.  The  patient  hes  down,  so  that  he  may  not  be  obhged  to 
move,  and  has  hardly  sufficient  strength  to  remain  standing.  There  is 
no  paralysis,  but  the  muscular  system  is  incapable  of  any  sustained  effort. 
If  the  patient's  first  attempt  registers  40  pounds  on  the  dynamometer,  the 
second  and  third  attempts  will  give  not  more  than  20  or  10  pounds.  A  fourth 
or  fifth  attempt  will  not  show  any  registration  at  all ;  his  muscular  strength 
is  exhausted.  One  of  my  patients  registered  a  force  of  80  pounds  at  his 
first  attempt,  but  his  fifth  and  sixth  efforts  only  registered  20  and  10  pounds. 
This  rapid  muscular  exhaustion  has  been  accurately  registered  by  means  of 
Mosso's  ergograph.  Several  of  these  charts  are  to  be  found  in  Dupaigne's 
thesis.  They  show  not  only  the  work  "  which  has  produced  the  fatigue, 
but  also  the  rapidity  and  the  form  of  this  fatigue." 

Tliis  muscular  weakness  is  due  to  the  suppression  of  the  function  of  the 
suprarenal  capsules.     Animals  after  the  removal  of  the  suprarenal  capsules 

1233 


1234  TEXT-BOOK  OF  MEDICINE 

become  intoxicated  by  their  mecliamcal  work.  Their  muscles  become  less 
and  less  capable  of  effort ;  but  if  suprarenal  extract  is  injected,  it  destroys 
in  part  the  muscular  toxines,  and  for  a  time  prevents  the  muscular  ex- 
haustion (Langlois), 

Pain. — The  pains  are  felt  in  the  epigastrium,  the  loins,  the  region  of  the 
kidneys,  the  hypochondrium,  the  limbs,  the  muscles,  and  the  joints.  They 
are  sometimes  very  severe,  being  lancinating  and  radiating  as  far  as  the 
groins  along  the  small  branches  of  the  ovarian  or  spermatic  plexus.  They 
may  simulate  the  gastric  crises  of  tabes,  mth  or  without  vomiting.  They 
remain  fixed  in  the  region  of  the  kidneys,  and  simulate  lumtcigo  ;  and  as 
they  cause  hjrpersesthesia  of  the  entire  beUy,  they  give  the  idea  of  peri- 
tonitis (Wurtz).  They  invade  the  muscles  and  the  joints,  just  as  rheu- 
matism does.  These  pains  generally  appear  after  the  onset  of  the  asthenia, 
In  some  cases,  however,  they  may  be  the  first  symptom  of  Addison's 
disease. 

Gastro-Intestinal  Troubles. — Anorexia,  vomiting,  and  diarrhoea  super- 
vene, either  from  the  commencement  or  during  the  course  of  the  disease. 
The  vomit  may  be  mucous,  as  in  alcohohsm,  or  it  may  consist  of  food- 
stuffs ;  it  may  be  uncontrollable  and  accompanied  by  gastralgia.  Diarrhoea 
is  a  frequent  symptom.  It  may  be  paroxysmal  or  continuous,  sometimes 
lasting  for  several  weeks.  It  disappears  and  reappears  without  interruption, 
especially  at  an  advanced  period  of  the  disease.  Loss  of  flesh  usually  super- 
venes from  the  first  in  Addison's  disease  ;  sometimes  it  is  rapid  and  con- 
siderable. 

Melanodermia. — Pigmentation  of  the  skin  is  very  rarely  the  initial 
symptom  of  Addison's  disease  (six  times  in  144  cases — Jaccoud).  Melano- 
dermia is,  as  a  rule,  preceded  by  asthenia,  pain,  and  gastro-intestinal  troubles. 
The  appearance  of  melanodermia  decides  the  diagnosis,  which  has  been 
previously  impossible  or  doubtful.  The  pigmentation  appears  at  first  on 
the  exposed  parts  of  the  body — ^the  face,  neck,  forearms,  dorsal  surface  of 
the  hands,  and  wrists — and  next  on  the  parts  normally  pigmented — the 
breasts,  the  genital  organs  (glans,  labia  minora),  the  groins,  and  the  axillse. 
At  first  the  skin  is  not  bronzed,  but  of  a  hght  slate  colour,  and  looks  dirty ; 
it  is  only  later  that  it  acquires  the  mulatto  tint.  Trousseau's  patient  ob- 
served that  for  some  three  months  his  hands  had  been  bistre -coloured  and 
dirty,  in  spite  of  repeated  washing.  His  face  had  a  smoky  look.  This 
brownish  tint  showed  itself  on  different  parts  of  the  body,  and  prolonged 
baths  caused  no  change.  At  first  the  discoloration  is  limited  to  brownish 
patches,  but  later  it  becomes  general,  and  resembles  the  complexion  of  the 
mulatto.  Darker  patches  sometimes  stand  out  on  the  uniform  background. 
There  are  sometimes  patches  where  the  pigment  is  entirely  absent  (vitiHgo). 
The  colouring  also  affects  some  of  the  mucous  membranes ;  the  lips,  gum^. 


DISEASI'iS  OF  THE  SUPRARENAL  CAPSULES  1235 

tongue,  palate,  and  internal  surface  of  the  cheeks  are  mottled  with  black 
patihos,  sucfi  as  are  seen  inside  the  mouth  of  certain  dogs. 

Course  of  the  Disease. — As  Trousseau  says,  the  onset  is  slow,  and  the 
disease  at  iirst  passes  unnoticed.  The  patient  cannot  fix  exactly  the  com- 
mencement of  the  symptoms.  There  is  general  malaise,  with  weakening  of 
the  physical  and  moral  forces.  The  appetite  grows  less,  the  digestion  is  dis- 
turbed by  uncontrollable  vomiting.  At  the  same  time  gastric  and  lumbo- 
abdominal  pain  supervenes.  Pigmentation  of  the  skin  soon  shows  itself. 
As  the  disease  progresses,  the  bronzed  tint  becomes  more  and  more  pro- 
nounced. Cachexia  appears,  prostration  becomes  extreme,  and  the  patient 
is  confined  to  bed,  unwilhng  to  move  and  refusing  all  food.  He  suffers  from 
irrepressible  vomiting,  with  continual  diarrhoea.  He  has  a  sensation  of 
vertigo,  fainting,  or  syncope,  and  complains  of  a  feehng  of  cold  in  the  hrabs, 
which  persists  in  spite  of  everything,  and  he  dies,  emaciated  to  the  utmost 
degree,  in  marasmus  or  coma. 

In  some  cases  Addison's  disease  has  a  rapid  course,  and  death  may 
supervene  in  a  few  weeks  or  months  (Starr).  Generally,  however,  its  course 
is  slower.  According  to  Ball's  statistics,  the  duration  was  less  than  a 
year  in  thirty-nine  cases,  and  in  thirty-nine  other  cases  it  was  more  than  a 
year.     In  any  event,  the  disease  ends  in  death. 

If  the  patient  is  attacked  by  secondary  or  primary  pulmonary  tuber- 
culosis, the  s}Tnptoms  of  tubercular  cachexia  are  added  to  those  of 
Addison's  cachexia,  the  loss  of  flesh  and  the  course  of  events  being  more 
rapid.  Addison's  disease  does  not  always  go  through  all  its  phases  without 
periods  of  arrest.  Remissions  of  longer  or  shorter  duration  may  occur. 
These  remissions  follow  as  the  result  of  absolute  rest,  and  cease  at  once 
as  soon  as  the  patient  resumes  his  ordinary  work. 

Sudden  Death. — Patients  with  Addison's  disease  do  not,  as  a  rule,  die 
suddenly ;  they  gradually  become  cachectic  and  die  of  marasmus  or  coma, 
the  pulmonary  and  suprarenal  lesions  helping  to  this  end. 

In  such  circumstances  death  is  not  unexpected,  and  the  physician  can 
foretell  the  fatal  termination.  In  some  cases,  however,  the  march  of  events 
is  different,  and  an  individual  with  Addison's  disease  is  suddenly  seized 
with  convulsions,  coma,  or  syncope,  and  death  rapidly  follows.  To  quote 
examples  : 

Hiller :  A  man  suffering  from  pulmonary  tuberculosis  had  also  an  anal  fistula, 
which  was  operated  on.  Next  morning  the  patient's  condition  was  good.  The  patient 
was  suddenly  seized  with  epileptiform  convulsions  and  loss  of  consciousness.  The 
con\Tilsive  attack  recurred  during  the  day,  and  the  patient  died.  At  the  post-mortem 
examination  a  few  tubercles  were  found  at  the  apices  of  the  lungs.  All  the  other  organs 
were  normal,  ■with,  the  exception  of  the  suprarenal  capsules,  which  showed  tubercular 
degeneration.  The  patient  had  no  bronzed  tint.  (The  case  is  an  example  of  the 
defaced  type.) 


1236  TEXT-BOOK  OF  MEDICINE 

Chauflfard ;  A  lady,  thirty-five  years  of  age,  had  all  the  symptoms  of  Addison's 
disease  :  the  asthenia  was  so  great  that  she  could  not  drive  in  a  carriage  without  fatigue  ; 
the  patient  passed  her  days  stretched  out  on  a  long  chair,  incapable  of  the  least  muscular 
movement ;  the  pigmentation  was  typical.  Without  warning  the  patient  was  seized 
with  angina,  pain,  and  acceleration  of  the  pulse  to  160,  and  she  succumbed,  intoxicated 
by  the  toxine,  acting  here  "  like  curare,  and  causing  paralytic  tachycardia." 

Letulle :  A  man,  twenty-eight  years  of  age,  who  for  some  weeks  had  felt  great 
lassitude  and  depression,  was  admitted  to  St.  Antoine  Hospital.  His  skin  was  of  an 
earthy  colour  ;  this  was  ascribed  to  an  old  attack  of  malaria.  The  examination  revealed 
a  suspicious  tubercular  lesion  at  the  left  apex.  Nine  days  later,  without  apparent  cause, 
death  supervened  suddenly,  just  as  the  patient  was  about  to  sit  up.  The  post-mortem 
examination  showed  that  each  suprarenal  capsule  was  transformed  into  a  fibro-caseous 
block  of  the  size  of  a  small  tangerine  orange.  The  man  had  died  suddenly  of  Addison's 
disease. 

Sudden  death  has  been  noted  in  children,  who  may  also  suffer  from 
Addison's  disease.  With  regard  to  this  point,  Variot  relates  the  following 
case  : 

A  thin  httle  girl,  fourteen  years  of  age,  was  admitted  into  the  Trousseau  Hospital 
for  weakness  and  a  tired  feehng  in  the  legs.  Her  uncle  was  said  to  have  noticed  that 
the  skin  had  been  getting  brown.  The  hyperpigmentation  of  the  skin  was,  in  fact, 
general.  Addison's  disease  was  diagnosed.  One  morning  the  child  got  up  to  use  the 
chamber  ;  she  got  back  to  bed,  became  pale,  and  died.  At  the  post-mortem  examination 
miHary  tubercles  were  found  in  both  lungs.  Both  suprarenal  capsules  were  enlarged, 
and  converted  into  tubercular  tissue. 

These  cases  show  that  Addison's  disease  may  terminate  in  sudden 
death.  This  sudden  ending  may  happen  in  the  cachectic  stage,  or  at  a 
period  of  the  disease  when  nothing  could  have  caused  it  to  be  foreseen. 

I  consider  it  important  to  mention  that  sudden  death  has  been  noted 
several  times  in  Addison's  disease  of  the  defaced  type,  where  the  patient  had 
no  bronzed  tint.  The  importance  of  these  cases  will  be  apparent  from  the 
medico-legal  point  of  view.  An  individual  dies  suddenly,  and  as  the  bronzed 
tint  is  wanting,  attention  is  not  called  to  the  nature  of  the  disease.  The 
post-mortem  examination  reveals  the  fatal  lesion  in  the  suprarenal  capsules. 

Defaced  Type. — In  one  of  my  chnical  lectures*  I  proposed  the  name 
defaced  for  cases  of  Addison's  disease  in  which  pigmentation  of  the  skin  and 
of  the  mucosae  was  absent.  I  quote  the  case  upon  which  the  lecture  was 
based : 

In  January,  1898,  a  youth  of  seventeen  years  of  age  came  into  my  wards  very  much 
exhausted.  He  understood  the  questions  put  to  him,  but  his  answers  were  slow  and 
difficult.  He  awoke  from  his  somnolence,  as  it  were,  with  regret,  and  fell  back  into  it 
again  as  soon  as  I  ceased  questioning  him.  I  was,  nevertheless,  able  to  obtain  some 
information.  He  had  come  to  the  hospital  for  extreme  lassitude.  He  was  not 
paralyzed,  but  the  shghtest  movement  was  an  effort.  He  was  pale,  remarkably  thin, 
motionless,  and  lay  in  his  bed  Mke  a  dying  man. 

The  patient  gave  the  following  history ;    Six   months   previously   he    began    to 

*  "  Forme  Fruste  de  la  Maladie  d' Addison  "  (Clinique  Medicale  de  VHotd-Dieu,  1898, 
9"^  lejon). 


DISEASES  OF  THE  SUPRARENAL  CAPSULES  1237 

cough  ;  no  fever,  no  hreraoptysis  ;  rapid  loss  of  flesh  and  extreme  weakness.  At  the 
Tonon  Hospital  tuborculur  bronchitis  was  diagnosed.  After  a  fortnight's  treatment 
the  patient  returned  homo.  The  cough  was  almost  gone,  but  his  strength  was  gradually 
faiUng ;  he  was  so  tired  that  ho  never  wished  to  leave  his  bcni.  This  condilitjn  of 
weakness  and  of  loss  of  flesh  became  still  more  pronounced  during  tlio  fortnight  preceding 
his  admission  into  my  wards.  There  was  no  other  symptom  to  be  noticed  excepting 
sUght  vomiting  of  food. 

It  was  necessary  to  make  a  diagnosis.  The  signs  of  pulmonary  tuberculosis  were 
xmdeniablc,  but  the  tubercular  lesion  was  not  sufficient  to  account  for  the  asthenia  and 
lassitude.  The  clinical  picture  was  not  that  of  early  phthisis.  Diabetes  sometimes  causes 
similar  symptoms,  but  the  patient  was  not  diabetic.  All  the  organs,  with  the  exception 
of  the  lungs,  were  healthy  ;  the  skin  showed  no  patches  and  no  eruption  ;  and  wo  were 
perhaps  face  to  face  with  comphcations  such  as  meningeal  or  miliary  tuberculosis.  The 
prostration,  vomiting,  constipation,  and  retraction  of  the  abdomen,  were  in  favour  of 
meningitis ;  but  meningitis,  even  supposing  it  were  present,  would  not  have  accounted 
for  the  progressive  asthenia,  which  in  six  months  had  ended  in  marasmus.  The 
following  morning,  the  situation  remained  the  same.  At  eleven  o'clock  in  the  morning 
he  took  a  glass  of  milk,  and  fell  back  again  into  his  apathy.  At  half-past  two  o'clock 
the  nurse  on  duty  foimd  liim  dead. 

The  results  of  the  post-mortem  examination  were  quite  a  surprise.  At  the  apices 
of  the  lungs  the  ordinary  tubercular  lesions  were  met  with.  The  brain,  liver,  kidneys, 
and  spleen  were  absolutely  healthy,  but  both  suprarenal  capsules  were  enlarged  and 
converted  into  tuberculo-caseous  tissue.  Thej'^  were  superimposed  on  the  kidneys  like 
large  mushrooms.  The  left  suprarenal  capsule  was  hypertrophied,  indurated,  and 
calcareous,  with  soft  points  ;  the  lower  portion  was  much  harder,  of  a  golden  yellow 
colour,  and  had  undergone  cretaceous  change.  The  right  suprarenal  capsule  was  like- 
wise transformed  into  tuberculo-caseous  tissue  ;  it  was  indurated  and  calcified  in  places. 

As  the  post-mortem  examination  showed  that  the  patient  had  died  of  Addison's 
disease, we  searched  with  the  greatest  care,  both  on  the  skin  and  on  the  mucosae,  for  some 
traces  of  pigmentation.  There  were  none  at  all.  The  disease  had  been  defaced.  Other 
examples  are : 

Lancereaux  :  A  woman  who  had  been  ill  for  a  month  with  vomiting  and  loss  of  flesh 
came  to  the  hospital  in  a  condition  of  complete  prostration.  Vomiting  and  weakness 
were  the  chief  symptoms.  The  patient  was  so  weak  that  she  would  not  even  move 
in  her  bed,  and  was  afraid  of  changing  her  position.  The  skin  was  normal.  The 
urine  contained  neither  sugar  nor  albumin.  The  patient  succumbed.  At  the  post- 
mortem examination  three  httle  tubercular  masses  were  foimd  at  the  apex  of  the  left 
limcr.  The  suprarenal  capsules  were  hard,  indiu-ated.  yellowish,  and  tuberculo-caseous. 
Death  was  due  to  Addison's  disease,  which  had  caused  no  melauodermia. 

Carpentier  :  A  man  within  six  months  had  grown  so  thin  and  weak  that  he 
lay  motionless  on  his  bed,  except  when  he  took  a  Uttle  food.  The  urine  contained 
neither  sugar  nor  albumin.  The  temperature  was  normal.  The  successive  examina- 
tion of  the  various  organs  gave  ordy  negative  results.  There  was  no  pigmentation.  For 
a  fortnight  no  change  was  noticed.  One  morning  he  experienced  a  feeling  of  distress 
and  cold.  Half  an  hour  later  the  pulse  became  thready,  the  extremities  grew  cold,  and 
the  patient  died,  remaining  conscious  until  the  very  end.  The  post-mortem  examina- 
tion revealed  old  tubercular  foci  at  the  apex  of  the  lungs.  The  suprarenal  capsules  were 
attacked  by  tuberculosis.  The  skin  and  mucous  membranes  were  examined  most 
carefully,  but  no  trace  of  pigmentation  could  be  found.  It  was  a  case  of  Addison's 
disease  without  melanodermia. 

Diagnosis. — It  is  quite  impossible  to  diagnose  Addison's  disease  before 
the  appearance  of  melanodermia.     The  character  of  the  muscular  asthenia 


1238  TEXT-BOOK  OF  MEDICINE 

furnislies  a  strong  presumption  in  favour  of  Addison's  disease,  especially  if 
gastric  troubles  and  pains  are  also  present.  The  appearance  of  melano- 
dermia  decides  the  diagnosis,  for  the  syndrome  is  then  complete  ;  and  yet, 
when  melanodermia  occurs  in  an  anaemic  or  neurasthenic  patient,  we  must 
not  diagnose  Addison's  disease  before  making  a  careful  examination.  Some 
syphiUtic  patients  (women  especially)  show  in  the  secondary  period  a  pig- 
mentation of  the  skin  of  the  neck  (pigmentary  syphihdes),  and  sufier  from 
muscular  weakness.  In  malarial  cachexia  the  pigmentation  of  the  skin  is 
less  pronounced,  the  patches  on  the  mucosae  are  wanting,  the  spleen  is 
hjrpertrophied,  and  the  causes  of  the  disease  are  known.  Patients  who  have 
been  treated  for  a  long  time  with  nitrate  of  silver,  either  through  the  diges- 
tive passages  or  by  injections,  have  sometimes  an  indehble  bluish  tinge, 
which  is  especially  marked  on  the  face  and  hands,  since  they  are  exposed  to 
the  hght.  In  bronzed  diabetes  there  is  a  lesion  of  the  hver,  and  more  or 
less  abundant  glycosuria.  In  the  defaced  forms  of  Addison's  disease  the 
diagnosis  presents  the  greatest  difl&culty. 

AddisoD's  disease  must  not  be  confounded  with  vagabond's  itch,  in 
which  the  pigmentation  is  due  to  Pediculi  corporis,  and  affects  the  parts  in 
contact  with  the  clothes.  The  presence  of  the  parasites  and  the  scratch- 
marks  give  the  diagnosis.  The  diagnosis  may,  however,  be  difficult  on 
account  of  the  pigmentation  of  the  buccal  mucous  membrane  that  sometimes 
occurs  in  vagabond's  itch.  In  such  a  case,  however,  asthenia,  gastro- 
intestinal troubles,  pain,  and  low  arterial  tension  are  absent. 

In  Addison's  disease  the  pseudo-peritoneal  symptoms  sometimes  simu- 
late appendicitis. 

Pathological  Anatomy. — The  essential  lesions  of  Addison's  disease  are 
seated  in  the  suprarenal  capsules  and  in  the  neighbouring  nerve  plexus. 
The  nature  of  the  lesion  matters  httle ;  the  important  point  is  the  seat  of 
the  lesion.  In  fact,  the  changes  of  the  capsules  are  very  diverse.  Tuber- 
cular lesions  are  the  most  common ;  then  come  cancer,  suppuration,  cystic 
degeneration,  the  echinococcus,  and  fibrous  suprarenalitis.  The  lesion  is 
almost  always  bilateral.  The  capsules  are  often  hypertrophied  and  adherent 
to  the  neighbourmg  organs.  In  tubercular  degeneration  they  are  mammil- 
lated,  and  their  substance  is  converted  into  a  lardaceous  mass,  showing 
opaque  yellowish  portions,  tubercular  granulations,  caseous  and  cretaceous 
masses,  and  islets  or  bands  of  connective  substance.  In  a  certain  number 
of  post-mortem  examinations,  lesions  of  the  semilunar  gangha  and  of  the 
solar  plexus  (sclerosis  and  fatty  degeneration)  have  been  noted.  The 
melanodermia  is  due  to  accumulation  of  pigment  in  the  corpus  mucosum. 

iEtiology — Pathogenesis. — Addison's  disease  is  most  frequent  between 
the  ages  of  twenty  and  forty  years.  It  is  sometimes  primary,  and  super- 
venes in  the  midst  of  good  health.     Sometimes  it  is  secondary,  and  super- 


DISEASES  OF  THE  SUPKAPtENAL  CAPSULES  1239 

VL'iies  ill  a  patient  who  is  already  tubercular.  In  a  case  reported  by 
Jacquet  and  Sezary  the  lesion  was  syphilitic,  many  treponemata  being 
I)rc'sent  in  each  suprarenal  capsule.  In  any  case,  the  syndrome  ot"  Addison's 
disease  does  not  answer  to  any  one  lesion  of  the  suprarenal  capsules. 
The  essential  factor  is  that  the  suprarenal  region  must  be  affected.  The 
lesion  is  usually  tubercular,  but  it  may  be  malignant  or  librous. 

The  patliogenesis  of  the  disease  may  be  stated  thus  :  Brown-Sequard, 
Abelous,  and  Langlois  have  proved  that  complete  extirpation  of  both  supra- 
renal capsules  in  the  frog,  guinea-pig,  or  dog,  causes  death  in  a  few  days. 
If  only  a  sixth  part  of  the  suprarenal  capsules  Ls  left,  this  part  is  sufficient 
to  carry  on  the  function,  and  the  animal  may  not  die.  The  animal,  after 
complete  extirpation  of  the  capsules,  succumbs  after  suffering  rapid  loss  of 
strength,  similar  to  the  muscular  asthenia  of  Addison's  disease. 

It  is  a  question  of  toxic  symptoms.  The  deficiency  or  the  suppression 
of  the  suprarenal  function  allows  the  accumulation  of  a  poison  in  the  blood. 
This  toxine  is  identical  with  the  toxine  obtained  from  the  muscles  of  an  over- 
worked animal,  and  seems  to  have  the  efifect  of  curare.  It  attacks  the  motor 
nerve  endings  (fatigue  and  muscular  paresis,  rapid  exhaustion  of  the  motor 
excitability).  It  may  even  involve  the  cardiac  nerves,  and  cause  paralytic 
tachycardia  (Chauffard).  The  suprarenal  capsules  have,  then,  an  antitoxic 
action  upon  the  waste  products  of  muscular  combustion,  neutralizing  or  de- 
stroying the  poisons  of  the  curare  type  that  are  elaborated  during  muscular 
work.     They  belong  to  the  group  of  glands  having  an  internal  secretion. 

Most  of  the  symptoms  of  Addison's  disease,  including  the  grave  and  fatal 
symptoms,  are  due  to  suprarenal  insufficiency,  to  the  resulting  auto-intoxica- 
tion, and  to  the  nature  of  the  toxines,  which  are  no  longer  neutraHzed  or 
destroyed  when  the  suprarenal  function  is  suppressed  (experiments  on 
animals),  or  when  the  function  is  destroyed  by  lesions  (tuberculosis,  cancer, 
fibroid  and  calcareous  changes,  or  abscess). 

The  melanodermia  has  still  to  be  explained.  It  is  said  to  be  due,  not  to 
the  suprarenal  insufficiency,  but  to  the  nervous  lesions  of  the  plexus  around 
the  capsules  (Jaccoud,  Alezais,  and  Arnaud).  Melanodermia  is  said  to  be 
absent  when  the  lesion  is  confined  to  the  interior  of  the  gland.  It  is  said 
to  appear  when  the  lesion  involves  the  gangUa  and  the  nerve  plexus  in  the 
fibrous  covering  of  the  suprarenal  capsule.  It  will,  therefore,  be  understood 
that  a  lesion  may  attack  either  the  gland  or  the  nerve  plexus.  Lesions  of 
the  nerve  plexus  without  direct  lesions  of  the  gland  might  reproduce  the 
sjmdrome  of  Addison's  disease,  as  the  glands  only  function  definitely  through 
their  nerves  (Caussade). 

Treatment. — Hygiene  occupies  a  prominent  place  in  the  treatment  of 
Addison's  disease.  A  few  days  of  complete  rest  are  sometimes  sufficient 
to  make  a  patient  recover  who  appears  to  have  reached  an  advanced  state 

79—2 


1240  TEXT-BOOK  OF  MEDICINE 

of  asthenia.  The  most  approved  line  of  treatment  consists  in  supplementing 
the  insufficiency  by  giving  suprarenal  extract.  Brown-Sequard  deserves 
the  highest  credit  as  the  pioneer  in  this  branch  of  therapeutics.  Supra- 
renal insufficiency  causes  symptoms  of  auto-intoxication  in  much  the  same 
way  as  thyroid  insufficiency  causes  an  auto-intoxication.  The  introduction 
of  thyroid  extract  into  the  system  has  an  extraordinary  effect  on  myxoedema. 
It  was,  therefore,  reasonable  to  hope  that  the  introduction  of  suprarenal 
extract  into  the  system  would  give  good  results. 

The  first  attempts  in  this  direction  were  not  encouraging  (Abalous, 
Langlois,  Charrin,  and  Chauflard).  Several  cases  have  since  been  pubhshed 
(Beclere,  Dupaigne,  Gilbert,  and  Marie).  I  made  use  of  this  remedy  in  the 
following  case  : 

A  man,  twenty-nine  years  of  age,  was  admitted  into  my  wards  on  Jime  14,  1895, 
for  muscular  exhaustion,  preventing  any  efiort.  The  muscular  asthenia  began  four 
months  after  the  military  manoeuvres.  Three  months  before  admission  vomiting  and 
pain  appeared,  and  soon  after  diarrhoea.  The  vomit  contained  bile  and  food-stuff ; 
the  vomiting  recurred  several  times  daily  for  several  weeks.  The  pains  were  very  sharp 
in  the  epigastric  region,  in  the  hypochondria,  and  in  the  calves  of  the  legs.  The  diarrhoea 
had  been  continuous  for  several  days — up  to  twelve  and  fourteen  stools  a  day.  The 
patient  was  very  thin.  On  looking  at  him  we  were  immediately  struck  with  the  bistre 
colour  of  his  face,  neck,  forearm,  and  the  dorsal  surface  of  his  hands.  There  were 
pigmentary  patches  on  the  lower  Umbs.  We  also  fotmd  bronzed  patches  on  the  buccal 
mucosa,  on  the  velum  palati,  and  behind  the  labial  commissure.  The  patient  told  us 
himself  that  during  the  past  few  months  his  skin  had  "  become  the  colour  of  ginger- 
bread." 

It  was  a  case  of  Addison's  disease.  We  had  still  to  discover  the  nature  of  the  lesion 
in  the  suprarenal  capsules.  As  the  left  subspinal  fossa  showed  some  signs  of  early 
tuberculosis,  it  was  evident  that  the  suprarenal  capsules  were  invaded  by  tuberculosis. 
An  injection  of  1  c.c.  of  glycerinated  suprarenal  extract  was  administered  every  other 
day.  The  symptoms  rapidly  improved  ;  the  vomiting,  pain,  and  diarrhoea  disappeared. 
The  appetite  was  excellent,  and  the  muscular  asthenia  diminished  so  much  that  the 
patient,  who  during  his  first  days  in  hospital  could  not  leave  his  bed,  now  helped  to 
clean  the  floors.  He  asked  to  be  discharged.  He  returned  three  months  afterwards 
in  a  state  of  muscular  asthenia  more  pronounced  than  on  his  first  visit.  He  was  carried 
on  a  stretcher.  The  vomiting,  diarrhoea,  and  pains  had  reappeared,  the  bronzed  tint 
had  increased,  and  the  loss  of  flesh  was  so  great  that  the  patient  only  weighed  110  poimds. 
The  signs  of  pulmonary  tuberculosis  were  unchanged,  and  bacilh  were  found  in  the 
sputum.  I  again  prescribed  suprarenal  extract,  but  in  view  of  threatening  lymphangitis 
I  replaced  the  injections  by  capsules,  each  capsule  containing  IJ  grains  of  dried  supra- 
renal gland.  Four  capsules  were  administered  daily.  The  improvement  was  even 
more  rapid  than  on  the  first  occasion,  all  the  symptoms  yielding  in  a  few  days.  The 
patient  put  on  flesh  visibly,  gaining  20  pounds  in  a  month.  He  again  left  the  hospital 
and  resumed  his  work,  but  he  was  obhged  to  come  back  on  December  5,  for  the  same 
symptoms ;  he  only  weighed  106  poimds.  For  a  third  time  the  treatment,  to  which 
large  doses  of  cod-liver  oil  were  added,  caused  the  symptoms  (except  the  pigmentation) 
to  disappear,  and  tAvo  months  and  a  half  later  the  patient,  who  had  regained  his  strength, 
weighed  125  poimds.  The  pulmonary  lesions  had  improved,  the  expectoration  was 
almost  absent,  and  contained  no  more  baciUi. 

Surgeon-Lieutenant  Pech,  of  Sidi-bel-Abbes,  sent  me  the  following  notes  of  a 
patient  suffering  from  advanced  Addison's  disease,  and  treated  with  grilled  suprarenal 


DISEASES  OF  THE  SITRAREXAL  rwisiLKS  1241 

eapsnIoM  from  bullocka.  After  taking  tliis  Utnd  for  a  fow  duyH  thu  iiiiprovoriifint  in  tlia 
patit'nt  was  surprising.  Ho  folt  strong  and  well.  Tlio  vomiting  did  not  reappear,  an<l 
tlie  striking  thing  was  that  ho  was  losing  his  bronzed  comph?xion.  Ho  walked  up  tho 
fltaira  and  about  the  garden,  although  ho  had  been  incapable  of  tho  slightest  movi-rnr-nt. 
Ho  ate  voraciously  and  without  vomiting,  although  ho  had  been  a  prey  to  uncontrolhiblo 
vomiting. 

The  amelioration  obtained  by  suprarenal  opotherapy  is,  unfortunatflv, 
not  of  long  duration — at  least,  we  are  not  absolutely  certain  as  to  the  value 
of  the  remedy.  In  a  case  published  by  Beclere,  however,  the  pigmentation 
disappeared,  the  dpiamometric  force  increased  to  quite  an  unexpected 
degree,  and  the  cure  was  maintained  three  years  afterwards.  AVhatever 
the  future  may  have  in  store  for  opotherapy  in  Addison's  disease,  it  remains 
none  the  less  true  that  the  remedy  has  given  undeniable  results.  I  propose, 
therefore,  in  cases  of  Addison's  disease  of  the  masked  t}^e  to  clear  up  the 
diagnosis  by  the  remedy  in  question.  Grilled  suprarenal  capsules,  or  else 
subcutaneous  injections  of  glycerinated  extract  of  the  capsules,  will  be 
given,  and  if  the  asthenia  Is  improved  in  a  few  days,  there  is  a  vahd  reason 
for  making  a  diagnosis  of  Addison's  disease. 

We  must  not,  however,  be  too  ready  to  regard  this  treatment  as  a 
specific.  Account  must  be  taken  of  the  hygienic  conditioas  and  of  absolute 
rest,  which  are  such  a  valuable  auxiliary ;  and  yet  it  appears  to  me  undeni- 
able that  the  ingestion  of  suprarenal  extract  is  in  certain  forms  of  Addison's 
disease  a  means  to  which  we  must  have  recourse.  I  do  not  ad\'ise  the  use 
of  subcutaneous  injections,  because  glycerinated  extracts,  even  if.  aseptic, 
cause  necrosis  of  the  tissues.  I  recommend  the  fresh  pulp  of  the  supra- 
renal glands,  or  capsules  of  the  dried  extract.  The  suprarenal  capsules  of 
young  calves  are  the  best  (Pettit).  For  many  reasons  they  are  preferable  to 
the  suprarenal  capsules  of  other  animals. 

II.  INSUFFICIENCY  OF  THE  SUPRARENAL  CAPSULES— 
ILEMORRHAGE— SUPRARENALITIS. 

The  role  of  the  suprarenal  glands  in  the  human  economy  is  so  important 
that  any  change  in  their  function  may  bring  on  certain  toxic  troubles.  We 
thus  have  a  s^nidrome  of  suprarenal  insufficiency,  comprising  the  following 
elements :  asthenia,  arterial  hypotension,  vomiting,  diarrhoea,  cerebral 
phenomena,  and  abdominal  pains. 

They  are  met  with  in  almost  all  more  or  less  pronounced  capsular  lesions, 
but  they  do  not  always  appear  with  the  same  severity.  Sometimes  supra- 
renal insufficiency  manifests  itself  suddenly  in  a  few  days  or  in  a  few  hours. 
This  is  acute  insufficiency,  very  analogous  to  that  seen  after  the  ablation 
or  the  sudden  destruction  of  both  glands  in  an  animal. 

It  sometimes  appears  in  an  insidious  manner.     This  is  chronic   insuffi- 


1242  TEXT-BOOK  OF  MEDICINE 

ciency,  resulting  from  tlie  slow  destruction  of  the  glands  by  diverse  poisons 
and  in  particular  those  of  the  tubercle  baciUus.  Caseous  tuberculosis 
and  epithelioma  of  the  suprarenal  capsules  were  for  a  long  time  considered 
as  the  only  lesions  capable  of  causing  insufficiency.  The  sjmdrome  was  com- 
plete, being  acute  or  chronic,  sudden  or  progressive,  and  causing  sudden 
death  or  gradual  weakening,  according  as  some  superadded  infection  did 
or  did  not  hasten  the  course  of  events. 

Eecent  researches,  however,  have  shown  that  this  syndrome  is  also 
found  in  other  affections  of  the  suprarenal  capsules. 

There  are,  first  of  aU,  cases  of  primary  haemorrhage  or  hsematomata, 
caused  by  rupture  of  an  atheromatous  vessel,  and  destroying  the  glandular 
parenchjnna  partially  or  entirely. 

The  symptoms  in  these  cases  are  those  of  internal  haemorrhage,  rather 
than  those  of  profound  intoxication. 

Next  infections  and  profound  intoxications  foUow:  in  the  animal,  diphther- 
itic and  phosphorus  poisoning  and  pneumo-bacillary  infection  (Roger,  Oppen- 
heim  and  Loeper) ;  in  man,  erysipelas,  smaU-pox,  measles,  scarlatina, 
diphtheria,  icterus  gravis,  and  appendicitis,  may  be  the  origin  of  acute 
suprarenahtis  (Oppenheim  and  Loeper). 

The  suprarenal  syndrome  is  not  always  easily  recognized  in  the  symptom- 
complex  of  the  infection,  or  of  the  intoxication  that  has  given  rise  to  it. 
Sometimes  there  is  a  very  marked  fall  in  the  arterial  tension,  sometimes 
there  is  a  sudden  and  rapidly  fatal  weakening,  sometimes  there  are  cere- 
bral troubles.  At  other  times,  as  in  some  of  Oppenheim  and  Loeper' s 
cases,  death  is  sudden. 

The  post-mortem  examination  then  reveals  intense  congestion,  which 
may  go  so  far  as  to  cause  haemorrhage,  abscesses,  and  very  extensive 
cellular  necrosis. 

The  frequency  of  these  lesions  in  individuals  who  have  died  of  infection 
or  of  grave  intoxication  testifies  even  more  than  the  suprarenal  symptoms  to 
the  part  which  the  suprarenal  insufficiency  must  play  side  by  side  with  the 
renal  and  hepatic  insufficiency. 

We  must  also  mention  the  cases  of  fibrous  suprarenalitis,  which  at 
times  show  the  classical  symptoms  of  Addison's  disease,  but  which  are 
more  often  defaced. 

The  only  rational  treatment  of  suprarenal  insufficiency  appears  to  be 
opotherapy.  The  very  rare  trials  which  have  been  made  do  not  allow  us 
to  draw  any  precise  conclusion. 


PART   TV 

DISEASES  OF  THE   NERVOUS  SYSTEM 

CHAPTER  I 
DISEASES  OF  THE  SPINAL  CORD 

I.  PROGRESSIVE  LOCOMOTOR  ATAXY— TABES  DORSALIS— 
DUCHENNE'S  DISEASE. 

Undkr  the  names  of  tabes  dorsalis,  and  spinal  paralysis,  the  German  school  had  studied 
the  disease  which  Duchenne  had  called  progressive  locomotor  ataxy,  and  though  the 
researches  undertaken  at  Vienna  and  at  Berlin  concerning  this  question  (Romberg, 
Wunderhch,  Rokitansky)  are  of  undoubted  value,  we  must  nevertheless  recognize  that 
our  present  knowledge  of  this  malady  is  largely  due  to  Duchenne.  "  Progressive 
abolition  of  the  co-ordination  of  the  movements  and  apparent  paralysis,  contrasting 
with  the  integrity  of  muscular  force,  are  the  fundamental  characteristics  of  the  disease 
which  I  propose  to  describe.  Its  symptoms  and  its  course  make  of  it  a  distinct  morbid 
entity.  I  propose  to  call  it  '  progressive  locomotor  ataxy.'  "  This  sentence  from 
Duchenne's  monograph  proves  how  this  accurate  observer  had  at  the  outset  brought 
into  reUef  the  striking  features  of  the  disease  which  bears  his  name. 

Description — Classical  Form, — Locomotor  ataxy  presents  two  types ; 
the  classical  and  the  defaced. 

It  is  customary  to  describe  three  periods,  although  the  chnical  picture 
of  the  disease  does  not  lend  itself  well  to  this  arbitrary  division,  created  to 
meet  the  needs  of  pathology. 

First  Period. — In  the  classic  type  the  scene  opens  with  pains.  They 
are  rapid  and  ephemeral,  and  are  known  as  "  hghtning  pains."  They  shoot 
through  the  lower  limb,  and  follow  one  after  the  other  in  the  shape  of  fits, 
that  sometimes  leave  as  a  mark  of  their  passage  various  eruptions  and 
ecchymotic  patches  on  the  skin.  The  attacks  are  repeated  day  and  night 
for  several  days  in  succession.  They  then  disappear,  and  leave  the  patient 
in  peace  for  weeks  and  months.  At  other  times  the  pains  are  lancinating, 
as  though  caused  by  a  pointed  instrument  which  is  plunged  into  the  flesh 
and  bones  and  twisted.  Sometimes  they  are  seated  around  a  joint,  and  have 
a  grinding  character. 

In  the  body  they  take  the  form  of  girdle  pains,  the  patient  feehng  as 

1243 


1244  TEXT-BOOK  OF  MEDICINE 

tliougli  he  were  being  held  in  a  vice.  The  extension  of  the  disease  to  the  upper 
limbs  is  announced  by  pains  in  the  ring  and  httle  fingers  (area  of  the  ulnar 
nerve).  In  the  face  the  pains  may  be  continuous  or  intermittent  (area  of 
the  trigeminal  nerve).  They  are  often  lancinating,  and  affect  in  some  cases 
the  temporal  or  the  occipital  region  (exit  point  of  the  suboccipital  nerve). 
These  troubles  in  the  area  of  the  trigeminal  nerve  are  said  by  Collet  to 
exist  in  two-fifths  of  the  cases. 

The  viscera  are  not  exempt  from  these  crises.  In  the  stomach  they 
sometimes  take  the  form  of  very  severe  gastralgia,  accompanied  by  great 
distress  and  vomiting  of  mucus,  food,  bile,  or  blood.  These  gastric  crises 
appear  and  disappear  suddenly  ;  they  last  a  few  hours  or  a  few  days  without 
remission,  and  recur  on  taking  any  food.  The  intensity  of  the  pains  and  of 
the  vomiting  sometimes  induces  collapse.  The  gastric  crises  are  purely 
nervous  in  most  cases,  although  they  may  be  associated  with  lesions  of  the 
stomach.  I  had  under  my  care  a  patient  who  suffered  from  agonizing 
gastric  crises.  The  autopsy  revealed  the  characteristic  lesions  of  tabes, 
and  also  marked  atrophy  of  the  stomach,  which  was  reduced  to  the  size  of 
a  coil  of  gut.  Histological  examination  showed  the  lesions  of  subacute 
gastritis  (Crouzon). 

In  the  case  of  the  kidneys  the  crises  cause  lumbar  pains,  with  retraction 
of  the  testicle  and  vomiting,  as  in  renal  coHc.  In  certain  patients  the  crises 
are  vesical  and  urethral,  simulating  stone  in  the  bladder.  The  patient 
suffers  from  poUakiuria,  sometimes  accompanied  by  dysuria  and  temporary 
retention  of  urine.  In  other  cases  the  crises  invade  the  rectum,  causing 
the  sensation  of  a  foreign  body,  or  of  burning  and  tearing.  Attacks  of 
angina  pectoris  have  even  been  noticed.  They  are  due  to  changes  in  the 
cardiac  plexus  found  post  mortem.  I  have  given  full  details,  under 
Angina  Pectoris  and  in  one  of  my  chnical  lectures,  of  the  relations  between 
angina  pectoris  and  tabes.  Amongst  these  different  painful  manifestations 
of  tabes,  the  lightning  pains  in  the  lower  limbs  are  the  most  common  and 
the  earhest  to  appear. 

At  this  period,  and  sometimes  even  from  the  very  first,  we  notice  the 
absence  of  the  patellar  reflex  (Westphal).  If,  in  the  normal  condition, 
we  cross  one  leg  over  the  other,  the  upper  leg  being  allowed  to  hang  with 
the  muscles  relaxed,  a  smart  blow  with  the  ulnar  border  of  the  hand  on  the 
tendon  of  the  patella  causes  contraction  of  the  quadriceps  extensor,  the 
leg  rising  and  falling  with  an  oscillatory  movement.  The  absence  of  the 
patellar  reflex  is  one  of  the  earhest  signs  of  tabes  dorsahs.  In  consequence 
of  the  degeneration  of  the  posterior  columns  of  the  spinal  cord,  the  nerve 
ending  in  the  tendon  no  longer  transmits  stimuh  to  the  cells  of  the  anterior 
cornua.  Side  by  side  with  the  patellar  reflex  we  must  mention  the  reflex 
of  the  tendo  Achillis.     This  reflex  is  obtained  in  the  following  manner : 


DISEASES  OF  THE  SPINAL  CORD  1245 

The  patient  kneels  on  a  chair,  and  the  muscles  of  the  calf  are  felt  to  make 
sure  that  thoy  are  relaxed.  The  tendo  Achillia  is  percussed  with  a  plessor, 
and  we  see  that  the  foot  is  extended  on  the  leg.  The  aljsence  of  the  reflex 
of  the  tendo  AcliilHs  is  an  early  sign  of  tabes  (Babinski). 

To  this  first  period  of  the  disease  also  belong  the  cerebral  symptoms 
and  the  ocular  symptoms  which  constitute  the  tabetic  eye.  The  tabetic 
eye  may  show  itself  by  paralytic  troubles,  disorders  of  accommodation, 
or  visual  troubles.  The  ocular  paralyses  may  occur  early  or  late  ;  they 
affect  the  motor  muscles  of  the  eyeball  and  the  levator  palpebrse  superioris 
(third,  fourth,  and  sixth  pairs  of  nerves).  The  early  paralyses  (preataxic 
period)  are  generally  slighter  and  more  transient  than  the  late  paralyses. 
They  last  only  a  few  weeks  or  even  only  a  few  hours  ;  they  appear  and  dis- 
appear rapidly.  Their  characteristic  feature  is  that  they  are  monocular 
and  partial,  affecting  only  a  single  terminal  branch,  or  a  few  terminal 
branches,  of  the  motor  nerves  of  the  eye.  According  to  the  nervous  branch 
involved,  the  patient  is  affected  with  very  troublesome  diplopia  or  with 
ptosis.  These  passing  troubles  are  subject  to  recurrences.  The  late  ocular 
paralyses,  which  occur  during  the  course  of  confirmed  tabes,  behave  very 
differently  to  the  early  paralyses.  They  run  a  slower  course,  and  they  do 
not  generally  retrocede.  They  often  affect  both  eyes,  involving  especially  the 
muscles  supphed  by  the  common  ocular  motor  nerve,  the  levator  palpebrae 
(ptosis),  the  recti,  and  the  obhque  muscles.  The  muscles  supphed  by  the 
fourth  and  sixth  pair  are  less  often  affected.  The  late  paralyses  of  the  four 
recti  and  of  the  two  obhque  muscles  cause  diplopia  and  permanent  strabis- 
mus, the  characters  of  which  vary  according  to  the  muscles  attacked.  If 
all  the  muscles  are  affected,  the  eyeballs  are  absolutely  immovable.  This 
condition  is  external  ophthalmoplegia. 

The  late  ocular  paralyses  differ,  then,  in  their  course  from  the  early 
paralyses.  They  differ  hkewise  in  the  lesion  which  causes  them,  the  early 
and  transitory  paralyses  being  due  only  to  peripheral  neuritis*  (Kahler, 

*  The  transient  oculo-motor  troubles  have  been  looked  upon  by  P.  Bonnier  a3 
reflex  phenomena,  which  most  frequently  depend  on  systematic  lesions  of  the  labjTin- 
thine  nerve,  of  its  nuclei  in  the  brain,  and  of  the  fibres  which  pass  from  it  to  form  a 
system  homologous  with  the  system  in  the  posterior  columns  of  the  cord.  The  system 
of  the  labyrinth,  in  fact,  peripheral  as  well  as  central,  is  very  frequently  diseased  in 
tabes.  It  may  be  asked  whether  certain  symptoms  may  not  be  caused  by  the  tabetic 
lesion  of  this  system  when  we  remember  the  frequency  with  which  these  same  symptoms 
appear  during  the  course  of  ear  affections  that  are  absolutely  independent  of  tabes. 
To  deafness,  buzzing,  vertigo,  agoraphobia,  nystagmus,  ptosis,  diplopia,  myosis,  and 
amblyopia,  which  have  been  noticed  in  non-tabetic  diseases  of  the  ear,  Bonnier  has 
added  Romberg's  sign,  uncertainty  of  walking  in  the  dark,  incoherent  movements 
of  the  balls  under  the  closed  eyeUds,  slowness  of  accommodation  to  hght,  paralysis 
of  accommodation,  and,  finally,  mydriasis,  observed  for  the  first  time  during  the  course 
of  otitis  in  a  nurse  in  mj'  wards.  All  these  troubles  exist  in  tabes,  and  it  is  by  relying 
on  the  well-established  anatomical  relations  between  the  labyrinthine  nuclei  and  the 


1246  TEXT-BOOK  OF  MEDICINE 

Dejerine),  wliilst  the  late  and  permanent  paralyses  are  due  to  the  lesions  of 
the  nuclei  in  the  bulb.  Certain  patients  with  tabes  are  attacked  by  hyper- 
secretion from  the  conjunctiva  (Trousseau),  which  generally  coincides  with 
the  hghtning  pains  (Fere,  Berger). 

Disorders  of  the  pupils  and  of  accommodation  are  likewise  very  im- 
portant. The  pupils  are  frequently  contracted,  often  unequal,  and  it  is 
a  curious  fact  that  in  cases  of  myosis  consequent  on  tabes  dorsahs  the 
contracted  pupils  still  react  to  accommodation.  They  dilate  if  the  patient 
looks  at  a  near  object,  whilst  they  remain  insensible  to  the  action  of  hght 
(Argyll-Robertson) . 

Robertson's  sign  is  of  the  utmost  importance  in  the  diagnosis  of  tabes. 
It  is  not,  however,  pathognomomc  of  the  afiection,  being  also  found  in 
general  paralysis.  According  to  Babinski  and  CTiarpentier,  this  sign  does 
not  exist  only  in  these  two  afiections,  which  they  look  upon  as  syphihtic 
diseases  of  the  nervous  system,  but  it  may  also  be  associated  with  other 
syphihtic  manifestations  in  the  ner^'^ous  system  (hemiplegia,  paraplegia, 
etc.).  It  may  even  exist  alone  in  syphihtic  patients.  In  a  word,  it  is  said 
to  be  a  function  of  syphihs. 

The  power  of  accommodation,  properly  so  called,  may  also  ba  paralyzed, 
making  it  impossible  for  patients  whose  eyes  were  normal  or  hypermetropic 
to  see  clearly  near  objects.  It  is  only  distant  vision  that  is  still  intact. 
Paralysis  of  accommodation  generally  accompanies  paralysis  of  the  two 
reflexes  of  the  iris  (Hght  and  accommodation),  and  the  union  of  these  symp- 
toms in  the  same  eye  constitutes  internal  ophthalmoplegia. 

I  must  now  refer  to  atrophy  of  the  optic  nerves.  Visual  troubles  due 
to  optic  atrophy  are  found  in  the  proportion  of  15  to  20  per  cent.  The 
atrophy  sometimes  develops  rapidly,  and  bhndness  may  supervene  in  less 
than  a  year.  At  other  times  the  lesion  progresses  slowly.  The  lesion  is 
not  bilateral  from  the  first.  It  invades  one  eye  after  the  other.  The  keen- 
ness of  the  sight  grows  weak  (amblyopia),  and  the  field  of  vision  becomes 
contracted  from  the  circumference  in  the  form  of  notches.  The  sense  of 
colour  is  afiected  in  the  following  order :  disappearance  of  green,  red, 
yellow,  blue,  and  white.  The  bhndness  is  then  complete.  If  the  fundus  is 
examined  with  the  ophthalmoscope,  we  see  at  first  paleness  of  the  optic 
papiUa,  the  normal  rosy  tint  tending  to  become  of  a  bluish-white.  This 
change  is  especially  marked  in  the  external  haK  (temporal)  of  the  disc. 
The  papilla  shows  no  change,  either  in  shape  or  size.  The  outlines  are 
always  very  clear.     At  a  more  advanced  period,  "  in  consequence  of  a  change 

oculo-motor  centres,  and  by  relying  also  on  the  physiological  necessities  of  this  associa- 
tion, and  on  the  systematic  character  of  the  tabetic  affection,  that  he  has  been  able  to 
propose  a  labyrinthine  phase  of  tabes  side  by  side  with  tabes  dorsaUs,  cerebral  tabes, 
and  bulbar  tabes  itself. 


DISEASES  OF  THE  SPINAL  PORD  1247 

in  the  texture  of  the  optic  nerve,  and  especially  in  conflequenoe  of  the  dis- 
appearance of  the  myelino  cylinder,  the  pa])ilhi  ceast^s  to  he  transparent. 
It  reflects  the  light  strongly,  and  does  not  allow  the  vessels  to  be  clearly  seen 
in  its  depths.  Accordingly  it  does  not  present  the  normal  rosy  tint,  hut 
is  of  a  chalky-white  colour  "  (Charcot).  The  central  vessels  become  more 
slender.     The  arteries  are  attacked  before  the  veins. 

Optic  atrophy  is  often  an  early  symptom  of  tabes.  There  is,  indeed, 
a  type  of  tabes  (tabes  superior)  in  which  the  symptoms  are  limited  to  atrophy 
of  the  optic  nerves  and  some  other  cephahc  signs  (pupillary  signs,  ocular 
paresis,  etc.).  The  late  appearance  of  optic  atrophy  is  far  less  common. 
It  has  been  said  that  optic  atrophy  may  arrest  the  lesions  in  the  cord. 

The  aural  troubles  are  sometimes  characterized  by  weakening  of  the 
sense  of  hearing,  with  or  without  buzzings  in  the  ears,  and  in  such  a  case 
there  is  a  lesion  of  the  auditory  nerve.  In  other  cases  the  buzzings  and 
ringings  in  the  ears  are  accompanied  by  vertigo,  by  impulsion,  and  even 
by  falhng,  and  by  agoraphobia,  although  the  sense  of  hearing  is  not  afEected. 
It  is  then  probable  that  the  lesion  does  not  involve  the  fibres  of  the  auditory 
nerve  which  govern  the  hearing  of  sounds,  but  the  fibres  which  come  from  the 
semicircular  canals,  and  govern  the  sense  of  space  (De  Cyon),  or,  more 
exactly,  the  sense  of  the  position  of  the  head  and  of  the  rest  of  the  body 
(P.  Bonnier). 

Laryngo-bronchial  troubles  may  supervene  from  the  first  in  tabes. 
They  are  characterized  by  attacks  of  cough,  with  spasms  of  the  glottis  and 
a  sensation  of  choking.  These  attacks  are  sometimes  violent,  accompanied 
by  vertigo,  vomiting,  and  even  in  some  cases  by  epileptiform  convulsions, 
loss  of  consciousness,  and  falling  down  of  the  patient.  The  attack  is  sudden 
or  preceded  by  piodromata.  It  lasts  a  few  seconds  or  minutes,  and  it  may 
recur  several  times  in  the  twenty-four  hours.  These  laryngeal  crises  are 
due  to  hypersesthesia  and  to  spasms  of  the  glottis.  In  one  case  they  dis- 
appeared after  tracheotomy.  In  some  patients  the  disease  affects  the  larynx, 
causing  paralysis  of  the  muscles,  especially  of  the  posterior  crico-arytenoids. 

Genital  troubles — spermatonhcBa,  impotence,  venereal  excitement,  etc. 
— occur  in  all  phases  of  the  disease.  They  may,  indeed,  precede  the  other 
symptoms.  Chtoridean  crises  have  also  been  noticed,  the  patients  being 
attacked,  without  cause,  with  voluptuous  sensations,  frequently  repeated, 
and  often  preceding  the  other  s^Tnptoms  of  the  disease  by  several  years. 
We  shall  see  later,  when  describing  the  defaced  types  of  locomotor  ataxy, 
that  many  other  s}Tnptoms  may  precede  the  painful  phase  of  the  first 
period.  It  would  be  more  true  to  say  that  there  is  not  a  single  symptom, 
rare  or  common,  that  may  not  appear  before  the  stage  of  ataxy. 

Second  Period. — Although  inco- ordination  may  exist  from  the  com- 
mencement, it  usually  marks  the  second  phase  of  the  disease.     It  is  the 


1248  TEXT-BOOK  OF  MEDICINE 

chief,  but  not  the  exclusive,  symptom,  because  the  pains  and  other  symptoms 
previously  described  also  belong  to  this  period.  The  ataxy  is  characterized 
by  gradual  aboUtion  of  the  co-ordination  of  movements.  It  shows  itself 
at  indeterminate  periods,  sometimes  many  years  after  the  appearance  of 
the  hghtning  pains  and  the  cerebral  troubles. 

The  ataxy  commences  in  the  lower  Hmbs,  the  patient  having  less  control 
of  his  movements  and  experiencing  difficulty  in  standing  erect.  If  he  is 
asked  to  stand  erect,  with  the  feet  close  together  and  the  eyes  shut,  he 
becomes  unsteady,  and  may  even  fall  over  (Romberg's  sign).  The  patient 
with  tabes  finds  it  difficult  to  stand  on  one  leg,  turns  round  with  difficulty, 
and  readily  loses  his  equihbrium.  If  he  is  lying  in  bed,  and  is  asked  to  cross 
his  legs,  he  will  suddenly  throw  his  leg  forward,  because  he  can  no  longer 
control  the  force,  the  direction,  or  the  extent  of  the  movement.  In  the  patient 
suffering  from  ataxy  tlie  movement  exceeds  the  object,  or  does  not  reach  it. 
Thus  in  walking  the  patient  has  his  eyes  continually  fixed  on  his  feet,  in 
order  to  guide  them,  and  this  explains  why  the  lack  of  co-ordination  is  more 
pronounced  in  the  dark,  or  when  the  patient  is  made  to  walk  with  his  eyes 
closed.  Later,  walking  becomes  difficult  and  disordered,  the  patient  being 
unable  to  take  a  step  without  the  aid  of  a  stick  or  other  support.  He  thrusts 
his  legs  wildly  forward,  and  strikes  the  ground  with  his  heel,  until  the 
disease  makes  such  progress  that  walking  and  standing  erect  become  im- 
possible. Brissaud  has  drawn  attention  to  the  impossibihty  of  patients 
assuming  the  position  of  semi-genuflexion.  The  sudden  giving  way  of  the 
legs  which  the  patient  fears,  and  which  takes  him  unawares,  obhges  him  to 
keep  his  legs  stiff  when  walking  and  standing  erect.  Prior  to  Duchenne's 
researches,  those  patients  were  looked  upon  as  suffering  from  paraplegia, 
but  there  is  no  question  of  paralysis — or,  at  least,  the  paralytic  symptoms 
are  secondary  and  late.  An  attempt  to  flex  or  to  extend  the  leg  of  a  patient 
suffering  from  ataxy  at  once  shows  the  power  of  resistance.  The  integrity  of 
the  muscular  force  is  retained  until  a  late  stage.  The  want  of  co-ordination 
of  the  muscular  force  is  the  striking  feature. 

When  the  ataxy  involves  the  upper  hmbs,  it  causes  disorder  in  the  use 
of  the  hands.  If  it  is  a  question  of  shaving,  tying  a  knot,  or  taking  a  small 
object  in  the  fingers,  the  patient  is  awkward,  and  his  mode  of  prehension 
is  fairly  characteristic. 

At  this  period,  and  even  earher,  the  sense  of  touch  is  changed.  The 
sensations  of  touch,  pain,  and  ticHing  are  diminished,  abohshed,  or  per- 
verted ;  it  is  only  the  sense  of  cold  which  is  exaggerated.  Furthermore, 
we  notice  retardation  of  the  sensibiUty.  Thus  a  patient  whose  foot  or  whose 
leg  has  been  pricked  only  feels  the  prick  three,  four,  or  five  seconds  later. 

The  stereognostic  sense— that  is  to  say,  the  faculty  of  recognizing  the 
shape  of  objects  by  palpation— may  be  diminished  or  abohshed.     Anaesthesia 


DISEASES  OF  THE  SPINAL  CORD  1249 

la  not  limited  to  the.  sUia  ;  it  also  attacks  the  niucosao,  notably  that  of 
the  larynx  and  the  entire  locomotor  system— muscles,  tendons,  and  articula- 
tions.* In  the  normal  condition  sensibihty  renders  us  an  account  of  the 
effort  of  our  muscles  less  by  the  sensation  of  contraction  (muscular  sense  of 
Bell,  sense  of  muscular  activity  of  Gerdy),  than  by  the  measure  of  the 
resistance  opposed  to  this  effort  by  the  tendons,  the  hgaments,  the  articular 
surfaces,  and  the  integument.  As  a  matter  of  fact.  Trousseau  was  the  first 
to  estabhsh  an  important  distinction  "  between  the  consciousness  of  the 
accomphshed  movement  and  the  consciousness  of  the  muscular  contraction 
that  accomplishes  the  movement."  Trousseau  in  no  way  denies  the 
sensibihty  which  the  muscle  possesses,  hke  all  hving  tissues,  but  he  denies 
the  sentiment  of  muscular  activity.  The  thing  appreciated,  and  conse- 
quently ruling  the  muscular  expense  itself  at  every  moment,  is  movement 
properly  so  called,  and  this  movement  is  perceived  in  that  it  causes  a  change 
in  the  attitudes. f 

Side  by  side  \\ath  these  various  forms,  of  anaesthesia  certain  varieties  of 
visceral  analgesia  may  be  observed — testicular,  epigastric,  or  mammary 
analgesia,  described  by  Pitres,  and  also  tracheal  and  hngual  analgesia, 
pointed  out  by  Sicard. 

*  This  appreciation  of  muscular  force  may  bo  easily  noticed  with  a  dynamometer. 
Jaccoud  makes  use  of  another  method.  To  the  feet  of  a  patient  lying  in  bed  he  suspends 
bags  of  known  weight,  and  whilst  a  healthy  man  Hfting  these  weights  with  his  foot 
can  recognize  perfectly  a  difference  of  100  to  150  grammes,  a  patient  suffering  from 
ataxy,  on  the  contrary,  fails  to  recognize  differences  of  1,000  to  3,000  grammes. 

t  P.  Bonnier  in  various  pubhcations  {Le  Verticje,  Paris,  1893)  proposes  to  replace  the 
too  exclusive  expression  muscular  sense  by  the  more  exact  idea  of  the  sense  of  the  atti- 
tudes. Whether  there  is  muscular  contraction  or  not,  whether  the  attitude  is  reaUzed 
actively  or  passively,  it  is  always  the  attitude  which  is  perceived,  and  in  no  wise  one  of 
the  numerous  sensorial  operations,  the  composition  of  which  defines  the  attitude  for  us. 
The  writer  distinguishes  segmentary  attitudes — that  is  to  say,  the  respective  positions 
of  the  various  segments  of  the  trunk  and  of  the  hmbs,  of  the  attitudes  of  the  head,  and  the 
attitudes  of  the  whole  body.  The  pictures  of  the  segmentary  attitudes  are  transported 
by  the  nerve  roots,  and  the  posterior  columns  to  the  cerebrum  and  the  cerebellum. 
The  pictures  of  the  attitudes  of  *the  head  and  of  the  whole  body,  of  a  labyrinthic  origin 
follow  the  vestibular  nerve,  and  Hkewise  end  in  the  brain  and  in  the  cerebellum. 

There  exists,  then,  a  medullo-cerebral  system  serving  for  the  conscious  adaptation 
of  partial  movements  and  for  voluntary  equihbration,  and  a  medullo-cerebellar  system, 
devoted  to  the  reflex  working  of  these  movements  and  of  equihbration.  In  tabes,  which 
is  a  medullo-labyrintho-cerebral  affection  (Bonnier),  the  movements  are  said  to  remain 
co-ordinated,  but  they  are  badly  adapted.  TeU  a  patient  to  close  his  eyes,  and  imme- 
diately the  absence  of  sight  betrays  itself  by  the  loss  of  volimtary  equihbrium,  by  the 
difltiurbance  of  equihbrium  (Romberg's  sign),  by  the  exaggeration  of  the  ataxic  move- 
ments, and  by  the  sensation  of  vertigo.  In  Friedreich's  disease,  and  in  cerebellar 
heredo -ataxia,  which  are  meduUo -cerebellar  affections,  the  sense  of  the  attitudes  is 
affected  as  far  as  the  reflex  acts  are  concerned,  but  it  is  preserved  as  far  as  the  conscious 
act  that  supplements  the  reflex  act.  Thus,  the  closing  of  the  evi^hds  scarcely  affects 
the  equilibration,  and  only  shghtly  influences  the  adaptation  of  the  movements. 


1250  TEXT-BOOK  OF  MEDICINE 

Cerebral  symptoms  may  appear  at  various  periods  of  tabes,  preceding 
in  a  third  of  the  cases,  says  Fournier,  the  pains  and  the  ataxia — a  further 
proof  that  the  lesions  of  this  disease  are  not  only  limited  to  the  medullary 
axis,  as  the  original  meaning  of  tabes  dorsalis  wrongly  indicates  ;  they  are 
spread  over  the  entire  nervous  system.  These  cerebral  symptoms  may  be 
divided  into  two  principal  varieties,  motor  and  psychical.  To  the  motor 
troubles  belong  vertigo,  impulsion,  gyration,  epileptiform  convulsions,  and 
apoplectiform  attacks,  and  certain  kinds  of  paralyses,  to  which  I  shall  refer 
in  a  moment. 

To  the  psychical  troubles  belong  aphasia,  intellectual  torpor,  loss  of 
memory,  intellectual  troubles,  constituting  a  sort  of  tabetic  madness,  and 
most  of  the  symptoms  of  general  pseudo-paralysis.  These  troubles  may 
be  temporary  or  permanent.  They  sometimes  appear  in  the  last  stage 
of  tabes  ;  at  other  times  they  are  the  first  symptoms  (Fournier). 

AHenists  have  for  a  long  time  noticed  in  patients  suffering  from  general 
paralysis  the  following  symptoms  :  Lightning  pains,  oculo-pupillary  and 
genito-urinary  troubles,  anaesthesia,  locahzed  paralysis,  arthropathy, 
abohtion  of  the  reflexes,  etc. — manifestations  indicating  the  participation 
of  the  cord  or  of  the  peripheral  nerves  in  the  morbid  process.  Neuro-patho- 
logists,  on  their  side,  had  noticed  in  several  cases  of  ataxy  the  appearance 
of  apoplectiform  and  epileptiform  attacks,  followed  or  not  by  hemiplegia, 
buzzing,  dehrium  of  an  ambitious  or  depressed  type,  all  pointing  to  ana- 
tomical changes  in  the  brain  centres.  We  may  add  to  these  Meniere's 
vertigo,  due  to  labyrinthine  apoplexy. 

The  result  was  that  a  patient  considered  to  be  suffering  from  general 
paralysis  at  the  commencement  of  the  disease  was  later  classed  as  a  case  of 
ataxy.  Often,  too,  a  patient  with  ataxy  was  admitted  into  an  asylum, 
and  condemned  to  end  his  days  amongst  lunatics.  The  study  of  these  com- 
plex cases  has  recently  been  resumed.  Some  regard  them  as  the  casual 
union  of  two  distinct  diseases  in  the  same  subject ;  others,  on  the  contrary, 
consider  them  as  locahzations  in  the  brain  and  in  the  cord  of  a  single  morbid 
entity. 

The  partisans  of  the  duahst  doctrine  rely  on  pathological  anatomy  to 
support  their  opinion.  According  to  them,  tabes  is  an  affection  of  central 
origin,  characterized  by  a  progressively  systematic  lesion  of  the  cerebro- 
spinal sensory  system,  whilst  general  paralysis  is  characterized  by  an 
essentially  diffuse  lesion  of  the  cerebrospinal  axis.  The  same  difference  is 
said  to  exist  between  these  two  affections  as  exists  between  amyotrophic 
lateral  sclerosis  and  disseminated  sclerosis.  Ballet  goes  even  further,  and 
admits  that  tabes  is  an  affection  with  a  perivascular  onset.  Finally,  one  of 
these  diseases  ends  in  induration  of  the  nerve  centres,  and  the  other  in 
softening.     The  duaUsts  recognize,   however,   that  if  these  two   diseases 


DISEASES  OF  THE  SPINAL  CORD  1251 

differ  as  to  their  essential  nature,  they  both  develop  in  subjects  who  are 
identical,  as  far  as  the  medium  is  concerned — that  is  to  suy,  in  neuropathic 
individuals,  especially  in  those  with  hereditary  predi.s])()sl1i()ii.  and  often 
also  in  syphilitic  and  alcohoUc  persons. 

The  partisans  of  the  unicist  theory,  on  the  contrary,  turn  this  (j[uestion 
of  the  medium  to  account,  and  especially  the  neuropathic  medium  on  which 
syphilis  has  been  grafted,  in  order  to  prove  the  identity  of  tabes  and  general 
paralysis.  According  to  them,  the  frequency  of  the  cerebral  and  spinal 
manifestations  in  the  same  subject  is  too  great  to  be  simply  a  coincidence. 
Finally,  they  rely  on  the  fact  that  in  tabes  the  systematization  of  the 
lesions  is  not  as  rigorous  as  some  maintain.  They  say  that  in  a  large 
number  of  cases  manifestly  diffuse  changes  are  found  in  the  lateral  columns, 
in  the  anterior  cornua,  and  in  the  peripheral  nerves.  The  unicists  say 
that,  as  for  stating  precisely  the  histological  starting-point  of  the  lesions 
in  general  paralysis,  and  making  it  an  argument  by  which  to  differentiate 
the  two  diseases,  histological  research  is  not  sufficiently  advanced  to  permit 
of  such  a  demarcation. 

Let  us  now  pass  to  the  motor  troubles.  We  may  notice  in  all  phases 
of  Duchenne's  disease  paralyses  of  various  kinds ;  such  are  hemiplegia, 
monoplegia,  paraplegia,  facial  and  radial  paralysis,  and  paralysis  of  the 
muscles  of  the  eye.  These  paralyses  are  often  incomplete  and  transient, 
subject  to  recurrences,  and  deserve  rather  the  name  of  "  paresis."  Some, 
nevertheless,  have  other  characters ;  thus  we  find  persistent  hemiplegia 
associated  with  cerebral  lesions,  hemiplegia  with  sensitivo-sensorial  hemi- 
anaesthesia,  due  to  the  association  of  tabes  with  hysteria.  Tabetic  para- 
plegia sometimes  has  a  sudden  onset,  improves,  and  may  be  cured  after  a 
few  weeks  or  months.  Central  lesions,  peripheral  neuritis,  and  hysteria 
play  various  parts  in  the  causation  of  these  paralyses.  Another  category 
includes  choreiform  movements  and  athetosis,  generally  accompanied  by 
contractures,  and  depending  on  an  accessory  lesion  of  the  lateral  columns. 

Third  Period. — After  some  ten  to  fifteen  years  or  more  the  disease 
may  improve,  but  more  frequently  it  ends  in  the  fiaial  period  of  paralysis 
and  cachexia,  often  comphcated  with  ulcerative  cystitis,  bedsores,  pul- 
monary tuberculosis,  bulbar  phenomena,  and  general  paralysis.  This 
period  really  merits  the  name  of  tabes,  the  patient  dying  of  cachexia  if  he  is 
not  carried  off  by  some  intercurrent  disease. 

Trophic  Troubles. — Trophic  and  vasomotor  troubles  may  appear  at 
any  period  of  the  disease.  The  hghtning  pains  in  the  hmbs  and  in  the  face 
are  sometimes  accompanied  by  cutaneous  eruptions,  ecch}T2ioses,  and 
temporary  oedema.  Shedding  of  the  nails  is  noticed,  especially  of  the  nail 
of  the  big  toe.  The  shedding  of  the  nail  may  or  may  not  be  preceded  by 
subungual  ecchymosis,  with    pain   or   numbness,  and    the    nail    falls  off 


1252  TEXT-BOOK  OF  MEDICINE 

without  ulceration,  "like  a  crust  of  ecthyma,"  being  replaced  by  a  friable 
nail,  which  faUs  ofE  in  its  turn.  Vitihgo,  ichthyosis  of  the  skin,  and  per- 
forating ulcer  of  the  foot  are  often  seen. 

One  of  the  first  cases  of  perforating  disease  of  the  foot  was  reported  by 
my  uncle,  Paul  Dieulafoy.  Tabes  accounts  for  75  per  cent,  of  the  cases  of 
perforating  disease.  It  usually  attacks  the  head  of  the  first  and  fifth  meta- 
tarsal bones ;  it  may  be  superficial  or  deep.  In  some  cases  it  afiects  the 
palm  of  the  hand,  the  face,  the  mouth,  the  aortic  valve,  the  oesophagus, 
the  intestine,  or  the  buttock.  In  a  case  at  the  Hotel-Dieu,  perforating 
disease  of  the  sacro-coccygeal  region  produced  a  large  cavity.  The  area 
around  the  cavity  was  anaesthetic ;  the  incontinence  of  urine  and  faeces,  the 
hghtning  pains,  and  the  abohtion  of  the  reflex  of  the  tendo  AchiUis,  proved 
the  diagnosis  of  tabes.  The  autopsy  showed  the  characteristic  lesions  in 
the  lumbo-sacral  cord  and  ascending  degeneration  in  the  posterior  columns. 

From  the  commencement  of  the  disease  well-marked  arthropathies  may 
be  seen,  afEecting  the  knee,  the  foot,  and  the  hip  (Ball,  Charcot),  and  some- 
times appearing  almost  suddenly.  They  are  generally  painless,  and  very 
rapidly  accompanied  by  hydarthrosis,  hard  oedema,  and  swelling,  which  gives 
to  the  affected  limb  the  appearance  of  elephantiasis.  In  spite  of  this  in- 
vasion, the  movements  are  practically  normal  for  some  time.  When  the 
arthropathy  is  benign,  there  may  be  resolution ;  but  when  it  is  grave,  the 
swelhng  and  the  oedema  persist,  the  capsule,  the  ligaments,  the  cartilage, 
the  ends  of  the  bones,  and  the  articular  cavities  are  destroyed  by  the  trophic 
disorders,  and  dislocations  and  intra-articular  fractures  occur.  These  dis- 
orders cause  considerable  deformity,  and  aUow  the  most  weird  movements 
of  the  diseased  joint.  The  arthropathy  is  not  always  of  the  atrophic  type. 
Thickening  of  the  synovial  membrane  and  osteocartilaginous  tumours  are 
also  seen. 

Let  us  also  notice  as  trophic  troubles  fractures  due  to  rarefying  osteitis. 
These  fractures  particularly  attack  the  bones  of  the  hmbs,  but  they  have  also 
been  observed  in  the  vertebrae.  The  characteristic  feature  is  that  they 
occur  without  pain.  They  are  sometimes  multiple,  and  result  from  very 
trifling  causes,  but  they  become  consohdated,  and  the  callus  is  exuberant, 
shapeless,  and  resisting.  Osteoporosis  of  the  maxillae  causes  the  painless 
falhng  out  of  healthy  teeth.  I  had  in  my  wards  a  patient  suffering  from 
tabes  who  lost  seven  teeth  in  a  few  days.  This  shedding  of  the  teeth  is  some- 
times followed  by  the  absorption  of  the  alveolar  border,  the  first  degree  of 
perforating  disease  of  the  mouth,  already  described  under  Syphilitic  Per- 
forations of  the  Vault  of  the  Palate.  Let  us  also  note  ulcerations  of  the 
nose  (Giraudeau),  velum  palati,  piUars  of  the  fauces  (Bonnier)  and  face 
(P.  Marie). 

In  suflerers  from  tabes  we  sometimes  see  deformity  of  the  foot  analogous 


DISEASES  OF  THE  SPINAL  CORD  1253 

to  the  coiigciiital  flat-foot.  The  internal  edge  oi  thu  foot  is  thickened,  the 
dorsal  surface  is  prominent,  especially  in  the  tarso-metatarsal  region,  and  the 
plantar  arch  is  flat  and  weakened.  The  foot  is  shortened.  These  deformities, 
easily  recognized  in  footprints,  are  caused  by  trophic  lesions  of  the  tarsal 
bones,  which  become  friable,  atrophied,  and  disjointed.  "  There  is  rather 
osteopathy  than  arthropathy  "  (Chauffard).  This  tabetic  foot  may  super- 
vene from  the  ooniniencoment  of  the  disease.  It  mast  not  be  confounded 
with  the  tabetic  club-foot,  due  to  atrophy  of  certain  muscles  of  the  leg, 
the  deformity  of  the  foot  being  constituted  by  an  exaggerated  extension, 
with  an  inward  curve  of  the  internal  edge,  and  a  deviation  of  the  toes 
towards  the  middle  line  of  the  body  (JofEroy). 

The  name  hypotonia  is  given  to  a  condition  in  which  the  muscles  are 
relaxed,  and  abnormal  mobihty  of  the  articulations  follows.  In  certain 
cases  of  hypotonic  tabes  we  can  produce  hyperextension  of  the  leg  on  the 
thigh,  so  as  to  form  an  obtuse  angle.  When  the  patient  is  lying  down,  it 
is  possible  to  abduct  the  legs  to  such  an  extent  that  their  axes  lie  in  a  straight 
line.  In  the  hands  it  is  possible  to  cause  h}^erextension  of  the  phalanges 
on  the  metacarpus  and  of  the  phalanges  on  one  another. 

Muscular  atrophy  appears  chiefly  at  an  advanced  period.  It  is  usually 
symmetrical,  and  always  commences  in  the  muscles  of  the  limbs,  more 
often  in  the  hands  than  in  the  feet.  In  the  lower  L'mbs  the  atrophy  causes 
pes  equinus,  with  plantar  flexion  of  the  toes.  In  the  upper  Hmbs  it  takes 
the  Aran-Duchenne  type,  but  very  rarely  the  scapulo-humeral  or  anti- 
brachial  one.  The  muscular  atrophy  is  not  accompanied  by  fibrillary  con- 
tractions. The  idio-muscular  contraction  is  diminished  or  abolished,  but 
the  reaction  of  degeneration  is  not  common. 

Atrophy  of  the  muscles  of  the  eye  and  of  the  upper  eyelid  has  also  been 
noticed,  as  well  as  hemiatrophy  of  the  tongue.  Lesions  of  the  aorta 
(atheroma  and  aortic  insufiiciency)  are  fairly  common  in  tabes.  It  may  be 
asked  whether  they  are  due  to  trophic  trouble  or  to  syphiUs  and  rheumatism, 
which  are  often  associated  with  tabes. 

The  secretory  troubles  are  diarrhoea,  occurring  in  a  continuous  form, 
or  in  crises,  with  or  without  cohc — it  may  last  for  months  and  years — sialor- 
rhoea,  and  vomiting,  which  supervene  apart  from  the  gastric  troubles. 
The  sweat  is  sometimes  suppressed,  sometimes  abundant.  The  sweating 
may  be  limited  to  the  feet,  the  hands,  one  side  of  the  body,  or  the  head. 

Defaced  Form. — In  more  instances  than  we  are  wont  to  think  the 
disease  is  defaced  at  its  commencement,  and  remains  defaced  for  months 
and  years.  It  only  reveals  itseK  then  by  an  isolated  s}Tnptom,  which  at 
first  sight  seems  to  have  no  relation  with  locomotor  ataxy,  of  which,  how- 
ever, it  is  the  precursor.  Patients  may,  for  example,  suffer  from  progressive 
amblyopia,  while  the  other  manifestations  of  locomotor  ataxy  do  not  show 
a.  80 


1254  TEXT-BOOK  OF  MEDICINE 

themselves  till  months  and  years  later.  The  same  remark  apphes  to  the 
ocular  paralyses  and  visceral  neuralgia.  The  crises  of  gastralgia,  with 
vomiting,  which  so  closely  simulate  ulcer  of  the  stomach ;  the  vesical, 
urethral,  and  rectal  crises ;  the  lumbar  pains,  with  retraction  of  the  testes, 
which  might  readily  be  taken  for  renal  cohc,  are  all  manifestations  which 
may  mark  the  commencement  of  tabes  with  an  isolated  symptom.  Auditory 
troubles ;  deafness,  with  or  without  vertigo  (lesion  of  the  auditory  nerve) ; 
laryngeal  troubles ;  spasms  of  the  glottis,  with  or  without  falling  of  the 
patient ;   and  angina  pectoris,  are  aU  early  manifestations  of  tabes  dorsahs. 

Bladder  troubles  (dysuria,  incontinence,  and  retention),  genital 
troubles  (impotence,  spermatorrhoea,  satyriasis,  and  chtoridea%  crises), 
secretory  troubles  (diarrhoea,  sialorrhoea,  sweating,  and  polyuria),  trophic 
troubles  (shedding  of  the  nails  or  teeth,  "  mal  perforant,"  and  ichthyosis), 
may  precede  the  customary  and  classical  troubles  of  tabes. 

Even  the  painless  arthropathy  of  the  first  period  may  be  looked  upon  as 
a  local  joint  affection,  when  it  really  belongs  to  the  trophic  troubles  of 
ataxy.  It  will  be  important  to  remember  these  facts  when  we  have  to 
discuss  the  diagnosis. 

Course — Diagnosis. — Locomotor  ataxy  has  been  divided  into  three 
periods,  but  these  periods  lend  themselves  but  httle  to  a  methodical  division, 
for  they  are  extremely  variable  as  to  duration  and  as  to  their  time  of 
appearance.  In  some  exceptional  cases  the  disease  runs  a  rapid  course, 
reaching  the  stationary  stage  within  the  first  year,  but  more  frequently  it 
lasts  from  six  to  twenty  years,  or  even  longer.  In  some  circumstances  the 
ataxic  symptoms  only  appear  years  after  other  tabetic  troubles.  Generally 
speaking,  the  cerebral  troubles  are  consecutive  to  the  medullary  troubles, 
but  in  some  cases  the  contrary  is  observed,  and  the  patient  is  attacked  at 
first  by  cerebral  troubles  (apoplectiform  congestion,  paralysis,  or  madness), 
and  only  becomes  ataxic  later  (Fournier). 

The  prognosis  of  locomotor  ataxy,  though  very  grave,  is  not  absolutely 
fatal,  because  the  posterior  sclerosis  is  sometimes  arrested.  Under  the  name 
of  benign  tabes,  Charcot  has  collected  cases  of  people  who  had  only  some 
few  tabetic  symptoms,  developing  with  extreme  slowness,  and  possibly 
ending  in  recovery. 

The  diagnosis  is  especially  difficult  in  the  defaced  cases.  An  error 
is  most  frequently  avoided  if  care  is  taken  to  inquire  into  the  nature  of  the 
painful  crises,  if  the  absence  of  the  reflex  of  the  tendo  AchiUis  is  found, 
if  the  patient  is  carefuUy  questioned  on  some  phenomenon  which  he  has 
failed  to  notice,  and  if  this  phenomenon  is  joined  to  another  phenomenon 
which  has  passed  unnoticed.  The  patient  must  be  asked  whether  he  has 
ever  had  Hghtning  pains,  or  suffered  from  diplopia,  strabismus,  achroma- 
topsia, amblyopia,  deafness,  or  some  of  the  numerous  genital,  vesical,  trophic, 


DISEASES  OF  THE  SPINAL  CORD  1255 

and  secretory  troubles  which  we  have  reviewed.  Tlie  condition  of  the 
reHexes  and  the  various  kinds  of  muscular  sense  must  be  carefully  examined. 
It  is  rare  if,  after  a  minute  examination,  we  do  not  succeed  in  discovering 
the  correct  diagnosis. 

The  cerebro-spinal  fluid  should  be  examined  in  most  cases.  Lympho- 
cytosis is  the  rule  in  tabetic  patients,  and  the  exception  in  pseudo-tabes  due 
to  peripheral  neuritis.  We  must,  further,  assure  ourselves  of  the  almost 
constant  presence  of  albumin  in  the  cerebro-spinal  fluid  in  tabetic  patients. 
On  boihng  the  Hquid,  we  see  a  marked  albuminous  cloud,  while  in  the  normal 
condition  heat  only  produces  very  shght  opalescence. 

Examination  by  cyto-diagnosis  and  the  albumin  test  will  be  considered 
in  conjunction  with  the  chnical  signs  in  doubtful  cases  and  in  cases  of 
pseudo-tabes.  Pseudo-tabes  associated  with  polyneuritis  is  seen  after 
infectious  diseases,  in  diabetes,  and  in  chronic  poisoning,  especially  by 
alcohol.  It  is  well  to  remember  the  possibihty  of  error,  in  order  to  avoid 
it.  In  alcohohc  pseudo-tabes  the  paresis,  the  ataxic  symptoms  and  the  pains 
are  early,  rapid,  and  dominant.  They  are  associated  with  symptoms  of 
alcohohc  intoxication  (trembUng  of  the  hands,  dreams,  nightmare,  etc.). 
They  are  sometimes  followed  by  muscular  atrophy,  but  they  are  hardly 
ever  accompanied  by  hghtning  pains,  visceral  crises,  ocular  paralyses, 
disorders  of  the  sphincters,  etc.,  which  in  true  tabes  form  the  preataxic 
period. 

Locomotor  ataxy  (Ducherme's  disease)  should  not  be  confounded  with 
Friedreich's  disease.  The  latter  malady  has  been  wrongly  called  "  hereditary 
ataxy."  It  is  indeed  hereditary,  and  especially  common  in  famihes,  but 
heredity  also  plays  a  considerable  part  in  Ducherme's  disease.  The  muscular 
ataxy  described  by  Friedreich  is  an  affection  which  has  somewhat  indefinite 
anatomical  characters,  although  its  clinical  features  are  well  recognized. 
It  is  an  affection  of  childhood  and  puberty.  While  it  is  not  locomotor 
ataxy,  disseminated  sclerosis,  or  a  combination  of  these  two  diseases,  it 
borrows  from  the  former  the  motor  inco- ordination  of  the  Hmbs  and  the 
absence  of  the  knee-jerk,  from  the  latter  nystagmus  and  scanning  speech. 
It  differs,  however,  from  both  in  its  other  symptoms,  its  aetiology,  its  mode 
of  evolution,  and  its  prognosis  (Charcot).  The  hghtning  pains,  the  vesical 
crises,  the  anaesthesias,  and  the  trophic  troubles  met  with  in  Duchenne's 
ataxy  are  absent  in  Friedreich's  ataxy.  Vertigo,  epileptiform  attacks, 
and  optic  neuritis,  are  also  absent  in  Friedreich's  disease. 

The  diagnosis  becomes  very  difficult  if  other  affections  of  the  nervous 
system  are  juxtaposed  with  tabes.  These  afiections  associated  with  tabes 
include  general  paralysis,  syphihs  of  the  nerve  centres,  hemiatrophy  of 
the  tongue,  progressive  muscular  atrophy,  Friedreich's  disease,  syringo- 
myeha,  and  hysteria.     Under  such  circumstances  the  diagnosis  may  present 

80—2 


1256 


TEXT-BOOK  OF  MEDICINE 


serious  difficulties,  for  the  similar  signs  are  more  mimerous  than  the  differ- 
ential ones. 

Pathological  Anatomy. — We  know  to-day  that  the  lesion  of  loco- 
motor ataxy  is  a  sclerosis,  affecting  to  an  unequal  extent  the  spinal 
cord,  the  mesencephalon,  the  encephalon,  the  great  sympathetic,  and  the 
nerves. 

1.  With  regard  to  the  encephalon,  the  changes,  though  frequent,  are 
not  constant,  and  the  locahzation  takes  place  without  order  and  without 
system,  thus  differing  from  the  medullary  lesion,  which  is  systematic. 
We  meet  with  sclerosis  in  the  inferior  peduncles  of  the  cerebellum,  and  in 
certain  cranial  nerves,  such  as  the  optic,  the  auditory,  and  the  common 
oculo-motor  nerve.  The  most  common  and  the  best  known  encephahc 
lesion  is  that  of  the  optic  nerves.  It  commences  in  one  nerve  before  in- 
vading the  other.     Like  peripheral  neuritis,  it  advances  progressively  from 


Fig.  68. — Section  ojf  the  Spi^tal  Coed  est  the  Dorsal  Region. 

A,  anterior  comu  ;  P,  posterior  cornu  ;  C,  Clarke's  column  ;  I,  direct  pyramidal 
tract ;  II,  crossed  pyramidal  tract ;  ///,  anterior  radicular  tract ;  IV,  direct  cerebellar 
tracts ;  V,  Gowers'  tract  ;  VI,  motor  and  vasomotor  portion  of  the  mixed  tract ; 
VII,  sensory  portion  of  the  mixed  tract ;  VIII,  Burdach's  tract,  containing  in  its 
external  third  the  fascicuh  cuneati  of  Charcot  and  Pierret ;  IX,  Goll's  column. 

the  periphery  towards  the  optic  tracts  and  the  geniculate  bodies,  and  gives 
rise  to  grey  induration  of  the  nerves ;  and  as  the  lesion  of  the  nerve 
fibre  seems  to  precede  the  invasion  of  the  connective  tissue,  the  neuritis 
might  be  called  parenchymatous. 

Locomotor  ataxy  may  precede,  follow,  or  coincide  with  general  paralysis 
of  the  insane.  In  these  special  forms  we  then  find  the  lesions  of  dif^se 
meningo-encephahtis.  These  forms  are  of  great  interest  from  the  point  of 
view  of  prognosis. 

2.  As  regards  the  bulb  and  the  pons,  we  see  in  some  cases  that  the 
sclerosis  of  the  posterior  columns  continues  under  the  floor  of  the  fourth 
ventricle.  It  invades  the  nuclei  of  the  restiform  bodies,  the  substantia 
gelatinosa  of  Rolando,   the  ascending  root  of  the  trigeminal  nerve,   and 


DISEASES  OF  THE  SPINAL  Cr)RD  1257 

flometimcs  caiiae.s  atrophy  of  the  sen?ory  nuclei  of  the  glosso-pharyngeal, 
flpinal  accessory,  and  pneumogastric  nerves. 

Dejerine  has  often  observed  atrophy  of  the  niuhnis  of  the  sixth  pair 
and  of  the  corresponding  radicular  fillets.  Several  writers  have  noticed 
atrophy  of  the  auditory  nerves  and  of  the  nuclei. 

Before  describing  the  lesions  of  the  spinal  cord,  I  give  here  a  diagram 
of  a  section  of  the  cord,  in  order  to  facihtate  the  description  of  these  lesions. 

3.  Of  the  changes  in  the  spinal  cord,  some  are  constant  and  others  in- 
constant. The  latter  are  situated  in  the  anterior  comua  and  the  lateral 
columns.     We  shall  return  to  them  later. 

The  constant  and  characteristic  changes  in  tabes  dorsaUs  invade  the 
posterior  spinal  system — that  is  to  say,  the  posterior  columns,  the  most 
posterior  portion  of  the  grey  matter,  the  posterior  nerve  roots,  and  the 
adjacent  meninges.  The  sclerosis  of  the  posterior  columns  commences 
in  the  lumbar  region,  where  in  general  it  is  more  pronounced  than  elsewhere. 
It  ascends  into  the  cervical  and  bulbar  regions,  and  it  may  even  reach  the 
floor  of  the  fourth  ventricle. 

When  the  sclerosis  is  of  long  .standing,  the  posterior  columns  are  in- 
durated, greyish,  and  atrophied.  They  are  soldered  together  "  by  the  forma- 
tion of  new  cormective  tissue,  at  the  expense  of  the  pia  mater,  which  thrusts 
itself  into  the  furrow  separating  them  in  the  healthy  condition  "  (Comil 
and  Ranvier).  This  chronic  posterior  meningitis  is  constant,  according  to 
Vulpian,  who  questions  whether  it  does  not  play  an  important  role  "  as  a 
productive  cause  in  the  pathogenesis  of  tabes  dorsaUs."  According  to 
Dejerine,  the  meningitis  and  cortical  meningo-myelitis  explain  the  propaga- 
tion of  the  lesions  to  the  lateral  columns  in  cases  where  lateral  sclerosis 
complicates  posterior  sclerosis. 

P.  Marie  and  Guillain  attribute  the  chief  part  in  the  development  of 
tabetic  lesions  to  posterior  meningitis,  and  to  the  changes  in  the  posterior 
lymphatic  system  of  the  spinal  cord. 

Is  the  grey  matter  of  the  posterior  cornua  afiected  ?  At  first  sight  it 
would  seem  as  though  it  must  be  so,  on  account  of  its  intimate  relations 
with  the  posterior  columns.  And  yet  the  cells  of  the  posterior  cornu  are 
almost  unaffected,  but  the  radiating  fibres  from  the  posterior  column  are 
involved  (Lissauer).  In  Clarke's  columns,  tabes  attacks  the  reticulum, 
but  not  the  cells. 

The  posterior  roots  of  the  spinal  nerves  are  shrunken  to  less  than  half 
their  normal  size.  We  know  that  as  soon  as  the  fibres  of  the  posterior 
roots  enter  the  cord  they  di\^de  into  two  terminal  branches.  One  descends 
in  Burdach's  column,  which  in  its  external  third  contains  the  external 
band  of  Charcot  and  Pierret,  and  soon  ends  in  the  cord  ;  the  other  ascends 
verticallv  in  the  posterior  cord,  to  end  at  different  levels  in  the  posterior 


1258  TEXT-BOOK  OF  MEDICINE 

cornu.  Some  fibres  reach  ttie  bulb.  These  terminal  branches  give  out 
collateral  branches,  which  penetrate  the  grey  matter  by  fine  arborizations. 
The  shortest  soon  terminate  around  the  nearest  cells.  Those  of  average 
length  form  a  rich  plexus  around  the  cells  of  Clarke's  column,  which  send  a 
tract  of  fibres  to  the  cerebellum.  Others  pass  through  the  posterior  grey 
commissure,  and  lose  themselves  in  the  posterior  cornu  of  the  opposite 
side.  Finally,  there  are  long  collaterals  forming  Kolhcker's  reflex  collateral 
bundle  (sensitive -motor  tract  of  Ramon  y  Cajal),  and  ending  in  the  anterior 
cornu. 

This  collateral  system,  described  by  Ramon  y  Cajal,  is  the  seat  of  constant 
and  early  lesions  in  tabes,  as  Lissauer  and  Weigert  have  shown.  Pierret, 
in  1871,  had  noticed  the  degeneration  of  the  nerve  fibrils  in  the  grey  matter 
of  the  posterior  cornua.  The  degeneration  of  the  reflex  collaterals  and  of 
the  collaterals  of  Clarke's  column  exists  from  the  commencement  of  tabes 
(Marinesco).     It  always  coincides  with  the  change  in  the  posterior  cords. 

The  posterior  roots  are  the  seat  of  very  evident  lesions  in  old  tabes ; 
their  integrity  has  only  been  noted  at  the  commencement  of  tabes.  Vulpian, 
in  1874,  and  Schultze,  Leyden,  and  Dejerine  later,  held  that  the  medullary 
lesion  was  due  to  neuritis  of  the  posterior  roots.  The  lesions  of  the  gangha 
are  much  more  vague  and  uncommon.  The  result  of  Vulpian's  interesting 
researches  is  that  the  posterior  roots,  which  are  much  afiected  between  the 
spinal  cord  and  the  ganghon,  are  perfectly  healthy  beyond  the  ganghon. 
This  fact  would  seem  to  prove  that  the  lesion  does  not  commence  in  the 
periphery  of  the  nerves,  in  order  to  ascend  towards  the  spinal  cord,  any 
more  than  it  commences  in  the  roots,  because  we  find  the  posterior  roots 
almost  healthy,  while  the  posterior  columns  are  diseased.  Tabes  com- 
mences, then,  in  the  posterior  columns,  and  extends  to  the  neighbouring 
parts,  and  this  systematic  sclerosis  leads  us  to  suppose  that  the  myehtis  is 
at  first  parenchymatous  (Hallopeau),  before  becoming  interstitial,  the 
initial  irritation  aflecting  the  nerve  fibre  before  it  attacks  the  connective 
tissue. 

The  primary  and  constant  lesion,  as  we  have  said,  is  the  systematic 
sclerosis  of  the  posterior  column  of  the  spinal  cord.  This  fact,  however, 
requires  explanation.  The  posterior  column  of  the  spinal  cord  is  itself 
divided  into  several  independent  territories,  the  distinct  lesions  of  which 
cause  various  symptoms.  Knowledge  gained  from  embryology,  anatomy, 
and  pathology  shows  us  that  each  posterior  column  of  the  marrow  is  divided 
into  two  secondary  bundles,  the  one  median  and  the  other  external,  the 
respective  size  of  the  bundles  varying  according  to  the  regions  of  the  spinal 
cord. 

The  median  bundle,  which  is  thin  in  the  lumbar  region,  larger  in  the 
dorsal  region,  and  threadlike  in.  the  cervical  region  (Goll's  column),  ends  in 


DISEASES  OF  THE  SPINAL  CORD  12r,9 

the  posterior  pyramids.  This  median  bundle  exists,  then,  throui^hout  the 
entire  length  of  tlie  spinal  cord,  it  is  composed  of  longitudinal  libres, 
arising  in  the  grey  matter  at  various  levels  and  in  relation  with  the  cells  of 
Clarke's  vesicular  columns.  The  longer  the  tract  that  these  longitudinal 
fibres  have  to  pass  through,  the  more  superficial  they  arc.  Some  of  them 
are  of  sufficient  length  to  unite  the  lumbar  swelhng  with  the  posterior 
pyramids. 

The  external  or  Burdach's  column  contains  in  its  outer  tliird  the  fasci- 
culus cuneatus,  which  is  also  found  throughout  the  entire  length  of  the 
cord.  It  is  formed,  on  the  one  hand,  of  commissural  fibres,  that  estabUsh 
intimate  relations  between  the  various  points  of  the  posterior  grey  matter 
(Todd,  Vulpian),  and,  on  the  other  hand,  of  fibres  having  a  transverse  and 
obhque  direction,  arising  in  the  posterior  roots  of  the  nerves,  and  joining 
the  cells  of  the  posterior  cornu. 

The  posterior  columns  of  the  cord  are  formed  by  Goll  and  Burdach's 
columns,  containing  the  fascicuh '  cuneati.  In  tabes  dorsahs  does  the 
change  invade  the  entire  posterior  column,  or  does  it  remain  Hmited  to 
one  of  the  two  secondary  bundles  ?  And  in  this  case  which  one  of  them 
is  affected  ?  Is  it  Goll's  or  Burdach's  column  ?  When  post-mortem 
examinations  are  performed  at  an  advanced  period  of  the  disease,  we  find 
that  the  sclerosis  affects  all  of  the  posterior  bundles ;  but  when  the  anatomical 
examination  is  carried  out  at  less  advanced  stages,  the  lesion  may  be  ob- 
served in  various  phases  of  its  evolution  (Pierret),  and  we  see  side  by  side 
with  the  primary,  characteristic  and  constant  lesion  other  lesions  that  are 
secondary  and  inconstant. 

The  characteristic  and  constant  lesion  is  in  Burdach's  column.  Amongst 
the  secondary  lesions  we  find  degeneration  of  Goll's  column.  Isolated 
sclerosis  of  Goll's  column  in  the  cervical  region  occurs  as  a  secondary 
ascending  sclerosis  when  the  dorsal  portion  of  the  spinal  cord  is  affected 
(Pott's  disease,  tumours).  It  is  accompanied  neither  by  hghtning  pains 
nor  by  ataxy.  This  is  a  proof  that  the  isolated  sclerosis  is  not  dependent 
on  the  tabetic  sjmiptoms,  and  if  it  is  frequently  found  post  mortem  in  tabes 
dorsahs,  it  is  simply  consecutive  to  the  dorso-lumbar  lesion  of  tabes  (Pierret), 
just  as  it  is  consecutive  to  a  tumour  or  to  Pott's  disease.  We  must  not, 
therefore,  seek  for  the  lesion  of  tabes  in  the  sclerosis  of  GoU's  column. 

The  constant  and  characteristic  lesion  of  tabes  is  situated  in  the  fasciculi 
cuneati,  and  Pierret  has  collected  several  cases  in  which  the  disease  was 
only  in  the  stage  of  hghtning  pains  and  sclerosis  was  present  in  the  fasciculi, 
without  any  change  in  GoU's  columns.  The  medullary  lesion  commences, 
then,  in  the  fascicuh  cuneati  of  Burdach's  column,  invades  the  posterior 
spinal  roots  and  the  posterior  grey  matter,  and  causes,  secondarily,  ascending 
sclerosis  of  Goll's  columns. 


1260  TEXT-BOOK  OF  MEDICINE 

Philippe  stained  a  series  of  sections  of  the  cord  according  to  the  Weigert- 
Pal  process.  He  was  thus  able  to  determine  the  early  and  the  more  advanced 
lesions  of  tabes.  At  the  commencement  the  fascicuH  cuneati  are  the  first 
to  be  attacked  in  their  middle  radicular  fibres.  If  the  disease  is  of  long 
duration,  the  lesions  constantly  affect  the  descending  bundle,  and  in  a 
lesser  degree  the  ascending  bundle.  The  invasion  of  the  endogenous  bundles 
is  characteristic  of  advanced  tabes.  GoU's  cord  undergoes  a  secondary 
degeneration  in  the  cervical  region  (Pierret),  but  it  may  be  primarily  attacked 
in  the  lumbar  region.  The  histological  process  is  essentially  parenchy- 
matous. "  The  parench}Tnatous  lesions  exist  from  the  commencement  of 
tabes  in  the  nerve  fibre.  The  ceU  of  the  vertebral  ganghon  remains  intact. 
The  parenchymatous  lesions  are  especially  primary  "  (Phihppe). 

4.  The  lesions  of  the  great  sympathetic  are  at  present  imperfectly 
worked  out.  Lesions  of  the  ganglia  have,  however,  been  met  with,  which 
is  not  to  be  wondered  at,  seeing  that  the  spinal  origin  of  the  great  sym- 
pathetic appears  to  be  in  the  posterior  vesicular  columns  and  in  Clarke's 
intermedio-lateral  tract  (Pierret).  Neuritis  has  been  noticed  in  various 
plexuses. 

5.  Peripheral  Neuritis. — Some  of  the  peripheral  nerves  are  attacked 
by  neuritis.  This  lesion,  though  not  constant,  is  very  frequent.  These 
changes  affect  the  periphery  of  the  nerves,  and  are  most  frequently  peri- 
pheral from  the  outset.  As  a  matter  of  fact,  the  corresponding  spinal 
gangha,  up  to  a  certain  distance,  are  healthy.  The  peripheral  neuritis  may 
be  very  pronounced,  even  in  early  tabes,  and,  inversely,  the  peripheral 
nerves  may  be  healthy  in  cases  in  which  the  posterior  columns  of  the  marrow 
have  for  a  long  time  been  sclerosed.  In  some  cases  peripheral  neuritis  has 
been  met  with  on  one  side  only,  whereas  the  lesion  in  the  spinal  cord  is 
symmetrical.  These  facts  prove  that  peripheral  neuritis  in  tabes  may 
evolve  on  its  own  account  parallel  with  the  lesion  in  the  cord,  but  without 
being  directly  associated  with  it.  Besides,  this  autonomy  of  peripheral 
neuritis  does  not  afiect  Waller's  law,  but  proves  that  peripheral  lesions  of 
the  nerves  may  arise  independently  of  lesions  in  the  trophic  centres. 

The  peripheral  neuritis  may  attack  the  sensory,  mixed,  or  visceral 
nerves.  It  is  very  frequent  in  the  cutaneous  nerves,  and  has  also  been 
met  with  in  the  branches  to  the  muscles.  Amongst  other  nerves  attacked 
by  peripheral  neuritis  I  may  mention  the  nerves  of  the  levator  palpebrse 
superioris  (Dejerine),  the  recurrent  and  the  pneumogastric  (Oppenheim), 
the  cardiac  plexus,  the  coehac  plexus,  and  the  abdominal  sympathetic 
(Groeeo  and  Fusari).  The  neuritis  is  of  a  parenchymatous  nature- 
atrophied  nerve  fibres,  or  fibres  in  course  of  destruction,  interstitial 
lesions,  and  perineuritis.  In  some  cases  the  peripheral  neuritis  is  curable 
(Pierret). 


DISEASES  OF  TEIE  SPINAL  CORD  12C1 

Pathological  Physiology. — Is  tho  appoaranre  of  tho  symptoms  of  loro- 
motor  atuxy  in  n-latiou  with  tlic  systematic  invasion  of  the  lesion  ?  This 
question  will  now  be  discussed. 

Pain. — In  the  stage  of  the  hghtning  pains  the  lesion  is  confined  to  the 
fasciculi  cimeati  in  the  shape  of  a  very  thin  and  limited  band  of  sclerosis. 
As  the  posterior  roots  of  the  spinal  nerves  are  not  attacked  at  this  period, 
it  must  be  admitted  that  the  pains  of  tabes  dorsaUs  are  due  to  the  change 
in  the  posterior  roots  during  their  intraspinal  course.  These  lesions 
fully  explain  the  pains  in  the  Umbs  and  in  the  trunk,  but  when  it  is  a 
question  of  the  crises  of  the  stomach,  bladder,  rectum,  and  kidneys,  it  is 
probable  that  we  must  refer  them  to  peripheral  neuritis  in  the  corresponding 
visceral  plexuses.  Peripheral  neuritis  of  the  laryngeal  and  pneumogastric 
nerves  explains  the  laryngeal  crises. 

Anaesthesia. — The  diminution,  loss,  and  perversion  of  the  senses  of 
touch,  pain,  temperature,  and  orientation,  as  well  as  of  the  muscular  and 
articular  sensibility,  are  phenomena  observed  only  at  a  fairly  advanced 
period  of  the  disease.  The  anaesthesia  and  analgesia  are  often  patchy. 
They  are  sometimes  complete  (foot,  leg,  and  face),  and  there  is  often  a  delay 
of  several  seconds  in  the  perception  of  the  sensations.  What  are  these 
phenomena  due  to  ? 

This  question  has  been  carefully  discussed  by  Vulpian.  It  may  be  thus 
summed  up  :  The  impressions  received  at  the  periphery  are  carried  by  the 
fibres  of  the  posterior  nerve  roots  to  the  grey  matter  of  the  spinal  cord. 
It  is  probable  that  the  impression  passes  from  the  grey  matter,  in  which  it 
is  elaborated,  into  the  posterior  coliimns,  which  transmit  it  to  the  brain ; 
and  if  these  columns  are  destroyed  for  a  certain  extent,  it  is  the  grey  matter 
which  undertakes  to  re-establish  the  path  of  the  sensory  impressions.  One 
thing  is  certain — viz.,  that  the  sensory  impressions  have  not  an  exclusive 
route  in  their  medullary  passage.  The  path  of  transmission  may  vary 
according  to  the  need,  and  the  paths  of  communication  supplement  one 
another  so  well  that  sensory  troubles  presuppose  an  already  extensive 
lesion  in  the  cord.  The  diminution  and  the  loss  of  sensibiUty  are  conse- 
quently due  to  the  multiple  lesions  of  the  posterior  cords,  of  the  posterior 
grey  matter,  and  of  the  corresponding  spinal  roots ;  and  as  to  the  delay  in 
the  transmission  of  sensory  impressions,  it  may  be  asked  "  whether  it  is 
not  due  to  the  atrophy  of  the  posterior  columns,  and  to  the  necessity  of  the 
impressions  abandoning  the  direct  path  of  the  white  bundles,  to  foUow  more 
slowly  the  tortuous  path  of  the  grey  matter  "  (Vulpian). 

Another  cause,  no  doubt,  exists  to  explain  the  patches  of  hyperaesthesia 
and  of  anaesthesia  and  the  delay  of  the  sensations — viz.,  the  neuritis  of  the 
peripheral  cutaneous  nerves.  We  must  admit  the  important  part  played 
by  peripheral  neuritis,  because  the  disturbances  in  the  senses  of  touch, 


1262  TEXT-BOOK  OF  MEDICINE 

pain,  and  of  temperature  are  more  marked  at  the  extremities,  and  diminish 
from  below  upwards  (Dejerine). 

Ataxy. — It  is  exceptional  for  the  loss  of  co-ordination  of  movements 
to  appear  from  the  commencement  of  the  disease.  It  shows  itseK  two  or 
three  years,  and  even  longer,  after  the  Hghtning  pains  and  visceral  crises. 
Raynaud  has  found  that  in  certain  cases  where  visceral  crises  were  present, 
to  the  exclusion  of  the  pains  in  the  extremities,  the  symptom  of  ataxy  was 
indefinitely  delayed.  However  this  may  be,  ataxy  of  the  lower  or  upper 
hmbs  always  shows  itself  by  the  same  symptoms.  Muscular  force  persists 
as  to  quantity  at  least  for  a  long  time,  but  it  lacks  regulating  power,  the 
movements  either  exceeding  their  object  or  faihng  to  reach  it.  The  patient 
with  ataxy  cannot  regulate  the  quality  or  the  amplitude,  so  that  we  find 
want  of  co-ordination  of  the  voluntary  movements  and  "  disorder  of 
mechanical  co-ordination"  (Jaccoud).  The  pathogenesis  of  this  ataxy 
has  given  rise  to  much  discussion. 

According  to  Charcot  and  Pierret,  the  ataxy  appears  when  the  sclerosis 
of  the  fasciculi  cuneati  extends,  both  internally  and  externally,  and  they 
interpret  this  fact  by  admitting  that  the  commissural  fibres  and  the 
fascicuh  cuneati  "  serve  in  the  co-ordination  of  the  movements  of  the  hmbs." 
This  hypothesis  is  not  yet  based  on  a  sure  foundation. 

Other  writers  have  advanced  a  theory,  based  on  cutaneous  anaesthesia, 
both  muscular  and  articular.  The  troubles  of  sensibihty  destroy,  on  the 
one  hand,  the  source  of  the  reflex  actions,  and,  on  the  other,  they  deprive 
the  muscles  of  the  ideas  of  force,  resistance,  extent,  and  duration,  which 
govern  the  synergy  of  the  contractions  (muscular  sense).  This  theory, 
which  at  first  sight  is  seductive,  appears  to  be  overthrown  by  these  two 
facts.  We  find  hysterical  patients  who  are  deprived  of  sensibihty,  and 
who  do  not  suffer  from  ataxy,  and  also  patients  suffering  from  ataxy  who 
have  very  advanced  motor  inco-ordination,  when  their  sensibihty  is  almost 
normal  (Duchenne).  Nevertheless,  the  peripheral  lesions  of  the  sensory  nerves 
and  the  consequent  anaesthesia  might  well  be  comiected  with  the  troubles 
of  inco-ordination. 

According  to  Jaccoud,  sclerosis  of  the  posterior  columns  produces  ataxy 
by  causing  disturbance  of  the  reflex  actions  and  of  the  spinal  radiations — 
that  is  to  say,  by  destrojdng  the  nerve  fibres  which,  arising  from  the  pos- 
terior roots,  extend  as  far  as  the  anterior  cornua  of  the  grey  matter  (reflex 
motor  fibres),  or  as  far  as  Gerlach's  nervous  network.  These  fibres  appear 
to  have  a  regulating  action  on  the  previously  estabhshed  synergic  contrac- 
tion of  the  groups  of  muscles. 

According  to  Pierret,  "  the  prime  cause  of  locomotor  ataxy  is  said  to 
be  an  irritation  of  the  sensory  fibres  of  the  nervous  centres."  The  irrita- 
tion of  these  fibres  has  the  effect  of  paralyzing  certain  muscles,  or  groups 


DISEASES  OF  THE  SPINAL  CORD  VlCr, 

of  muscles,  by  reflex  action,  and  "  as  soon  as  an  attempt  at  movement  is 
madi^  in  which  the  parotic  muscle  is  autagonistic  to  the  healthy  miLscle, 
the  former  overrides  the  latter,  and  the  movement  exceeds  its  ohject." 
The  ataxy  would  thus  Ix^  explained.  "  There  is  no  need  for  me  to  dwell,*' 
says  Grasset,  '"  on  the  objections  to  this  theory,  which  has  need  of  fresh 
proofs." 

Onimus  has  put  forward  the  view  that  the  want  of  co-ordination  is  due 
to  contractures.  The  word  "  contracture  "  must  not  be  taken  here  in  its 
most  common  acceptation,  wliich  supposes  rigidity  of  the  muscular  fibre. 
There  are  less  marked  degrees,  and  it  may  be  said  that  contracture  exists 
in  a  muscle  as  soon  as  its  natural  suppleness  is  lessened,  and  as  soon  as  it 
experiences  a  difficulty  in  relaxing  after  voluntary  contraction.  In  patients 
suffering  from  ataxy  these  phenomena  of  muscular  rigidity  accompany 
the  disease  throughout  its  course,  but  they  are  more  marked  as  the  malady 
progresses.  What  happens  then  ?  When  the  patient  suffering  from  ataxy 
wishes  to  make  a  movement,  he  experiences  a  certain  resistance,  due  to  this 
state  of  contraction,  and  in  order  to  overcome  this  resistance  he  employs  a 
force  that  outstrips  the  desired  object,  because  the  disturbance  of  the 
muscular  and  cutaneous  sensibility  gives  wrong  information  to  the  spinal 
cord. 

Leyden  has  more  recently  sought  for  the  point  of  departure  of  tabes 
in  the  periphery  itself,  in  the  irritation  of  all  kinds  which  develops  a  centri- 
petal process  of  degeneration,  attacking  and  paralyzing  the  ganghon  cells. 

Brissaud  attributes  the  want  of  co-ordination  to  the  constant  ignorance 
of  the  patient  as  to  the  extent  of  the  resistance  experienced.  The  muscular 
effort,  therefore,  is  always  excessive.  He  is  of  opinion  that  the  primary 
lesion  of  tabes  is  an  affection  of  "  the  centripetal  protoneuroma  " — that  is 
to  say,  of  that  part  of  the  centripetal  system  wliich  is  made  up  of  the  afferent 
nerve  fibres,  the  ganglion  cell,  and  its  afferent  fibres. 

Bonnier  opposes  the  idea  of  motor  inco-ordination  in  the  strict  sense  of 
the  word.  The  elementary  movements  are  said  to  be  weU  co-ordinated, 
but  ill  advised.  A  military  officer,  ignorant  of  the  ground  over  which  he  is 
manoeuvring,  of  the  forces  to  which  he  is  opposed,  and  of  the  condition  of 
his  troops,  might  give  iU-advised  orders,  which  will,  however,  be  perfectly 
executed  by  his  men.  The  sufferer  from  ataxy  executes  movements  that 
prove  the  co-ordination  of  muscular  efforts,  but  these  movements  are  un- 
suitable to  the  end  in  view,  because  the  sufferer  from  ataxy  does  not  know 
how  to  begin,  is  ignorant  when  he  reaches  the  point  of  arrival,  and  cannot 
grasp  the  various  attitudes  required.  It  is  not  the  muscular  sense  that  is 
affected,  but  the  sense  of  the  attitudes. 

The  diversity  of  these  theories  proves  that  the  pathogenesis  of  ataxy 
is  still  a  matter  of  speculation.      Taking   up  the  question,  not  from  the 


1264  TEXT-BOOK  OF  MEDICINE 

pathological,  but  from  tlie  physiological,  point  of  view,  we  see  that  the 
explanation  of  the  co-ordination  of  the  movements  given  by  Duchenne 
is  true.  Even  the  simplest  movement  can  only  be  carried  out  by  the  co- 
operation of  several  muscles.  It  requires  the  contraction  of  the  muscles 
which  are  to  produce  this  movement,  and  the  contraction  of  the  antagonistic 
muscles  which  are  to  hmit  this  movement.  The  flexor  muscles  have  the 
extensor  muscles  as  antagonists,  just  as  the  adductor  muscles  have  the 
abductor  ones.  The  regularity  of  a  movement  supposes,  then,  the  harmony 
of  contraction  of  the  muscles  which  produce  the  movement,  and  the  harmony 
of  the  antagonistic  muscles  destined  to  limit  this  movement.  If  one  of 
these  factors  is  wanting,  the  movement  is  no  longer  co-ordinated,  and  ataxy 
results. 

Why  are  one  or  both  of  these  factors  compromised  in  posterior  spinal 
sclerosis  ?     The  preceding  theories  are  attempts  to  solve  this  problem. 

Paralysis  and  Atrophy. — I  have  said  that  in  the  different  periods  of 
muscular  ataxy  we  sometimes  see  transient  or  persistent  paralyses.  These 
paralyses  may  be  due  to  focal  lesions  in  the  brain,  to  the  extension  of  the 
posterior  sclerosis  to  the  lateral  columns  of  the  cord,  to  the  peripheral 
changes  in  the  motor  nerves,  and  to  the  association  of  hysteria  with  tabes. 
The  muscular  atrophies  are  in  some  cases  due  to  change  in  the  cells  of  the 
anterior  cornua,  especially  in  those  of  the  external  group.  According  to 
certain  observations,  however  (Dejerine),  the  muscular  atrophy  is  said  to 
be  due  to  peripheral  neuritis,  the  motor  cells  and  the  grey  matter  of  the  cord 
being  intact.  In  hemiatrophy  of  the  tongue  degeneration  of  the  bulbar 
nucleus  of  the  hypoglossal  nerve  has  been  found. 

Trophic  and  Secretory  Troubles. — It  seems  certain  that  most  of  the 
trophic  and  secretory  troubles  are  due  to  lesions  in  the  roots,  the  gangha, 
and  the  terminal  branches  of  the  great  sympathetic.  The  peripheral 
neuritis  will  explain  the  trophic  troubles  in  the  skin — various  eruptions, 
oedema,  perforating  disease,  and  shedding  of  the  nails.  Peripheral  neuritis 
may  also  be  responsible  for  the  spontaneous  fractures  and  arthropathies, 
which,  according  to  some  writers,  are  put  down  to  the  lesions  of  the  anterior 
cornua  or  of  the  root  zones.  The  trophic  influence  of  the  trigeminal  nerve 
and  the  neuritis  of  the  branches  of  this  nerve  explain  the  troubles  affecting 
the  teeth  and  the  maxiUa. 

iEtiology — Treatment. — The  causes  of  locomotor  ataxy  are  obscure. 
The  disease  is  more  frequent  in  men  than  in  women,  and  almost  always 
occurs  in  middle  age — from  twenty  to  forty  years.  According  to  certain 
writers  (Fournier,  Vulpian,  Erb,  Marie),  syphihs  is  ahnost  always  to  be 
blamed.  Fournier  has  sustained  this  opinion,  which  is  now  accepted,  but 
it  remains  to  be  seen  whether  syphihs  can  of  itself  produce  locomotor  ataxy, 
or  whether  it  only  acts  as  a  provoking  agent.     A  patient  whom  I  attended 


DISEASES  OF  THE  SPINAL  CORD  1265 

some  years  ago  at  the  Necker  Hospital  for  syphilitic  haemoptysis  had 
at  a  later  date  come  back  into  the  Hotel-Dieu  with  confirmed  tabes. 
Heredity  is  an  inii)ortant  factor.  Sometimes  it  is  direct,  and  then  it  is 
a  case  of  heredo-syphilis  ;  otherwise  it  is  indirect.  How  many  sufferers 
from  tabes  are  there  not  in  whose  family  we  find  madness,  general  paralysis, 
epilepsy,  and  diabetes  a.ssociated  with  the  preceding  causes !  Traumatism 
plays  an  important  role  in  the  development  of  tabes,  and  the  first  s^Tnptoms 
have  often  appeared  after  a  fall  or  a  violent  contusion.  Cases  of  conjugal 
ayphiUtic  tabes  have  been  noticed. 

Treatment. — Raymond  has  discussed  the  treatment  of  tabes  in  detail. 
According  to  him,  true  tabes  is  a  disease,  the  cure  of  which  is  most  prob- 
lematical. 

Pain. — The  pains  may  be  relieved  with  the  following  remedies  :  Injec- 
tions of  morphia,  antipyrin,  acetanilide,  phenacetin,  chloral,  or  sahcylate 
of  soda.  These  remedies  are  of  undoubted  value,  but  their  constant  ad- 
ministration may  have  bad  results.  It  \vill  be  enough  to  remember  that 
sufferers  from  tabes  furnish  an  important  contingent  of  morphomaniacs. 
Other  remedies  have  also  been  recommended — faradization,  continuous 
currents,  refrigeration,  massage,  and  especially  suspension.  Intraspinal 
injections  of  cocaine  can  only  be  given  under  exceptional  conditions. 

The  means  of  treating  the  anaesthesia  and  paraesthesia  are  reduced  to 
faradization  and  carbonic  acid  baths. 

The  remedies  for  the  ocular  troubles  are  multiple.  In  order  to  limit 
papillary  atrophy  and  amblyopia,  we  may  use  subcutaneous  injections 
of  cyanide  of  gold,  silver,  or  platinum  (Galezowski).  The  paralyses  are 
amenable  to  faradization,  and  especially  to  specific  treatment  with  mercury 
and  iodide  of  potassium,  when  the  patient  has  recently  had  syphilis. 

The  ataxy  should  be  treated,  on  the  one  hand,  by  suspension,  and, 
on  the  other,  by  the  so-called  Fraenkel  method,  based  on  the  re-education 
of  the  muscles.  Raymond  speaks  of  the  value  of  this  method.  It  consists 
in  the  systematic  execution  of  movements  which  at  first  are  simple,  and 
become  gradually  more  and  more  complicated,  thus  bringing  into  play 
the  dexterity,  and  not  the  muscular  force,  of  the  patient.  Its  use  is  especially 
indicated  in  cases  of  tabes  with  early  ataxy,  when  the  lower  limbs  are  from 
the  first  so  severely  affected  that  standing  and  walking  are  impossible 
without  a  support.  It  is  contra-indicated  when  the  tabes  has  a  rapid  onset, 
with  acute  and  obstinate  lightning  pains.  It  is  likewise  contra-indicated 
in  patients  suffering  from  spontaneous  fracture,  rupture  of  tendons,  arthro- 
pathy or  cardiopathy,  and  in  obese  patients  poisoned  by  morphia  or 
alcohol.  The  remedy  always  fails  in  tabetic  patients  suffering  from 
amaurosis,  motor  paresis,  and  muscular  atrophy. 

Suspension  has  a  great  advantage  over  Fraenkel's  treatment,  in  that  it 


1266  TEXT-BOOK  OF  MEDICINE 

aims  at  the  improvement  of  the  ataxy,  the  hghtning  pains,  and  the  genito- 
urinary troubles.  On  the  other  hand,  the  method  is  more  severe.  It 
requires  special  education  on  the  part  of  the  physician,  and  it  exposes  the 
patient  to  fatal  risks.  Its  use  is  counterindicated  in  tabetic  patients  suffer- 
ing from  cardio-vascular  troubles  (valvular  lesions,  and  especially  aortic 
lesions) ;  in  tubercular,  emphysematous,  or  stout  persons ;  and,  finally,  in 
those  who  have  had  apoplectiform  or  epileptiform  attacks,  or  who  have  a 
tendency  to  vertigo  or  syncope. 

Does  a  curative  remedy  for  tabes  exist  ?  Raymond  thinks  there  is  none, 
and  I  share  his  opinion.  I  have  seen  tabes  persist  indefinitely,  without 
causing  death.  I  have  seen  some  cases  of  tabes  remain  stationary,  and  others 
improve  up  to  the  point  of  an  apparent  cure,  but  I  doubt  whether  true 
tabes  can  be  cured.  Nitrate  of  silver,  bromide  of  potassium,  preparations 
of  phosphorus,  hydrotherapy,  injections  of  artificial  serum  and  of  testicular 
fluid,  have  aU  enjoyed  well-merited  favour.  They  are  excellent  aids  in 
treatment,  but  they  do  not  bring  about  a  cure.  A  place  apart  must  be 
reserved  for  the  antisyphihtic  treatment,  as  far  as  the  cure  of  tabes  is  con- 
cerned. Nearly  all  tabetic  patients  are  syphihtic.  This  fact  cannot  be 
questioned  (Fournier).  Are  we  to  say  that  the  antisyphihtic  treatment  has 
chances  of  curing  tabes,  or  of  markedly  improving  the  syphihtic  patient 
suffering  from  tabes  ?  If  syphihtic  tabes  is  of  recent  date,  intensive  anti- 
syphihtic treatment,  continued  for  a  long  time,  may  be  of  real  service. 
If  the  tabes  is  inveterate,  heroic  antisyphihtic  treatment  rarely  gives  good 
results.  The  right  treatment  is  prophylactic;  it  consists  in  treating 
syphilis  carefully  with  mercurial  preparations,  or  with  Ehrlich's  606,  as 
soon  as  the  medullary  lesions  have  unmasked  their  batteries. 

n.  FRIEDREICH'S  DISEASE  AND  HEREDITARY  CEREBELLAR 
ATAXY— SPASMODIC  FAMILY  PARAPLEGIA. 

This  disease,  first  described  by  Friedreich,  was  considered  by  its  author 
as  a  variety  of  locomotor  ataxy.  Others  regarded  it  as  a  variety  of  dis- 
seminated sclerosis,  but  it  was  Brousse  who  affirmed  its  autonomy,  and 
gave  it  the  name  of  "  Friedreich's  disease." 

Description. — ^Friedreich's  disease  commences  in  early  hfe.  Difi&culty 
in  walking  opens  the  scene.  The  child  walks  with  heavy,  irregular  steps 
and  legs  apart,  so  that  the  staggering  gait  recalls  drunkenness,  or  the  walk 
due  to  lesions  of  the  cerebellum.  Some  lack  of  co-ordination  is  also  present, 
and  the  gait  was  therefore  called  "  tabeto-cerebellar  "  by  Charcot. 

There  is  also  difl&culty  in  standing,  which  Friedreich  calls  "  static  ataxy." 
The  child,  having  some  difiiculty  in  standing  erect  and  motionless,  on  account 
of  the  oscillations  of  its  body,  is  obhged,  in  order  to  maintain  equihbrium, 
to  change  its  feet  frequently.     The  fine  of  march,  instead  of  being  straight,  is 


DISEASES  OF  THE  SPINAL  CORD  1267 

du'cctod  altcruately  to  the  right  and  to  thu  lul't.  To  these  troubles  are 
added  choreifomi  movements  and  intention  tremors,  resembhng  those  of 
insular  sclerosis.     In  some  cases  athetoid  movements  arc  present. 

Sensory  troubles,  which  play  such  a  prominent  part  in  Duchenne's 
disease,  are  absent  or  insignificant  in  Friedreich's  disease.  Lightning  pains 
are  exceptional,  but  have  nevertheless  been  noted  (Brissaud).  Anaesthesia 
and  analgesia  are  very  rare  and  but  shghtly  marked. 

The  muscular  sense — or,  rather,  "the  sense  of  attitudes"  (Bonnier) — 
the  abohtion  of  which  is  characteristic  of  locomotor  ataxy,  seems  to  bo 
intact  in  Friedreich's  disease.     Choreiform  instabihty  is,  however,  noticed. 

The  tendon  reflexes  are  abohshed.  The  cutaneous  reflexes  are  pre- 
served.   Babinski's  phenomenon  is  seen. 

The  ocular  troubles  principally  affect  the  muscular  system  of  the  eye. 
Nystagmus  is  frequent.  Paralysis  of  the  muscles,  with  or  without  diplopia, 
is  extremely  rare.     Vision  is  normal,  whilst  it  is  often  afiected  in  tabes. 

The  genito-urinary  troubles  are  practically  absent.  The  cerebral 
troubles  are  shght.  The  intelhgence  remains  intact  throughout  the  disease. 
Speech  is  somewhat  halting,  as  in  ataxy. 

Muscular  atrophy  is  sometimes  seen  in  certain  muscles  of  the  trunk  or 
of  the  hmbs. 

Deformities  may  exist  in  the  trunk  in  the  form  of  scoUosis,  and  are 
common  in  the  feet,  the  type  being  that  of  equino-varus,  with  exaggerated 
extension  of  the  big  toe.  This  deformity  is  known  as  "  the  foot  of  Fried- 
reich's disease." 

Such  are  the  S3nnptoms  of  Friedreich's  disease.  After  some  years  the 
troubles  involve  the  upper  hmbs,  and  the  patient  is  absolutely  helpless, 
being  condemned  to  remain  indefinitely  in  bed  or  in  a  chair.  The  disease 
is  rarely  fatal. 

The  diagnosis  of  Friedreich's  disease  is  given  under  Insular  Sclerosis 
and  Tabes. 

etiology. — ^Friedreich's  disease  is  a  family  disease — ^that  is  to  say,  it 
attacks  several  children  of  the  same  family.  It  is  also  hereditary,  and 
Friedreich  therefore  called  it  hereditary  ataxy.  These  two  conditions  are, 
however,  not  absolute.  The  disease  commences  before  the  age  of  fourteen 
years  in  two-thirds  of  the  cases  (Sottla),  and  in  the  same  family  the  "  age 
at  which  the  disease  commences  is  the  same  for  each  member  attacked." 

Pathological  Anatomy. — The  lesions  found  have  not  always  been 
constant  in  the  few  post-mortem  examinations  that  have  been  performed. 
Sclerosis  is  found  in  GoU's  and  Burdach's  columns,  in  the  direct  cerebellar 
tract,  and  the  lateral  tracts  (combined  sclerosis).  The  grey  matter  in  the  reti- 
culum of  Clarke's  columns  is  affected.  Some  writers  have  noticed  changes 
in  the  anterior  cornua.     The  posterior  roots  only  show  irregular  lesions. 


1268  TEXT-BOOK  OF  MEDICINE 

According  to  Dejerine  and  LetuUe,  the  sclerosis  of  the  posterior  columns 
in  Friedreich's  disease  is  said  to  be  a  ghosis,  whereas  that  of  the  cerebellar 
and  of  crossed  pyramidal  tracts  is  said  to  be  a  vascular  sclerosis.  These 
views  are  not  generally  accepted  (Marie). 

Treatment  seems  to  have  no  effect  on  the  disease. 

Hereditary  Cerebellar  Ataxy. 

Let  us  now  refer  to  a  morbid  condition  having  many  relations  with 
Friedreich's  disease,  and  described  by  Marie  under  the  name  of  "  hereditary 
cerebellar  ataxy."  Marie  thus  describes  this  morbid  condition  :  "  Hereditary 
cerebellar  ataxy  is  a  family  disease,  hke  Friedreich's  disease.  It  attacks 
several  generations  more  often  than  Friedreich's  ataxy  does — ^that  is  to  say, 
it  is  more  directly  hereditary.  Its  onset  usually  occurs  at  a  more  advanced 
age  than  Friedreich's  disease,  either  after  the  twentieth  or  sometimes  after 
the  thirtieth  year.  The  initial  symptom  consists  in  motor  disturbances 
in  the  lower  limbs,  perfectly  analogous  to  those  of  Friedreich's  disease — 
staggering  gait,  dif&culty  in  standing  erect  with  or  without  Romberg's 
sign,  pseudo-tremors  of  the  upper  hmbs,  and  nystagmus.  So  much  for  its 
resemblances  to  Friedreich's  disease.  The  principal  differences  consist 
in  the  exaggeration  of  the  patellar  reflexes;  in  the  existence  of  various 
spasmodic  phenoinena ;  in  visual  troubles,  consisting  in  dichromatopsia, 
restriction  of  the  visual  field,  diminution  of  visual  acuity,  and  changes  in 
the  papilla  ;  in  the  loss  or  diminution  of  the  hght  reflex  ;  and,  finally,  in  the 
presence  of  objective  troubles  in  the  cutaneous  sensibihty,  as  weU  as  in  the 
absence  of  trophic  troubles,  such  as  scoHosis,  or  the  club-foot  of  Friedreich's 
disease." 

The  fundamental  lesion  is  atrophy  of  the  cerebellum.  The  atrophy  is 
general  or  partial.  The  cerebellum  may  be  reduced  to  haK  its  normal  size. 
It  is  not  a  question  of  sclerosis.  Perhaps  even,  says  Londe,  it  may  be 
possible,  according  to  the  nature  of  the  lesion,  to  estabhsh  a  difference 
between  sclerotic,  accidental,  non-family  atrophy  of  the  cerebellum  and  the 
family  atrophy  of  hereditary  cerebellar  ataxy.  Spinal  lesions,  which  were 
clearly  defined  and  constituted  the  sole  anatomical  substratum  in  the  cases 
of  Vincelet  and  Switalski,  Thomas  and  Roux,  have  been  noticed.  The 
condition  was  a  combined  sclerosis  of  the  posterior  columns,  of  Gowers' 
tracts,  and  of  the  direct  cerebellar  tracts. 

To  sum  up,  as  Londe  says,  hereditary  cerebellar  ataxy  and  Friedreich's 
disease  seem  to  be  two  forms  of  hereditary  ataxy.  The  lesion  in  the  one  is 
said  to  commence  in  the  cerebellum,  the  lesion  in  the  other  in  the  spinal  cord. 
They  may  both  hmit  themselves  to  the  organ  first  attacked,  but  they  may 
also  be  comphcated,  the.  one  with  spinal  lesions,  the  other  with  cerebellar 
lesions,  thus  forming  types  of  transition  frequent  in  family  diseases  (Charcot). 


DISEASES  OF  TILE  SPINAL  CORD  12G'J 

Spasmodic  Family  Paraplegia. 

Striimpell  noticed  spasmodic  paraplegia  in  two  brothers,  and  at  the  post- 
mortem examination  of  each  one  he  found  in  the  spinal  cord  lesions  in  the 
posterior  and  lateral  columns.  The  condition  was  a  primary  combined 
systematic  sclerosis.  Other  writers  have  seen  cases  of  spasmodic  family 
paraplegia,  and  in  some  cases  other  symptoms  were  superposed  on  this 
syndrome,  giving  to  the  disease  an  aspect  different  from  the  primary  type — 
either  that  of  spasmodic  tabes  or  of  insular  sclerosis.  We  may  agree  with 
Lorrain  that  this  disease  may  be  regarded  as  a  group  of  family  affections, 
united  one  \vith  another  in  transition  forms. 

III.  COMBINED  SCLEROSIS. 

We  designate  under  the  name  of  combined  scleroses,  not  a  clinical 
entity,  but  an  anatomo-pathological  grouping  which  is  the  substratum 
of  several  clinical  types.  The  characteristic  feature  is  the  combination  of 
sclerotic  changes  in  the  posterior  and  in  the  lateral  columns  of  the  spinal 
cord. 

Description  of  the  Clinical  Types. — The  cHnical  types  of  combined 
scleroses  may  be  classified  in  the  following  manner  : 

1.  Combined  Congenital  or  Family  Sclerosis. — These  are  Friedreich's 
disease,  hereditary  cerebellar  ataxy  of  Pierre  Marie,  and  spasmodic  family 
paraplegia  of  Striimpell. 

2.  Combined  Acquired  Sclerosis. — These  are :  (a)  Combined  tabetic 
sclerosis  (in  the  form  of  ordinary  tabes  and  combined  tabes)  ;  (b)  the  com- 
bined scleroses  of  general  paralysis  ;  (c)  the  combined  scleroses  of  spasmodic 
form ;  {d)  the  subacute  combined  scleroses,  and  those  due  to  ansemia  and 
intoxication. 

Tabetic  Form  (Combined  Tabes). 

The  chnical  aspect  of  patients  attacked  by  this  form  is  as  follows  :  A 
patient  has  aU  the  classical  signs  of  tabes — Robertson's  sign,  Romberg's 
sign,  loss  of  tendon  reflexes,  hghtning  pains,  urinary  troubles,  etc.  There 
is  no  reason  a  priori  to  suspect  an  abnormal  form  of  tabes,  and  patients 
suffering  from  this  form  were  for  a  long  time  considered  as  cases  of  ordinary 
ataxy,  although  the  post-mortem  examination  revealed  the  presence  of 
combined  lesions  in  the  posterior  and  the  lateral  columns. 

Marie  and  Crouzon  have  shown  that  it  is  possible  to  make  a  diagnosis 
of  combined  sclerosis  by  the  three  following  signs  : 

1.  Gait,  with  Dragging  of  the  Feet. — The  patient  does  not  push  his 
feet  forward,  as  in  ataxy,  and  does  not  walk  on  his  heels.  He  walks  on 
crutches  or  rides  in  a  carriage.  When  he  moves,  he  drags  his  legs  behind 
u.  81 


1270  TEXT-BOOK  OF  MEDICINE 

him,  the  body  bent  forward.     Each  leg  moves  forward  with  difficulty, 
dragging  the  point  of  the  toe,  as  though  it  were  dragging  a  heavy  weight. 

2.  Paraplegia. — A  patient  suffering  from  tabes  whose  muscular  power 
in  the  lower  hmbs  is  either  diminishing  or  is  so  weak  that  he  remains  con- 
fined to  his  bed,  hke  a  paraplegic  patient,  has  not  only  lesions  in  the  pos- 
terior columns,  but  also  lesions  in  the  lateral  columns.  The  excessive  want 
of  co-ordination,  or  the  muscular  weakness  that  may  be  associated  with 
the  amyotrophy  seen  in  some  patients,  must  not  always  be  taken  for 
paraplegia. 

3.  Babinski's  Sign. — Babinski,  in  1900,  noticed  this  sign  in  certain 
tabetic  patients,  and  put  forward  the  hypothesis  that  it  showed  the  presence 
of  combined  sclerosis.  Marie  and  Crouzon  have  verified  this  view  by  post- 
mortem examination.  The  three  cardinal  signs  just  enumerated  enabled 
Marie  and  Crouzon  to  prove  combined  sclerosis  once  in  every  thirteen 
cases  of  tabes.     This  clinical  form  is  therefore  relatively  frequent. 

Combined  Scleroses  of  General  Paralysis. 

Combined  spinal  lesions  in  the  course  of  general  paralysis  were  noticed 
by  Westphal,  and  later  by  Raymond  (1892).  They  were  present  seventy- 
three  times  in  145  post-mortem  examinations  made  by  Fiirstner. 

These  lesions,  however,  are  difficult  to  trace  chnically.  Crou  on,  consider- 
ing them  solely  from  the  point  of  view  of  the  chnical  signs  of  lesions  of  the 
posterior  columns  in  patients  suffering  from  general  paralysis  (Fere  and  Seglas's 
wards  at  Bicetre),  found  them  only  in  one  out  of  every  four  cases,  while  the 
spinal  lesions  existed  in  two-thirds  of  the  post-mortem  examinations. 

Combined  Spasmodic  Scleroses. 

The  fundamental  character  of  this  form  is  the  existence  of  spasmodic 
phenomena,  combined  with  symptoms  of  tabes,  due  to  the  lesions  in  the 
posterior  columns.  We  may  thus  have  to  deal  with  a  tabetic  patient  who 
shows  some  of  the  classical  signs  of  tabes — Romberg's  sign,  Robertson's 
sign,  lack  of  co-ordination,  urinary  troubles,  etc.  The  tendon  reflexes  are 
examined,  and  we  expect  to  find  them  abohshed ;  but  we  find,  on  the  con- 
trary, preservation  or  exaggeration  of  the  patellar  reflexes,  ankle- clonus, 
and  Babinski's  sign. 

Another  patient  is  attacked  by  spasmodic  paraplegia  and  lack  of  co- 
ordination of  the  movements,  but,  unhke  the  preceding  patient,  he  does 
not  show  the  other  phenomena  of  classical  tabes— no  hghtning  pains,  no 
Robertson's  sign,  no  Romberg's  sign,  etc.  This  type  was  described  by 
Gowers  in  1886  under  the  name  of  ataxic  paraplegia. 

Finally,  Striimpell,  Dejerine,  and  Sottas  have  been  able  to  verify  the 
presence  of  combined  sclerosis  at  the  post-mortem  examination  of  patients 


DISEASES  OF  THE  SPINAL  CORD  1271 

who  tliuiiig  their  lifetime  had  only  shown  slow  and  progressive  spasmodic 
paraplegia,  without  any  sign  of  associated  tabes. 

Ataxo-Spasmodic  Paraplegia  in  Old  People.  Marie  and  Crouzon 
have  seen  at  Bieetrc  a  certain  number  of  old  men  suffering  from 
spasmodic  paraplegia,  with  inco-ordination  and  cerebellar  symptoms. 
Tliis  disease  developed  at  an  advanced  age  and  ran  a  slow  course.  Crouzon 
has  described  this  clinical  type,  and  has  classed  it  with  the  cases  formerly 
described  by  Demange  under  the  name  of  "  progressive  tabetic  contracture." 
Recent  autopsies  have  shown  that  the  lesion  to  which  this  morbid  entity 
corresponds  is  a  primary  parenchymatous  atrophy  of  the  cerebellar  cortex. 

Subacute  Combined  Scleroses, 

In  certain  cases  post-mortem  examination  has  shown  the  existence  of 
a  combined  sclerosis  of  the  spinal  cord,  causing  a  disease  with  the  following 
symptoms  : 

The  patient  has  first  of  all  trouble  in  walking,  with  shght  inco-ordination 
and  spastic  paraplegia.  In  the  second  stage  the  paraplegia  becomes  marked, 
and  anaesthesia  of  the  lower  limbs  and  of  the  trunk  is  noticed.  In  the 
third  stage  the  paraplegia  becomes  complete  and  flaccid.  The  tendon 
reflexes  are  aboUshed,  and  muscular  atrophy,  with  incontinence  of  the 
sphincters,  appears. 

In  this  disease  we  notice  more  or  less  marked,  but  not  characteristic, 
anaemia.  Death  supervenes  in  one  to  three  years.  This  form  was  described 
in  1900  by  Eisien  Russell,  Batten,  and  CoUier,  under  the  name  of  "  subacute 
combined  degeneration  of  the  spinal  cord."  It  has  not  yet  been  observed 
in  France,  although  it  is  not  rare  in  London.  The  total  number  of 
cases  observed  in  the  Queen's  Square  Hospital  since  1898  numbers  over 
twenty. 

We  also  see  in  pernicious  ansemia  combined  sclerosis  of  the  spinal  cord, 
which  may  be  recognized  chnically,  or  may  be  revealed  only  at  the  post- 
mortem examination.  When  the  clinical  signs  exist,  they  are,  according  to 
Dejerine  and  Thomas,  most  frequently  troubles  of  subjective  and  objective 
sensibihty,  as  well  as  motor  troubles,  which  are  a  mixture  of  ataxy  and 
paraplegia.  The  reflexes  are  usually  abohshed,  though  they  are  sometimes 
exaggerated.     The  course  is  rapid,  and  death  occurs  in  a  few  months. 

Finally,  in  pellagra,  ergotism,  lathyrism,  and  cachexia  we  find  com- 
bined sclerosis,  the  cHnical  picture  being  sometimes  that  of  pseudo-tabes, 
at  other  times  that  of  spastic  paraplegia. 

Pathological  Anatomy. — The  definition  of  the  disease  indicates  the 
topography  of  the  lesions.  The  foUo^ying  combinations  may  be  seen : 
(a)  Combined  lesions  of  the  posterior  columns  and  of  the  crossed  pyramidal 
tracts  ;  (6)  combined  lesions  of  the  posterior  columns  and  of  the  direct 

81—2 


1272  TEXT-BOOK  OF  MEDICINE 

cerebellar  tracts  ;  (c)  combined  lesions  of  the  posterior  and  lateral  columns 
with  lesions  of  tbe  anterior  pyramidal  tracts. 

Pathogenic  Varieties. — Combined  scleroses  are  divided  into  two  large 
classes,  according  as  they  are  locahzed  in  a  system  of  fibres  or  are  diffuse, 
having  only  a  systematic  appearance. 

The  systematic  scleroses  may  be  created  by  changes  in  the  nerve  cells, 
producing  exogenous  (spinal  gangha)  or  endogenous  degeneration.  This  type 
of  combined  sclerosis  is  seen  in  general  paralysis  and  in  tabes  (lesions  of  the 
direct  cerebellar  tracts,  consequent  on  lesions  of  the  cells  in  Clarke's  columns). 
The  sclerosis  may,  however,  be  primary,  and  independent  of  any  cellular 
atrophy,  as  well  as  of  any  meningeal  or  vascular  lesion  (Dejerine  and  Sottas). 

The  combined  pseudo-systematic  scleroses  have  only  a  systematic 
appearance.  In  reahty  they  are  diffuse,  and  associated  with  meningeal 
or  vascular  lesions.  In  the  pseudo -systematic  scleroses  of  meningeal  origin 
the  sclerosis  penetrates  the  cord  from  the  surface  towards  the  deep  parts 
in  the  form  of  marginal  sclerosis.  Some  cases  of  combined  tabetic  sclerosis 
are  due  to  a  process  of  this  kind  (meningitis  by  propagation).  The  value 
of  posterior  meningitis  in  the  theory  of  Marie  and  Guillain  relative  to  tabes 
helps  to  confirm  this  pathogenesis. 

The  combined  scleroses  of  vascular  origin  are  explained  by  the  distribu- 
tion of  the  vessels  in  the  spinal  cord.  They  coincide  with  toxic  changes  in 
the  cord  (pernicious  anaemia,  cystoma,  lathjoiism,  etc.). 

etiology. — SyphiHs  plays  an  important  part  in  the  combined  scleroses. 
It  is  almost  always  the  cause  of  tabes  and  of  general  paralysis.  According 
to  Gowers,  it  is  rare  in  ataxic  paraplegia.  The  senile  form  seems  to  depend 
on  atheroma,  and  the  subacute  scleroses  are  associated  with  the  anaemias 
and  the  intoxications. 

Treatment. — In  the  combined  syphihtic  scleroses  of  tabes  and  of  general 
paralysis  we  employ,  as  in  tabes  and  general  paralysis,  the  intensive 
mercurial  treatment. 

IV.  SYRINGOMYELIA. 

The  word  syringomyelia  {crvpLy^,  canal ;  yitpeAos,  marrow)  signifies  a  canal  in  the 
marrow.  This  expression,  employed  for  the  first  time  by  OUivier,  of  Angers,  in  1827,  ■ 
was  almost  abandoned,  when  the  recent  labours  of  Mile.  Baumler,  and  especially  of 
Schultze  and  Kahler,  rescued  it  from  obhvion.  These  writers  did  more  :  whilst  rehabili- 
tating the  word  they  also  apphed  it  to  a  morbid  entity,  having  its  own  symptomatology 
and  pathological  anatomy.  Their  researches,  which  were  at  first  favourably  received 
(Debove,  Bruhl),  were  later  criticized,  especially  as  regards  the  nature  of  the  lesions 
(Charcot,  JoJEfroy,  and  Achard),  and  the  pathological  interpretation  of  the  symptoms 
(Dejerine,  Zambacco). 

Pathological  Anatomy. — The  cord,  when  removed  from  the  spinal 
canal,  becomes  flat  hke  a  ribbon.     The  consistency  is  less  firm,  and  the  cut 


DISEASES  OF  THE  SPINAL  CORD  1273 

• 

section  is  diffluent,  so  that  we  must  be  very  careful  lest  we  should  ronder 
any  further  examination  impossible.  The  changes  are  sometimes  limited 
to  a  small  segment.  In  most  cases  they  measure  from  3  to  4  inches,  but 
the  spinal  cord  may  be  affected  throughout  its  entire  length.  The  lesions 
are  chiefly  situated  at  the  cervico-brachial  enlargement  of  the  cord. 

In  the  centre  of  the  spinal  cord  we  find  a  cavity,  containing  a  fluid 
analogous  to  the  cerebro-spinal  fluid,  and  of  the  size  of  a  knitting-needle, 
of  a  probe,  or  of  a  pencil.  The  cavity  is  sometimes  double  or  triple,  and 
presents  several  diverticula.  This  cavity  was  for  a  long  time  thought  to  be 
formed  at  the  expense  of  the  central  canal  (hydromyelia).  Schultze  and 
Kahler  held  that  it  is  due  to  a  glioma  commencing  in  the  deep  parts  of  the 
spinal  cord.  This  glioma  generally  develops  at  the  expense  of  the  posterior 
half  of  the  cord,  pushing  back  the  grey  and  white  matter,  first  in  the  pos- 
terior half,  and  then  in  the  anterior  half  of  the  spinal  cord. 

This  tumour  is  formed  of  proliferated  neuroglial  elements.  A  felting 
is  thus  formed  of  fine  cells,  with  a  central  swelhng  and  multiple  interlacing 
prolongations,  plunged  into  the  midst  of  a  thin  fibrillarv  network.  At 
the  central  canal  we  fuid  some  trace  of  a  limiting  membrane,  but  in  general 
this  is  merely  neuroglial  cells  piled  up  one  against  the  other.  Sometimes, 
however,  an  incomplete  layer  of  cyUndrical  cells  is  found,  arising  from  the 
central  canal  of  the  spinal  cord.  The  arteries  are  often  thickened,  and 
their  lumen  is  constricted.  This  peculiarity  has  led  several  writers  (Joffroy 
and  Achard)  to  ask  whether  aU  cases  of  syringomyelia  are  really  caused  by 
ghomata,  or  whether  certain  of  them  are  not  due  to  a  central  myelitis 
of  vascular  origin.  The  latter  would  be  related  to  periependymal  myelitis 
(Hallopeau).  Finally,  Charcot  recognizes  three  varieties  of  syringomyefla  : 
(1)  medullar}'  malformation ;  (2)  periependjrmal  myelitis  ;  (3)  medullary 
ghoma. 

Description. — From  what  we  have  just  said,  it  follows  that  the  symp- 
toms of  syringomyelia  vary  according  to  the  seat  of  the  lesions  and  the 
direction  of  their  development.  As,  however,  the  lesions  chiefly  affect  the 
posterior  half  of  the  spinal  cord,  especially  at  the  commencement,  the 
principal  manifestations  are  of  the  sensory  type. 

These  sensory  troubles,  in  the  absence  of  which  it  is  almost  impossible 
to  make  the  diagnosis,  consist  in  a  special  anaesthesia  of  the  upper  hmbs, 
though  it  often  attacks  in  a  less  degree  the  lower  hmbs.  It  may  be  ex- 
clusively limited  to  them.  The  ansesthesia  is  frequently  more  marked  on 
one  side  than  on  the  other,  never  following  the  distribution  of  the  nerves 
and  ceasing  suddenly  in  certain  regions,  wliich  vary  according  to  the  par- 
ticular case.  The  anaesthesia  sometimes  occupies  the  hand,  and  ends 
like  a  ruffle.  It  sometimes  reaches  to  the  elbow,  or  even  as  far  as  the 
shoulder,  terminating  then  hl:e  a  sleeve.     It  invades  the  legs,  in  the  shape 


1274  TEXT-BOOK  OF  MEDICINE 

• 

of  a  stocking,  or  it  attacks  the  whole  lower  Hmb,  hke  a  pair  of  drawers.  It 
sometimes  attacks  the  whole  body,  leaving  the  face  intact.  This  last 
character,  for  a  long  time  regarded  as  pathognomonic,  loses  its  value  in 
view  of  certain  recently  pubhshed  cases. 

This  special  anaesthesia  consists  in  a  dissociation  of  the  various  forms 
of  sensibility.  The  sense  of  heat  and  cold  is  abohshed,  or  simply  blurred. 
Patients  often  have  burns  for  which  they  cannot  account.  The  sense  of 
pain  is  hkewise  abohshed,  so  that  patients  may  be  pricked  and  pinched 
without  feehng  any  pain.  Some  of  them  have  even  fractured  an  ansesthetic 
limb  without  feehng  any  pain.  The  anaesthesia  is  both  superficial  and 
deep-seated.  In  some  cases  thermo-ansesthesia  exists  alone  ;  in  one  case 
the  sense  of  heat  only  was  abohshed  (Dejerine).  The  sense  of  touch  is, 
on  the  contrary,  preserved ;  the  patient  feels  the  ground  when  walking, 
but  a  pin-prick  is  interpreted  as  a  tactile  sensation. 

These  troubles  of  sensibihty  are  divided  in  zones,  the  upper  hmit  being 
perpendicular  to  the  axis  of  the  body  or  the  axis  of  the  hmbs.  There  is 
no  agreement  between  these  girdles  of  anaesthesia  and  the  topographical 
distribution  of  the  nerves.  The  anaesthesia  may  be  hmited  to  the  hand, 
in  the  shape  of  a  glove,  and  the  three  nerves  affected  (ulnar,  radial,  and 
median)  have  quite  a  different  peripheral  distribution.  This  circular  dis- 
tribution of  the  anaesthesia  can  only  be  explained  by  the  persistence  of  the 
primary  metamerism  of  the  nerve  centre  (Brissaud).  I  shall  again  mention 
spinal  metamerism  under  the  distribution  of  Herpes. 

The  motor  troubles  are  hkewise  subordinate  to  the  regions  of  the  spinal 
cord,  compressed  from  within  outwards.  They  consist  in  muscular  atrophy 
of  the  Aran-Duchenne  type.  It  is  usually  hmited  to  the  hands  and  the  fore- 
arms. It  sometimes  affects  only  the  lower  hmbs,  and  is  accompanied  by 
fibrillary  tremors.  When  the  antero  -  lateral  columns  are  attacked, 
contractures  appear;  the  reflexes  are  then  exaggerated.  Sometimes  the 
ataxic  s3niiptoms  predominate,  being  most  common  in  the  lower  hmbs. 

The  existence  of  dorso-lumbar  scohosis  has  often  been  noted.  The  skin 
shows  trophic  lesions — bhsters,  puf&ness,  white  or  blue  oedema  of  the  hmbs, 
glossy  skin,  eschars,  repeated  whitlows,  shedding  of  the  nails,  phlegmons, 
etc.  The  trophic  troubles  in  the  bones  are  fractures,  with  rapid  con- 
sohdation,  and  depression  of  the  anterior  thoracic  wall.  In  the  joints  we 
find  arthropathies  hke  those  seen  in  ataxy.  Ulceration  and  perforation  of 
the  bladder  also  occur. 

The  nervous  troubles  sometimes  reach  the  superior  cervical  region,  and 
even  the  region  of  the  bulb  :  sensory  troubles  in  the  tongue,  dyspnoea,  and 
palpitations.  We  must  also  remember  inequahty  of  the  pupils,  unilateral, 
paralytic  mydriasis,  myosis,  and  Argyll-Robertson's  sign.  Nystagmus  is 
fairly  frequent.     Paralysis  of  the  motor  muscles,  ptosis,  and  diplopia  are 


DISEASES  OF  THE  SPINAL  T'oRD  127' 

more  rare.  Conceiitrio  narrowing  i»f  the  field  of  visimi  is  duo  to  tli<>  con- 
comitant livstj'iia  rather  than  tlic  syriiigoniyeha.  Finally,  we  must  mention 
defaced  cases — unilateral  nature  of  the  lesions,  comph^te  loss  of  all  kinds 
of  sensation,  absence  of  atrophy,  etc. 

Guillain  has  isolated  a  spasmodic  form  of  syringomyelia,  characterized 
by  contractures  and  exaggeration  of  the  reflexes  in  all  four  limbs.  The 
three  last  fingers  are  firmly  flexed,  so  that  the  thumb  and  the  index- 
finger,  which  are  almost  free,  can  alone  be  used  by  the  patient  {main  en 
fince). 

Syringomyelia  commences  generally  in  the  young.  Its  course  is  very 
slow,  and,  at  the  end  of  many  years,  death  is  due  to  exhaustion,  syncope, 
or  some  intercurrent  disease.  Syringomyeha  is  not  hereditary,  and,  accord- 
ing to  those  who  admit  only  the  existence  of  the  central  glioma,  it  is  a  disease 
of  evolution. 

Diagnosis. — The  special  troubles  of  sensation  distinguish  syringomyeha 
from  progressive  muscular  atrophy,  amyotrophic  lateral  sclerosis,  and  the 
various  forms  of  progressive  myopathy.  In  hysteria  the  dissociation  of 
the  sensor}^  troubles  may  exist,  as  may  also  the  limitation  of  the  anaesthesia 
to  the  wrist,  to  the  shoulder,  etc.  Constriction  of  the  field  of  vision  and 
atrophy  are  Ukewise  common  to  both  diseases.  It  is  obvious  how  difficult 
the  diagnosis  may  be  in  the  absence  of  any  convulsive  attack,  or  of  any 
hysterogenous  zone.  Their  presence  even  does  not  settle  the  question, 
because  syringomyeha  and  hysteria  may  exist  in  the  same  subject. 

Morvan's  disease,  or.  painless  whitlow,  is  considered  by  some  authors 
as  a  variety  of  syringomyeha.  In  this  disease  recurrent  whitlows,  with 
loss  of  the  phalanx,  finally  causing  marked  mutilation,  and  evohdng  without 
pain,  constitute  the  capital  syndrome.  Although  the  anaesthesia  is  almost 
always  complete,  it  may  happen  that  dissociation  of  the  sensory  troubles 
may  be  found  in  certain  patients  with  painless  whitlows.  The  unilateral 
nature  of  the  lesions  is  only  an  element  in  the  diagnosis,  because  it  may 
exist  in  certain  cases  of  syringomyeha.  Besides,  Jof!roy  and  Achard  have 
twice  found  ghomatous  changes  in  the  spinal  cords  of  patients  with  painless 
whitlow. 

The  existence  of  peripheral  neuritis,  characterized  by  nodules  on  the 
nerves,  and  particularly  on  the  uhiar  nerve  at  the  elbow,  the  sensory 
troubles,  and  the  mutilations  that  accompany  them,  have  led  Zambacco  to 
unite  syringomyeha  and  Morvan's  disease  under  one  heading.  He  holds 
that  they  are  an  attenuated  form  of  leprosy.  The  microscopic  examination 
of  a  nodule  on  the  ulnar  nerve  made  by  Pitres  revealed  the  leprosy  bacillus, 
but  this  finding  does  not  prove  that  all  cases  of  nodular  neuritis  are  of 
leprous  origin. 

In  five  patients  with  haematomyeha  of  traumatic  origin  Minor  has  noted 


1276  TEXT-BOOK  OF  MEDICINE 

most  of  the  symptoms  of  syringomyelia  ;  the  patient's  gait  alone  permitted 
the  diagnosis  to  be  made. 

Compression  of  the  spinal  cord  (Charcot)  may  lead  to  confusion.  One 
of  Charcot's  patients  showed,  as  a  distinctive  sign,  thermo-ansesthesia  in 
the  region  of  the  internal  cutaneous  nerve  of  the  arm,  but  it  did  not  ter- 
minate in  a  ruffle. 

Thermo-ansesthesia  has  been  noticed  in  alcohohsm  and  diabetes  (Vergely). 
In  these  two  diseases  neuroses  are  frequent,  and  cause  sensory  troubles. 
The  diagnosis  will  be  faciHtated  by  the  symptoms  pecuhar  to  these  diseases. 
The  coexistence  in  the  same  subject  of  exophthalmic  goitre  and  sjrringo- 
myeUa  has  been  observed  by  Joffroy  and  Achard.  The  coexistence  of 
syringomyeha  and  spasmodic  hemiplegia  has  been  noted  by  Charcot  and 
Brissaud. 

Certain  lesions  causing  cavities  in  the  spinal  cord  have  chnical  signs 
identical  with  those  of  syringomyelia  (Dejerine  and  Thomas). 


V.  PROGRESSIVE  MUSCULAR  ATROPHY. 

The  muscular  atrophies  play  an  important  part  in  the  diseases 
of  the  spinal  cord  which  we  are  now  about  to  describe.  They  are, 
furthermore,  met  with  in  many  cases  of  myehtis.  They  are  due  to  a  lesion 
in  the  cells  of  the  anterior  cornua  of  the  spinal  cord.  The  muscular  atrophy 
is  sometimes  inconstant,  shght,  and  appears  without  order  and  without 
any  fixed  date  in  the  course  of  myehtis  (insular  sclerosis).  At  other  times 
the  atrophy  is  the  most  important,  whilst  being  at  the  same  time  associated 
with  other  symptoms  which  of  themselves  are  of  great  value  (amyotrophic 
lateral  sclerosis,  syringomyeha,  atrophic  paralysis  of  infants).  Finally,  in 
other  cases  the  muscular  atrophy  shows  a  systematic  and  progressive 
course.  It  forms  a  weU-defined  morbid  entity,  and  is  known  as  Duchenne's 
progressive  muscular  atrophy. 

And  yet,  whatever  the  kind  and  the  variety  of  these  muscular  atrophies, 
they  are  all  of  spinal  origin,  and  are  myelopathic  atrophies,  whilst  there  are 
other  diseases  of  the  muscular  system  which  are  also  progressive,  and  run 
their  course  with  or  without  atrophy  of  the  muscle,  but  which  are  primary 
and  independent  (at  least,  in  appearance)  of  lesions  in  the  spinal  cord. 
These  family  myopathies  are  described  later.  There  are  two  kinds : 
(1)  pseudo-hypertrophic  muscular  paralysis  (Duchenne's  type)  ;  (2)  pro- 
gressive atrophic  myopathy  (Landouzy-Dejerine  type). 

These  muscular  atrophies  of  myelopathic  and  myopathic  origin  must  be 
contrasted  with  the  muscular  atrophies  of  neuritic  origin,  as  exempHfied  in 
alcohohc  paralysis  and  lead  palsy. 

The  existence,  however,  of  a  progressive  muscular  atrophy,  which  occurs 


DISEASES  OF  THE  SPINAL  TORD  1277 

in  families  and  is  of  myelopathic  origin  (Werding  and  Hoffmann),  seems  to 
establisli  a  bond  of  union  between  the  Aran-Diiclienne  ty{)e  and  the  various 
primary  myopathies,  and  to  bring  us  back  to  the  unitary  doctrine  (Raymond). 
"  There  is  no  insurmountable  line  of  demarcation  between  the  progressive 
family  amyotrophies  and  tlie  progressive  muscular  atrophy  of  the  Aran- 
Duchenne  t^-pe.  The  various  types  of  progressive  muscular  atrophy  are 
but  varieties  of  the  same  morbid  entity.  It  has  as  a  substratum  the  same 
organic  system,  the  spino-muscular  neuron,  and  its  prolongation,  the  muscle. 
The  weak  portion  of  this  organic  system  seems  to  be  the  muscle  in  the  early 
stages  of  life,  and  the  tropho-motor  cell  of  the  neuron  in  adult  age. 
This  does  not  prevent  in  exceptional  cases  the  dystrophy,  which  gives  rise 
to  progressive  muscular  atrophy,  from  commencing  in  the  tropho-motor  cells 
of  the  spinal  cord  and  manifesting  itself  in  the  first  years  of  life ;  just  as  it 
may  commence  in  the  muscles  and  hmit  itself  there  in  an  adult  subject. 
Progressive  muscular  atrophy,  as  Duchenne  conceived  it,  is  therefore  placed 
on  a  new  basis,  which  appears  to  me  to  be  permanent "  (Raymond).  I  shall 
now  describe  progressive  muscular  atrophy  of  the  Aran-Duchenne  type. 

Description. — The  disease  commences  insidiously  with  atrophy  of  the 
abductor  polUcis  ;  the  atrophy  spreads  to  the  muscles  of  the  hand,  invading 
both  hands  symmetrically,  and  then  affects  the  upper  hmbs  and  the  trunk, 
so  that  in  five  to  ten  years  the  muscles  of  these  various  regions  have  almost 
entirely  disappeared,  the  patient  preserving  the  absolute  integrity  of  the 
other  functions  until  the  atrophy  lays  hold  of  the  muscles  of  respiration,  of 
mastication,  and  of  deglutition. 

This  disease  has  received  from  Aran  and  Duchenne  the  name  of  pro- 
gressive muscular  atrophy.  The  work  pubHshed  in  1850  by  Aran  has 
largely  contributed  to  its  recognition.  It  must,  however,  be  added  that 
in  1849  Duchenne  had  already  presented  a  monograph  to  the  Institute 
which  estabHshes  the  question  of  priority,  and  leaves  him  the  honour  of 
the  discovery. 

Progressive  muscular  atrophy  almost  always  commences  in  the  upper 
limbs.  In  159  cases  collected  by  Duchenne  it  commenced  only  twice  in 
the  lower  hmbs,  and  twelve  times  in  the  muscles  of  the  trunk  ;  it  never 
attacks  the  face.  On  the  other  hand,  there  is  an  amyotrophy  which  often 
commences  in  the  face,  especially  in  children.  Duchenne  wrongly  con- 
sidered it  to  be  a  progressive  myelopathic  amyotrophy,  and  included  it 
under  progressive  muscular  atrophy.  It  should  be  classed  with  the  primary 
myopathies,  and  we  shall  meet  with  it  in  the  diseases  of  the  muscular  system 
under  the  name  of  progressive  atropine  myopathy  (Landouzy-Dejerine 
type). 

In  progressive  muscular  atrophy  the  atrophy  of  the  muscle  is  the 
prominent  feature.    The  muscle  loses  its  function,  not  because  it  is  paralyzed, 


1278  TEXT-BOOK  OF  MEDICINE 

but  because  it  is  destroyed.  The  atrophy  does  not  attack  a  limb  or  a  group 
of  muscles;  it  attacks  certain  bundles  of  the  muscle,  whilst  the  neighbouring 
bundles  are  intact,  but  they  will  be  attacked  in  turn.  As  soon  as  the 
muscle  is  afiected,  it  loses  its  consistency,  becoming  soft  and  contracting 
with  less  vigour  ;  but  the  intact  bundles  of  the  muscle  contract  and  preserve 
the  electrical  reaction.  Although  the  muscle  on  the  way  to  atrophy  has 
preserved  its  electrical  contractihty,  this  electrical  excitabihty  is  exhausted 
quicker  than  in  the  healthy  condition.  According  to  some  writers,  the 
diseased  muscle  is  said  to  have  a  momentarily  exaggerated  electrical  ex- 
citabihty (reaction  of  degeneration). 

As  a  general  rule,  when  a  muscle  or  a  group  of  muscles  becomes  atrophied, 
the  succession  of  the  phenomena  is  always  the  same.  The  atrophy  of  the 
muscle  modifies  the  shape  of  the  affected  part,  the  bones  becoming  prominent, 
while  flattening  replaces  the  muscular  contour.  Furthermore,  as  the  anta- 
gonistic muscles  are  rarely  atrophied  at  the  same  time,  their  action  becomes 
predominant,  and  hence  vicious  attitudes  result,  which  are  nowhere  more 
appreciable  than  in  the  hand. 

Atrophy  of  the  Muscles  of  the  Hand.— The  atrophy  commences  most 
frequently  in  the  thenar  eminence  of  the  right  hand  (Aran).  The  short 
abductor  muscle  of  the  thumb  is  the  first  affected.  The  action  of  this 
muscle,  abductor  and  extensor  of  the  last  phalanx,  is  to  oppose  the  ball  of 
the  thumb  to  the  ball  of  the  index  firger  and  of  the  middle  finger  when 
flexed  (Duchenne).  This  muscle  is  therefore  indispensable  in  holding  a  pen 
or  a  pencil,  and  in  working  with  a  brush  or  a  graver.  Its  atrophy  is 
therefore  quickly  noticed,  and  the  hand  immediately  becomes  useless. 
As  the  atrophy  also  invades  the  other  muscles  of  the  thenar  eminence,  the 
normal  prominence  is  replaced  by  a  flattening  ;  the  opposition  of  the  thumb 
is  impossible,  and  the  antagonistic  muscle,  the  long  extensor  of  the  thumb 
being  unopposed,  draws  the  first  metacarpal  backwards  and  outwards. 
The  hand  then  assumes  the  aspect  of  a  monkey's  hand  (Duchenne). 

When  the  lumbricales  and  the  interossei  are  atrophied,  the  meta- 
carpal bones  appear  to  be  stripped  of  the  flesh,  and  adduction  and  abduction 
of  the  fingers  become  impossible.  The  interossei  and  the  lumbricales,  how- 
ever, have  another  action  :  they  flex  the  metacarpal  phalanx  and  extend 
the  two  last  phalanges.  Their  antagonists  are  the  flexors  and  extensors 
of  the  fingers,  which  flex  the  two  last  phalanges  and  extend  the  metacarpal 
phalanx.  As  the  action  of  these  antagonistic  muscles  is  unopposed,  the 
interossei  being  atrophied,  we  find  the  main  en  griff e  (Duchenne). 

At  a  later  period  the  hand  is  so  emaciated  that  it  resembles  the  hand  of 
a  skeleton. 

Atrophy  of  the  Muscles  of  the  Arm  and  of  the  Shoulder. — In  the 
forearm  the  muscles  of  the  anterior  and  external  regions  are  first  attacked. 


DISEASES  OK  TIIR  SPINAL  ToFlD  1279 

In  tho  arm  tlie  triceps  is  the  muscle  which  resists  longest.  In  the  shoulder 
the  iliroe  l)utull(>s  of  IIk^  diMtoid  an^  invaded,  so  that  elevation  of  tlin  arni 
becomes  inijiossiMc  (DiicIkmhic). 

Atrophy  of  the  Muscles  of  the  Trunk.— The  upper  part  of  the  trapezius, 
wliicli  receives  its  nerv'e  supply  from  multiple  sources,  is  not  atrophied, 
the  atrophy  being  limited  to  its  lower  part ;  the  scapula  stands  out  from 
the  spinal  column.  The  pectoral  muscles,  the  serrati,  the  rhomboid  muscles, 
and  the  sacro-lumbar  muscles,  become  atrophied  without  any  fixed  rule. 
AVlien  the  pectoral  muscles  are  atrophied,  the  normal  mass  of  the  muscles  is 
replaced  on  each  side  of  the  sternum  by  a  hollow.  The  atrophy  of  the  ex- 
tensor or  flexor  muscles  of  the  trunk  displaces  the  centre  of  gravity,  and  to 
remedy  it  curvatures  of  the  spinal  column  are  produced.  The  head  falls 
in  every  direction  after  the  atrophy  of  the  extensor  and  flexor  muscles. 
The  contrast  is  striking  when  we  examine,  on  the  one  hand,  the  wasted  trunk 
and  the  emaciated  upper  limbs,  and,  on  the  other,  the  lower  limbs,  still 
clothed  with  masses  of  muscles.  The  lower  limbs  are  either  spared  or  do  not 
become  atrophied  until  a  very  advanced  period. 

The  chief  functions  of  the  general  economy  are  so  far  intact.  The  general 
s}inptoms  are  trifling  ;  they  are  fibrillary  contractions  in  the  muscles  on 
the  road  to  atrophy,  some  pain  and  a  sensation  of  cold  in  the  atrophied 
limbs,  with  actual  lowering  of  the  temperature.  At  a  more  advanced 
period  of  the  disease,  usually  after  several  years,  the  atrophy  lays  hold  of 
the  depressors  of  the  jaw,  and  mastication  becomes  impossible.  Some- 
times the  muscles  of  deglutition  are  invaded.  More  frequently  the  muscles 
of  respiration  become  atrophied,  the  intercostals  first,  and  costal  respiration 
is  aboUshed.  Later  the  diaphragm  is  attacked,  and  respiration  then  be- 
comes so  laboured  that  any  lesion  of  the  respiratory  apparatus,  even  the 
least  bronchitis,  may  carry  off  the  patient.  The  duration  of  the  disease 
is  variable,  being  rarely  less  than  two  years,  and  most  often  more  than  ten 
or  twelve  years. 

The  above  description  applies  to  a  typical  case,  but  there  are  cases  in 
which  we  find  anaesthesia,  contractures,  bulbar  paralysis  (glosso-labio- 
laryngeal  paralysis),  or  external  ophthalmoplegia. 

In  some  cases  progressive  muscular  atrophy,  instead  of  commencing  in  the 
muscles  of  the  thenar  eminence,  attacks  at  first  the  muscles  of  the  shoulder 
and  of  the  arm.  This  is  Vulpian's  scapulo-humeral  type.  The  atrophy  is 
generally  symmetrical,  and  remains  confined  for  a  long  time  to  the  root  of 
the  hmb  before  attacking  the  other  regions.     It  never  affects  the  face. 

Pathological  Anatomy. — The  atrophy  of  the  muscles  has  been  said  by 
some  writers  to  be  fatty,  but  recent  researches  (Hayem)  have  estabHshed 
that  it  is  most  often  simple,  without  fatty  degeneration.  The  muscles 
preserve  their  striation  tiU  the  last  moment ;  they  gradually  diminish  in  size 


1280  TEXT-BOOK  OF  MEDICINE 

and  take  on  a  dead-leaf  colour,  whole  bundles  finally  disappearing.  In 
some  cases  the  nuclei  of  the  sarcolemma  proHferate  and  give  rise  to  fibrosis. 
The  fatty  elements  sometimes  accumulate  in  the  interior  of  the  sheath, 
giving  rise  to  a  steatosis,  which  may  mask  the  disappearance  of  the  muscle, 
and  at  first  cause  a  behef  in  its  preservation. 

In  fact,  as  Kanvier  has  shown,  the  fundamental  lesions  of  the  muscles 
in  muscular  atrophy  of  myelopathic  origin  are  equivalent  to  those  seen  in 
muscles  separated  from  their  trophic  centres.  The  non-differentiated 
protoplasm  of  the  primary  fibre  becomes  hypertrophied ;  the  nuclei  of  the 
sarcolemma  prohferate  ;  their  phagocytic  action  is  then  exercised,  and 
causes  the  differentiated  tissue  to  disappear. 

It  was  at  first  thought  that  the  lesion  of  the  muscles  comprised  the 
entire  disease,  but  Cruveilhier  soon  showed  that  the  lesions  of  the  nervous 
system  claimed  a  preponderant  part,  and  in  a  post-mortem  examination 
that  has  remained  celebrated  he  discovered  the  atrophy  of  the  anterior 
roots  of  the  spinal  cord. 

Cruveilhier  went  even  farther,  and,  divining  the  lesion  which  he  did  not 
see,  announced  that  the  grey  matter  of  the  spinal  cord  must  be  involved. 
To  Luys  belongs  the  honour  of  having  been  the  first  to  describe  clearly  the 
real  lesion  of  muscular  progressive  atrophy.  In  1860  Luys  stated  that  the 
anterior  cornua  of  the  grey  matter  were  partially  destroyed  at  points  corre- 
sponding to  the  anterior  roots  of  the  atrophied  nerves  ;  and,  in  fact,  subse- 
quent post-mortem  examinations  (Hayem,  Charcot,  Vulpian,  Joffroy,  etc.) 
have  proved  that  the  primary  and  constant  lesion  of  muscular  atrophy  is 
seated  in  the  anterior  cornua  of  the  grey  matter.  The  cells  of  the  anterior 
cornua  disappear  by  pigmentary  or  by  sclerotic  atrophy,  the  capillary 
vessels  are  thickened,  and  connective  prohferation  is  found  in  the  neurogha 
of  the  anterior  cornua.  There  is,  then,  a  lesion  which  is  at  first  locahzed  in 
the  nerve  cell,  but  it  is  difficult  to  say  whether  this  lesion  is  irritative  or 
degenerative.  In  any  event  the  disease  may  be  regarded  as  a  systematic 
affection  of  the  medullary  parenchyma. 

The  morbid  process,  starting  in  the  nerve  cells  of  the  anterior  cornua 
(atrophic  degeneration  of  the  cell,  with  connective  prohferation),  extends 
to  the  anterior  roots  of  the  nerves  (atrophy  of  the  roots),  and  ends  in  the 
muscles  (simple  atrophy,  with  or  without  sclero-fatty  transformation).  The 
change  in  the  anterior  roots  of  the  spinal  nerves  is  often  visible  to  the  naked 
eye.  The  roots  are  obviously  atrophied,  and  in  some  cases  are  greyish. 
Under  the  microscope  healthy  nerve  fibres  are  found  side  by  side  with 
diseased  fibres,  irregularly  distributed.  Lesions  of  the  great  sympathetic 
have  been  noticed,  but  they  are  inconstant  and  secondary.  Why  does  an 
irritative  lesion  of  the  anterior  nerve  cells  of  the  spinal  cord  cause  muscular 
atrophy  ?     The  spinal  cord,  by  means  of  its  anterior  grey  matter,  exercises 


DISEASES  OF  TIIK  SI'INAL  PoRD  1281 

a  trophic  action  on  the  muscles.  The  fact  is  evident,  but  the  question  arises 
as  to  lunv  this  action  is  exercised. 

It  is  not  transmitted  from  the  spinal  cord  to  the  muscles  by  the  vaso- 
motor fibres,  because  section  of  the  fibres  of  the  sympathetic  or  tearing  oul, 
of  tlie  ganglia  does  not  produce  muscular  atropliy  (Vuli)ian).  It  appears 
to  be  transmitted  by  the  motor  nerves,  because  crusliing  or  section  of  a 
motor  nerve — the  sciatic  nerve,  for'example — causes  atrophy  in  the  corre- 
sponding muscles.  According  to  some  authors,  muscular  atrophy  is  said 
to  be  due  to  irritation  of  the  nerve.  There  is  an  excess  of  action,  and  this 
excess  of  function  is  said  to  lead  to  malnutrition  (Brown-Sequard,  Charcot). 
According  to  another  theory  (Vulpian,  Hayem),  the  muscular  atrophy  is 
due,  not  to  an  excess  of  action,  but  to  a  deficiency  of  action,  the  affected 
nerve  no  longer  transmitting,  or  transmitting  imperfectly,  to  the  corre- 
sponding muscle  the  trophic  pow^er  received  from  the  spinal  cord.  It  appears 
evident  that  the  nutrition  of  the  muscles  is  connected  with  the  cells  of  the 
anterior  cornua,  and  the  situation  of  the  muscular  lesion  always  corresponds 
to  a  definite  site  as  regards  the  medullary  lesion.  When  the  muscular  atrophy 
was  limited  to  the  muscles  of  the  hand  on  one  side  (Prevost*),  atrophy  of 
the  anterior  cornua  of  the  same  side  was  found  in  the  region  of  the  spinal 
cord,  extending  from  the  seventh  cervical  to  the  first  dorsal  pair  (exit  of 
the  roots  of  the  median  and  ulnar  nerves). 

Muscular  atrophy  with  atrophy  of  the  anterior  cornua  of  the  spinal 
cord  has  been  produced  by  injection  of  cultures  of  streptococci  into 
animals. 

Diagnosis — .ffitiology — Treatment.— Progressive  muscular  atrophy 
must  not  be  confounded  with  secondary  atrophy  supervening  in  a  more  or 
less  irregular  maimer  during  the  course  of  other  affections  of  the  spinal  cord, 
either  in  posterior  or  in  lateral  sclerosis. 

Progressive  myopathy  often  commencing  in  children  in  the  face  was 
for  a  long  time  described  as  forming  part  of  progressive  muscular  atrophy. 
We  shall  see  under  Diseases  of  the  Muscular  System  that  this  progressive 
atrophic  myopathy  (Landouzy-Dejerine  type)  has  nothing  in  common  with 
progressive  muscular  atrophy. 

The  atrophy  of  the  muscles  of  the  hand,  due  to  a  lesion  of  the  ulnar 
nerve  at  the  elbow  or  at  the  wrist,  presents  the  following  characters  :  The 
muscles  of  the  hypothenar  eminence,  the  interossei  and  lumbricales,  are 
atrophied,  but  the  muscles  of  the  thenar  eminence  supphed  by  the  median 

*  Prevost  and  David,  Arch,  de  Physiol,  1874,  p.  595.  This  case  is  as  conclusive  as 
it  is  remarkable.  The  muscular  atrophy  was  limited  solely  to  the  muscles  of  the  right 
thenar  eminence,  and  this  atrophy  dated  from  infancy.  At  the  autopsy  there  was 
evident  atrophy  of  the  right  anterior  root  of  the  eighth  cervical  pair,  and  under  the 
microscope  there  was  seen  atrophy  of  the  anterior  cornu  of  the  grey  matter  at  tliis  level 
throughout  a  length  of  from  2  to  3  centimetroa. 


1282  TEXT-BOOK  OF  MEDICINE 

nerve  are  normal.  The  claw  only  extends  to  the  last  two  fingers,  because  the 
interossei  and  lumbricales  of  the  two  first  spaces  have  a  double  supply  from 
the  ulnar  and  the  median  nerves. 

Progressive  muscular  atrophy  wiU  not  be  confounded  with  atrophic 
rheumatism  of  the  deltoid  and  with  muscular  atrophy  in  the  neighbourhood 
of  rheumatic  joints.  In  such  a  case  the  painful  stage  at  the  onset  of  the 
disease  sufiiciently  indicates  its  nature. "  The  deformity  of  the  hand,  conse- 
quent on  nodular  rheumatism  or  on  contraction  of  the  palmar  fascia,  simu- 
lates but  very  imperfectly  the  claw-hke  hand  of  muscular  atrophy. 

The  paralyses  of  the  brachial  plexus  are  accompanied  by  atrophy  of  the 
deltoid,  the  biceps,  the  brachiahs  anticus  and  supinator  longus,  the  infra- 
spinatus, the  teres  major  and  minor,  and  the  rhomboid  muscles  in  the  superior 
type,  and  by  the  other  muscles  of  the  upper  Hmb  in  the  inferior  type.  In 
the  latter  type  the  sensibihty  of  the  hand  is  abohshed,  while  it  is  preserved 
over  the  inner  side  of  the  arm,  and  to  some  extent  on  the  posterior  surface, 
these  parts  being  supphed  by  the  branches  of  the  first  intercostal  nerves. 
The  existence  of  oculo -pupillary  troubles  (inferior  type),  of  trophic  troubles, 
and  of  the  reaction  of  degeneration  are  signs  of  lesions  in  the  brachial  plexus, 
and  are  not  met  with  in  Aran-Duchenne's  disease. 

Charcot  and  Marie's  progressive  muscular  atrophy  commences  in  the  mus- 
cles of  the  feet  and  legs.  The  atrophy  is  for  years  hmited  to  these  regions 
before  invading  the  upper  hmbs.  In  the  arms  it  first  attacks  the  muscles 
of  the  thenar  and  hypothenar  eminences  and  the  interossei,  producing  the 
claw  hand.  The  muscles  of  the  trunk,  shoulders,  and  face  remain  free,  and 
those  of  the  arms  and  of  the  thighs  are  relatively  normal.  The  atrophied 
regions  only  show  sHght  fibrillary  contractions.  At  an  advanced  period 
the  reaction  of  degeneration  is  seen.  Sensory  troubles  are  sometimes  seen 
in  the  form  of  a  dissociated  ansesthesia,  which  leaves  the  tactile  sense  immune. 
The  disease  commences  in  childhood,  more  rarely  in  youth ;  it  is  a  family 
disease.  These  characteristics  suffice  to  distinguish  it  from  atrophy  of  the 
Aran-Duchenne  type. 

Syringomyelia  presents  numerous  points  of  resemblance  to  progressive 
muscular  atrophy  (Aran-Duchenne  type).  In  both  diseases  the  muscular 
atrophy  comjnences  in  the  upper  Hmbs,  attacking  by  preference  the  thenar 
and  hypothenar  eminences,  the  interossei,  next  the  muscles  of  the  fore- 
arm, and  finally  those  of  the  arm.  In  both  cases  the  deformities  and  the 
vicious  attitudes  of  the  hand  and  of  the  forearm  are  similar.  Finally,  in 
both  cases  fibrillary  contractions  are  seen  in  the  diseased  muscles.  In 
syringomyeha,  however,  we  notice  sensory  troubles,  which  are  always 
absent  in  progressive  muscular  atrophy.  Certain  trophic  troubles  are  also 
present — glossy  skin,  eschars,  fragihty  of  the  bones,  swelhng  of  the  epi- 
physes, articular  lesions,  panaris  with  loss  of  the  phalanges,  and  increased 


D18KASKS  OK  THE  SP1>J.\I.  (OIH)  1283 

sweatinij  over  the  aiisosthetic  regions.  From  the  anatomo-pathological 
point  of  view,  the  reeent  researches  of  Kahler,  Debove,  and  Dejerine  liave 
shown  that  in  syriiigoniycHa  there  is  not  a  lesion  Uniited  to  the  cells  of  the 
anterior  eorniui ;  either  a  ghonia  develops  in  the  circumference  of  the 
central  canal,  and  compresses  the  cornua  of  the  spinal  cord  from  witliin 
outwards,  or  there  is  a  central  myelitis,  which  produces  a  cavity  (Joffroy 
and  Achard).  If  the  effects  are  more  marked  in  the  upper  limbs,  it  is 
because  the  lesion  is  especially  localized  in  the  cervical  region  of  the  cord. 

The  aetiology  of  progressive  muscular  atrophy  is  very  obscure.  Heredity 
and  excessive  muscular  fatigue  have  been  invoked.  Charrin  and  Claude,  by 
repeated  injections  of  pyocyanic  toxine,  were  able  to  produce  progressive 
muscular  atrophy  in  animals.  The  post-mortem  examination  revealed  a 
lesion  of  slow  evolution  in  the  grey  matter  of  the  spinal  cord.  The  diseases 
of  the  anterior  cornua,  and  especially  infantile  paralysis,  are  regarded  as 
favouring  the  ulterior  development  of  progressive  muscular  atrophy.  Accord- 
ing to  certain  authors,  however,  the  appearance  of  Aran-Duchemie's  disease 
is  said  to  be  independent  of  any  anterior  cornual  affection.  Both  diseases 
are  said  to  develop  successively,  in  consequence  of  a  congenital  weakness  of 
the  spinal  cord  {locus  minoris  resistenticB).  Rendu  has  further  pointed  out 
that  in  these  cases  the  muscular  atrophy  is  not  essentially  progressive,  but 
that  it  rapidly  attacks  certain  muscles  or  groups  of  muscles,  while  progressive 
atrophy  generally  involves  small  bundles  of  fibres.  The  atrophy  caused  by 
lead-poisoning  differs  markedly  from  the  classic  disease  just  described.  The 
prognosis,  though  grave,  is  not  always  fatal.  The  disease  sometimes  has 
long  periods  of  arrest ;  it  may,  indeed,  stop  in  its  evolution.  Faradization 
is  the  most  efficacious  treatment  for  progressive  muscular  atrophy. 

VI.  SECONDARY  AND  PRIMARY  LATERAL  SCLEROSIS- 
SPASMODIC  TABES  DORSALIS. 

Sclerosis  of  the  lateral  columns  of  the  spinal  cord  may  be  imilateral  or  symmetrical, 
primary  or  secondary,  and  isolated  or  associated  with  other  medullary  changes. 

Sclerosis  of  the  lateral  columns  is  generally  only  an  episode  in  the  course  of  some 
cerebral  or  spinal  disease  ;  at  other  times  the  whole  interest  of  the  question  is  concen- 
trated in  the  lateral  sclerosis.     The  following  forms  are  seen  : 

(o)  Descending  secondary  lateral  sclerosis. 

(6)  Symmetrical  lateral  sclerosis  ;  spasmodic  tabes  dorsahs. 

Lateral  Columns. — The  lateral  columns  of  the  spinal  cord  contain  the  longitudinal 
nerve  fibres,  some  long,  others  short,  which  cause  the  anterior  grey  matter  of  the 
spinal  cord  throughout  its  entire  length  to  communicate  with  the  brain,  and  which  unite 
the  various  segments  of  this  grey  matter.  The  crossed  pyramidp.l  tract  (described  in 
detail  under  Cerebral  Hsemorrhage)  forms  the  bulk  of  the  lateral  columns.  It  is  by 
means  of  the  fibres  of  the  pyramidal  tract,  situated  in  the  posterior  portion  of  the  lateral 
columns,  that  the  anterior  grey  matter  of  the  spinal  cord  receives  from  the  brain  the 
order  for  contraction,  which  it  subsequently  transmits  to  the  muscles  by  means  of  the 


1284  TEXT-BOOK  OF  MEDICINE 

motor  nerves  (voluntary  movement).  It  is  therefore  clear  that  the  destmction  of  these 
tracts  vrill  be  followed  by  paresis  or  paralysis  of  the  voluntary  muscles.  It  is  also  clear 
that  the  chronic  irritative  lesions  of  these  columns  (descending  or  primary  sclerosis), 
by  causing  abnormal  excitabihty  in  the  anterior  grey  matter,  will  give  rise  to  abnormal 
muscular  action,  or  tonus,  which  by  its  intensity  or  permanence  constitutes  con- 
tracture. In  a  disease  of  the  cord,  transient  or  permanent  contractiires,  the  tendon 
reflexes  and  the  tremors  that  so  often  accompany  the  contractures  are  phenomena 
associated  with  irritative  lesions  of  the  lateral  columns.  The  motor  troubles  of 
paralysis  and  of  contracture  may  exist  at  the  same  time,  or  may  foUow  each  other  in 
diverse  degrees.  If  they  are  often  found  together,  although  the  paralysis  is  the  result 
of  a  destructive  lesion  and  the  contracture  of  an  irritative  lesion,  it  is  because  both  kinds 
of  lesion  are  present  in  lateral  sclerosis. 

1.  Secondary  Descending  Lateral  Sclerosis. 

Wlien  the  crossed  pvramidal  tract  is  diseased  at  any  point  in  its  cerebral 
or  spinal  course,  the  portion  of  tie  cord  subjacent  to  the  lesion  (bsemorrliage, 
softening,  tumour,  etc.)  may  become  the  seat  of  a  secondary  descending 
sclerosis.  The  lateral  sclerosis  thu5  constituted  is  situated  on  the  side  of 
the  provoking  lesion,  if  the  lesion  is  in  the  spinal  cord,  and  on  the  opposite 
S:ide  if  the  provoking  lesion  is  above  the  decussation  of  the  pyramids.  This 
secondary  sclerosis  is  generally  unilateral.  Its  form  and  its  extent  vary 
according  as  its  origin  is  cerebral  or  spinal,  but  it  reveals  itseK  by  constant 
symptoms,  which  are  :  (1)  Exaggeration  of  the  tendon  reflexes  ;  (2)  con- 
tracture. The  contracture,  which  is  at  fiist  temporary  and  then  per- 
manent, attacks  the  upper  and  the  lower  limb,  according  to  the  extension 
of  the  spinal  lesion.  This  contracture  is  frequently  accompanied  by 
Babinski's  sign  and  tremors  (spontaneous  or  provoked)  of  var^niig  intensity. 

The  lesion  in  the  lateral  columns  does  not,  however,  always  remain 
limited  to  the  territory  first  invaded.  The  irritation  sometimes  spreads  into 
the  anterior  cornua  of  the  grey  matter,  "Rith  which  these  columns  are  directly 
related  (change  in  the  motor  cells),  in  which  case  we  notice  atrophy  of 
certain  muscles  or  groups  of  muscles.  This  variety  of  sclerosis  of  the  lateral 
columns  is  secondar}^  and  descending ;  and  if  it  is  sometimes  comphcated 
with  muscular  atrophy,  this  atrophy  is  limited,  and  has  no  progressive 
tendency. 

2.  Symmetrical  Lateral  Sclerosis— Spasmodic  Tabes  Dorsalis. 

Description.  —  This  sclerosis,  which,  according  to  certain  writers 
(Eichter),  is  said  to  be  a  double  primary  sclerosis  of  the  lateral  columns, 
has  been  described  under  the  name  of  spasmodic  paralysis  (Erb)  and  of 
spasmodic  tabes  dorsaUs  (Charcot).  Xo  proof,  however,  exists  that  it  is 
a  distinct  morbid  species — a  simple  primary  sclerosis  systematically  con- 
fined to  the  pyramidal  tracts — and  it  is  quite  possible  that  this  afiection 
is  really  a  variety  of  disseminated  sclerosis.     In  some  cases,  followed  by  post- 


DISEASES  OF  THE  SPINAL  CORD  1285 

mortem  examination,  the  degeneration  of  the  lateral  columns  was  secondary 
and  was  caused  by  foci  of  myelitis,  by  cerebral  lesions,  by  lesions  of  both 
capsules,  or  by  the  meningeal  lesions  of  general  paralysis. 

According  to  Little  and  Marie,  the  existence  of  spasmodic  tabes  may  be 
admitted,  but  it  must  be  considered  as  a  congenital  disease,  due  to  imperfect 
development  of  the  pyramidal  tract  throughout  its  whole  length.  In  four 
cases  of  Little's  syndrome,  Phihppe  and  Cestan  found  the  pyramidal  tract 
absolutely  normal,  both  in  the  bulb  and  in  the  spinal  cord.  The  symptoms 
commence  in  infancy.  The  disease  always  makes  its  appearance  in  the 
lower  hmbs,  and  may  be  confined  to  them  indefinitely. 

Both  lower  Hmbs  are  attacked,  either  simultaneously  or  subsequently, 
by  paresis.  The  loss  of  power  is  compUcated  by  exaggeration  of  the 
tendon  reflexes,  muscular  spasm,  and  later  by  contractures,  which  are  at 
first  transient  and  then  permanent.  The  legs  are  placed  in  the  position 
of  extension  and  adduction.  These  symptoms  are  often  accompanied  by 
twitchings  and  spinal  epilepsy,  which  are  sometimes  spontaneous,  some- 
times provoked  by  the  patient's  movements.  It  is  very  rare  for  these  symp- 
toms to  invade  the  upper  Hmbs.  Stiffness  of  the  neck,  strabismus,  and 
speech  troubles  may  be  observed.  The  disease  lasts  indefinitely,  until 
some  intercurrent  affection  carries  off  the  patient.  This  form  of  sclerosis 
is  not,  as  a  rule,  accompanied  by  muscular  atrophy. 

Of  the  affections  which  may  evolve  under  the  outward  appearance  of 
spasmodic  tabes,  some  may  recover  (Raymond). 

VII.  AMYOTROPHIC  LATERAL  SCLEROSIS. 

Since  the  date  of  Charcot's  work  we  designate  under  the  name  of 
amyotrophic  lateral  sclerosis  primary  and  symmetrical  sclerosis  of  the 
lateral  columns,  accompanied  in  the  invaded  segment  of  the  cord  by  a  change 
in  the  cells  of  the  anterior  cornua.  The  symptoms  of  lateral  sclerosis  are 
also  associated  with  the  symptoms  of  invading  muscular  atrophy. 

Pathological  Anatomy. — According  to  Charcot,  "  the  lesion  of  amyo- 
trophic sclerosis  commences  at  the  level  of  the  oHvary  bodies  in  the  pyra- 
midal tract.  The  sclerosis  spreads  along  the  direct  and  crossed  tracts  in 
such  a  manner  as  to  cause  total  atrophy.  This  anatomical  period  corre- 
sponds to  the  cHnical  period  of  paralysis."  The  sclerosis  does  not  remain 
confined  to  the  pyramidal  tract.  It  also  attacks  the  mass  of  the  antero- 
lateral tracts  and  Goll's  columns.  Later  or  simultaneously  changes  super- 
vene in  the  grey  matter  of  the  spinal  cord,  and  extend  through  the  entire 
extent  of  the  anterior  cornua,  causing  atrophy  of  the  large  gangHon  cells. 

These  spinal  lesions  are  always  accompanied  at  a  given  moment  by 
bulbar  lesions,  such  as  sclerosis  of  the  pyramids,  degeneration  with  pigmenta- 
tion, or  more  or  less  complete  disappearance  of  the  cells  in  the  inferior 
II.  82 


1286  TEXT-BOOK  OF  MEDICINE 

nucleus  of  the  hypoglossal  and  of  the  facial  nerves.  The  nuclei  of  origin  of 
the  mixed  nerves  and  of  the  trigeminal  nerves  are  not  always  exempt  from 
lesions.  The  pyramidal  tract  may  show  lesions  in  its  course  through  the 
peduncles,  the  internal  capsule,  and  as  far  as  the  motor  convolutions,  which 
in  some  cases  are  said  to  have  presented  atrophic  lesions,  with  disappearance 
of  the  nerve  cells  through  pigmentary  degeneration.  The  anterior  roots  of 
the  nerves  are  generally  atrophied,  and  the  small  intramuscular  nerves  are 
often  sclerosed,  whilst  the  trunks  of  the  motor  nerves  are  often  healthy. 
The  atrophied  muscles  show  simple  atrophy.  According  to  these  data, 
latent  amyotrophic  sclerosis  might  be  considered  as  an  afiection  attacking 
primarily  the  pyramidal  tract,  and  affecting  by  choice  a  portion  of  this  tract, 
but  in  some  cases  attacking  the  entire  tract,  and  even  the  motor  ceUs  in 
various  regions  of  the  brain,  medulla,  and  cord.  The  primary  lesion  in 
the  antero -lateral  column  is  not  subordinated  to  the  cellular  changes. 
Cellular  atrophy  causes  simple  atrophy  of  the  white  bundles,  but  not 
sclerosis.  The  disease,  therefore,  is  a  primary  lesion  of  the  antero -lateral 
tract  (Phihppe  and  Guillain). 

Symptoms. — In  amyotrophic  lateral  sclerosis  paralytic  and  spasmodic 
troubles  open  the  scene,  and  show  themselves  in  nearly  every  case  in  the 
upper  hmbs.  The  patient  experiences  paresis  in  the  arms,  often  preceded  by 
pains  and  accompanied  by  spasmodic  phenomena.  The  muscles  preserve 
their  electrical  contractihty,  but  muscular  rigidity,  exaggeration  of  the 
tendon  reflexes,  spasms,  and  contracture  are  early  troubles. 

The  exaggeration  of  the  tendon  reflexes  is  general ;  it  is  observed  in  the 
knee,  the  heel,  the  wrist,  and  the  masseter.  The  muscular  contracture 
exists  more  frequently  in  the  condition  of  stiffness  than  in  the  condition  of 
true  contracture. 

In  the  first  period  of  the  disease — that  is  to  say,  a  few  months  after  the 
commencement  of  symptoms — the  upper  limbs  show  invading  muscular 
atrophy  (lesions  of  the  anterior  cornua)  and  permanent  contracture  (lesion 
of  the  lateral  column).  The  fingers  are  bent  in  the  hand.  The  forearm  is 
semiflexed  on  the  arm,  and  the  arm  is  forcibly  adducted  to  the  side.  These 
symptoms  are  naturally  less  pronounced  in  proportion  as  the  muscular 
atrophy  progresses.  The  atrophy  especially  affects  the  muscles  of  the 
hands  and  of  the  forearms. 

In  the  second  period — that  is  to  say,  ten  to  twelve  months  after  the 
commencement  of  the  disease — the  lower  hmbs  are  involved.  Paresis, 
exaggeration  of  the  tendon  reflexes,  contracture,  and  tremors  (lesions  of 
the  lateral  columns)  are,  however,  the  dominant  symptoms,  and  the  muscular 
atrophy  (lesion  of  the  anterior  cornua)  is  much  less  pronounced  than  in  the 
upper  limbs.  The  lower  hmbs  are  extended  and  rigid,  with  inward  rotation 
of  the  internal  edge  of  the  feet. 


DISEASES  OF  THE  SPINAL  CORD  12«7 

The  paresis,  contracture,  unci  atrophy  may  also  attack  the  muscles  of 
the  neck.  The  positions  of  the  head  vary  according  to  tlic  muscles  most 
affected. 

Finally,  in  the  third  period,  the  bulbar  phenomena  supervene.  The 
patient  looks  like  a  crying  child  ;  the  saliva  drools  from  the  mouth  ;  the 
tongue,  which  is  often  atrophied,  moves  with  dilliculty  ;  the  velum  palati 
is  paralyzed  ;  the  lower  jaw  loses  its  movements  of  diduction ;  and  we  find 
successively  or  simultaneously  troubles  of  speech,  of  mastication,  of  de- 
glutition, and  of  respiration  (atrophy  of  the  nuclei  of  the  hypoglossal,  of 
the  facial,  of  the  motor  branch  of  the  trigeminal,  and  of  the  pneumogastric 
nerves).  Sometimes  the  onset  is  bulbar,  difficulty  in  the  articulation  of 
words  and  embarrassment  of  speech  being  the  first  symptoms  (Raymond). 

The  sphincters  remain  intact.  There  are  no  sensory  or  trophic  troubles. 
When  the  patient  is  not  carried  off  by  an  intercurrent  disease,  he  dies  of 
asphyxia,  syncope,  or  inanition. 

The  special  feature  of  amyotrophic  lateral  sclerosis  is  the  rapidity  of  its 
evolution.  In  two  or  three  years,  sometimes  in  one  year,  it  runs  its  course, 
ending  without  exception  in  bulbar  phenomena.  What  a  difference  from 
progressive  muscular  atrophy  and  spasmodic  tabes,  which  have  a  slow 
invading  course,  and  which  may  even  become  stationary  without  threaten- 
ing the  patient's  hfe  for  a  long  time  !  Although  writers  have  wished  to 
cast  these  two  affections  into  a  single  disease,  the  distinction  must  be 
rigidly  maintained  (Raymond  and  Rickhn). 

iEtiology — Diagnosis. — Nothing  is  known  as  to  the  causes  of  this 
disease.  It  is  almost  special  to  adult  age.  The  absence  of  all  cerebral 
symptoms,  the  presence  of  bulbar  symptoms,  and  the  evolution  of  musculal 
atrophy  distinguish  it  from  insular  sclerosis.  Spasmodic  tabes  differs  from 
it  in  the  absence  of  muscular  atrophy  and  in  the  initial  locahzation  of  the 
disease  to  the  lower  Umbs.  In  Duchenne's  progressive  muscular  atrophy 
the  initial  stage  of  paresis  and  the  contractures  are  absent. 

VIII.  INSULAR  SCLEROSIS. 

Pathological  Anatomy. — The  various  forms  of  myehtis  so  far  described 
are  both  systematic  (Vulpian)  and  parenchymatous  (Hallopeau)  :  systematic 
— that  is  to  say,  they  are  limited  to  a  system  of  fibres  or  ceUs  (posterior  or 
lateral  columns,  anterior  cornua) ;  parenchymatous — that  is  to  say,  the 
irritative  process  seems  to  commence  in  the  nerve  fibre  or  cell  before 
reaching  the  neurogha. 

Insular  sclerosis,  on  the  contrary,  is  a  diffuse  and  interstitial  chronic 
myehtis.  It  is  diffuse  because  it  invades,  in  the  shape  of  islets,  the  white 
matter  of  the  nerve  centres  and  the  columns  of  the  spinal  cord  without 


1288  TEXT-BOOK  OF  MEDICINE 

taking  account  of  the  furrows.  It  is  interstitial  because  the  irritative 
process  seems  to  commence  in  the  vascular  element  and  in  the  neurogUa. 
The  grey  matter  is  less  affected  than  the  white  matter.  The  patches  of 
sclerosis  may  be  superficial  or  deep,  greyish,  rosy,  of  a  firm  consistency, 
clearly  circumscribed,  and  rich  in  vessels.  The  sclerotic  lesion  is  very 
pronounced  in  the  centre  of  the  patch,  and  disappears  at  the  circumference 
by  insensible  transitions.  The  meninges  are,  as  a  rule,  neither  thickened 
nor  adherent. 

The  nerve  tubes  are  affected  in  the  midst  of  this  prohferating  con- 
nective tisue.  The  axis-cyhnder  remains  even  in  the  centre  of  the  patch 
until  a  very  advanced  period  (Charcot),  which  is  not  customary  in  scleroses 
of  the  tracts.  The  myehn,  however,  disintegrates,  and  the  leucocytes, 
which  have  passed  out  of  the  bloodvessels  by  diapedesis,  become  charged 
with  drops  of  myehn,  converted  into  granular  bodies,  which  infiltrate  the 
lymphatic  sheaths.  The  destruction  of  the  sheaths  of  myehn,  formerly 
supposed  to  be  due  to  compression  of  the  nerve  fibres  by  the  new  connec- 
tive tissue,  appears  to  result  from  the  nutritive  activity  of  the  neuroghal 
and  lymphatic  cells. 

The  neurogha  of  the  grey  matter  also  undergoes  a  sclerotic  process  ;  the 
nerve  cells  degenerate,  become  atrophied,  and  their  processes  disappear. 
The  bloodvessels  show  periarteritis  and  endarteritis,  the  wall  becoming 
thickened  and  the  lumen  constricted.  It  has,  indeed,  been  asked  whether 
the  vascular  lesions  were  not  the  origin  of  the  patches  of  sclerosis.  The 
patches  are  discrete  or  confluent ;  they  may  be  found  throughout  the  whole 
extent  of  the  nervous  centres  (spinal  cord,  bulb,  pons,  cerebellum,  cerebrum 
and  cranial  nerves),  and  their  predominance  in  certain  parts  explains  the 
spinal,  cerebral,  and  cerebro-spinal  forms  of  this  disease.  The  cerebral 
variety  is  the  least  common,  the  cerebro-spinal  form  the  most  common. 
The  lesions  of  insular  sclerosis  are  rarely  followed  by  secondary  degenera- 
tions, doubtless  because  the  axis-cyHnders  are  almost  always  intact. 

Description. — The  irregularity  and  the  predominance  of  the  patches 
in  various  parts  of  the  nervous  system  make  this  form  of  sclerosis  essentially 
a  polymorphous  disease.  I  shaU  nevertheless  base  my  description  on  the 
most  common  or  cerebro-spinal  type. 

In  some  cases  the  disease  makes  its  appearance  suddenly  by  hemiplegia, 
with  or  without  apoplexy,  by  vertigo,  or  by  visual  troubles.  The  com- 
mencement is  generally  slow  and  progressive,  the  dominant  symptom  con- 
sisting in  speech  troubles,  tremors,  particularly  of  the  hands,  and  increasing 
difficulty  in  walking.  The  last-named  trouble  is  the  most  common  initial 
symptom.  The  patient  experiences  paresis  in  the  lower  hmbs,  which 
gradually  becomes  more  marked,  but  which  presents,  as  its  characteristic, 
remissions  that  may  last  for  several  months. 


DISEASES  OF  THE  SPINAL  CORD  12R0 

At  an  earlier  or  later  period  the  paresis  in  the  Kiwer  limbs  is  complicated 
by  rigidity  and  contractures,  at  first  temporary  and  thfMi  permanent.  Tiie 
contracture  places  the  legs  in  the  position  of  extension  and  of  adduction, 
causing  the  spasmodic  gait.  As  the  rigidity  of  the  leg  does  not  allow  flexion 
of  the  knee,  the  patient  has  to  walk  forward  by  alternately  raising  the  pelvis 
and  the  trunk  on  each  side,  and  even  then  the  point  of  the  foot  which  is 
not  properly  raised  from  the  ground  causes  a  dragging  to  be  heard  at  every 
step.  The  tendon  reflexes  being  exaggerated,  Babinski's  sign  may  show 
itself  when  the  patient  stands  on  the  soles  of  his  feet.  The  walk  is  not  only 
of  a  spasmodic  character,  but  often  assumes  a  cerebellar  type,  the  patient 
walking  hke  a  drunken  man,  with  legs  apart  and  staggering  steps  (cere- 
bello-spasmodic  gait).  The  motor  troubles,  called  cerebellar  asynergy  by 
Babinski,  have  been  verified  by  Campbell  and  Crouzon  at  Bicetre  in  patients 
with  insular  sclerosis.  In  some  cases  walking  is  rendered  even  more  difi&cult 
by  a  general  tremor,  which  appears  as  soon  as  the  patient  tries  to  rise " 
and  walk. 

The  contracture  is  not  so  marked  in  the  arms  as  in  the  legs,  but  spas- 
modic paresis  is,  however,  noticed  in  them,  and  makes  the  movements 
very  awkward.  The  chief  factor,  however,  in  the  upper  Hmbs  is  a  tremor 
which  has  a  special  character  in  insular  sclerosis.  As  long  as  the  patient 
is  at  rest,  the  tremor  is  not  seen  ;  it  is  intentional,  and  only  produced  on  the 
occasion  of  voluntary  movements.  If  a  patient  is  told  to  drink  a  glass  of 
water,  he  will  seize  the  glass  and  clutch  it  tightly.  The  arm  commences 
to  tremble,  and  makes  the  glass  shake.  The  amplitude  and  the  rapidity 
of  the  oscillations  increase  as  the  patient  brings  the  glass  to  his  mouth, 
the  water  is  spilt  in  all  directions,  and  the  head  and  body,  which  have  been 
bent  forward  to  meet  the  glass,  are  seized  with  rhythmic  oscillations  as  the 
glass  reaches  the  mouth.  It  knocks  against  the  teeth,  the  nose,  and  the 
chin,  and  the  patient  can  only  take  the  glass  between  his  teeth  by  making 
a  fresh  attempt  with  both  hands.  This  intentional  tremor  may  invade 
every  part  of  the  body. 

Ocular  troubles  are  frequent  and  generally  well  marked ;  they  are  of 
great  importance  from  the  diagnostic  point  of  view.  Let  me  first  mention 
nystagmus,  which  is  present  in  half  the  number  of  cases,  and  which 
consists  in  rapid  involuntary  oscillations  of  the  eyeballs,  in  the  horizontal 
plane.  Besides  true  nystagmus,  due  to  a  bulbar  or  cerebral  lesion,  Uhthoff 
has  noticed  a  false  nystagmus,  due  to  paresis  of  the  motor  muscles.  The 
paralyses  of  the  oculo-motor  muscles  are  usually  incomplete  and  associated 
— associated  in  that  they  affect  in  both  eyes  the  muscles  entrusted  with 
the  function  of  movement.  They  are  sometimes  temporary,  and  have  a 
preference  for  the  external  or  internal  recti.  As  in  tabes,  we  notice  the 
inequahty  of  the  pupils  and  myosis.     Whilst,  however,  in  tabes,  myosis  is 


1290  TEXT-BOOK  OF  MEDICINE 

accompanied  by  Argyll-Robertson's  sign,  in  insular  sclerosis  the  pupil 
reflexes  are  preserved.  Amblyopia  is  frequent,  but,  contrary  to  that  of 
tabes,  it  rarely  ends  in  blindness.  The  ophthalmoscope  shows  that  the 
external  segments  of  the  optic  discs  are  pale  ;  atrophy  is  rare.  Retro-bulbar 
neuritis  may  provoke  similar  functional  troubles.  The  field  of  vision  fairly 
often  shows  a  central  scotoma.  The  dyschromatopsy  may  be  compared 
to  that  of  tabes.     Red  and  green  are  the  first  colours  to  disappear. 

Embarrassment  of  speech  is  almost  constant,  and  closely  resembles 
that  of  general  paralysis,  although  the  words  are  more  scanned,  spasmodic, 
and  monotonous  than  in  the  latter  disease. 

Sensory  troubles  do  not  form  a  part  of  the  chnical  picture  of  insular 
sclerosis  (Charcot).  Trophic  troubles  are  quite  exceptional.  G-lycosuria 
has  been  noticed  ;  it  indicates  a  lesion  in  the  fourth  ventricle.  For  several 
years  these  symptoms  follow  one  another,  combine,  improve,  or  grow  worse, 
and  finally  there  comes  a  period  characterized  by  the  appearance  of  loss  of 
flesh,  anorexia,  frequent  diarrhoea,  and  progressive  weakening  of  the  intelli- 
gence. The  excessive  embarrassment  reduces  the  speech  to  an  unintelli- 
gible sputtering.  Eschars  form,  the  sphincters  become  paralyzed,  and  the 
patient  succumbs  in  cachexia. 

Insular  sclerosis  lasts  from  two  to  twenty  years.  The  course  of  this 
disease  is  most  irregular.  In  the  first  place,  it  may  be  cured.  In  other 
cases  it  improves,  with  long  intermissions,  or  else  events  are  rapidly 
precipitated.  The  patient  is  sometimes  carried  ofi  by  phthisis  or  pneu- 
monia ;  sometimes  he  succumbs  with  symptoms  of  glosso-labio-laryngeal 
paralysis  or  of  general  paralysis,  Temporary  or  persistent  hemiplegia, 
accompanied  or  not  by  apoplexy  and  aphasia,  may  be  observed  in  all  stages 
of  insular  sclerosis  (Blanche,  Edwards).  Apoplectiform  attacks  sometimes 
supervene  at  the  onset  or  during  the  course  of  the  disease,  and  may  be 
followed  by  death.  The  important  point  is  that  they  cause  a  rise  in  tem- 
perature (Charcot),  unlike  apoplexy  from  cerebral  haemorrhage,  at  the 
commencement  of  which  the  temperature  is  lowered. 

Diagnosis. — In  addition  to  the  various  forms  already  described,  insular 
sclerosis  sometimes  presents  a  defaced  form,  in  which  the  ordinary  symp- 
toms are  absent.  In  several  cases  it  has  simulated  the  clinical  picture  of 
spasmodic  tabes  so  closely  that  certain  writers  have  considered  spasmodic 
tabes  to  be  a  variety  of  insular  sclerosis  rather  than  a  distinct  morbid  entity, 
due  to  the  primary  and  symmetrical  sclerosis  of  the  lateral  columns.  Insular 
sclerosis  is  sometimes  comphcated  by  muscular  atrophy,  and  these  cases  of 
atrophy,  with  contractures,  so  closely  resemble  amyotrophic  lateral 
sclerosis  that  it  has  been  asked  whether  the  latter  disease  deserves  to  be 
placed  as  a  morbid  entity  in  diseases  of  the  spinal  cord.  The  anatomical 
lesions,  however,  justify  this  distinction. 


DISEASES  OF  THE  SPINAL  CORD  1291 

Insular  sclerosis  was  for  a  long  time  confounded  with  paralysis  agitans, 

but  in  the  latter  disease,  amongst  other  distinctive  signs,  the  tremor 
particularly  affects  the  wrists  and  the  fingers,  and  is  continuous,  whilst  in 
sclerosis  it  is  intentional.  Although  the  speech  is  more  scanning  and  less 
tremulous  in  insular  sclerosis  than  in  general  paralysis,  it  must  neverthe- 
less be  noted  that  the  speech  troubles  are  sometimes  identical.  But  in 
general  paralysis  we  do  not  find  the  same  tremors  or  contractures,  and  tbe 
psychical  troubles  often  appear  early. 

The  mercurial  tremor  has  many  analogies  with  that  of  insular  sclerosis. 
It  has  a  certain  amplitude,  and  it  may  be  exaggerated  by  voluntary  move- 
ments, but  in  insular  sclerosis  the  tremor  is  absent  as  long  as  the  patient  is 
at  rest. 

In  some  cases  gastric  crises,  thoracic  pains,  and  troubles  of  equilibrium 
recall  locomotor  ataxy.  In  several  instances  predominance  of  the  para- 
lytic troubles  has  been  noted — partial  hemiplegia,  with  a  sudden  or  slow 
onset,  monoplegia,  and  paraplegia — so  that  the  diagnosis  from  cerebral 
haemorrhage  and  softening  of  cerebral  tumours  sometimes  causes  much 
difficulty.  This  difficulty  is  all  the  greater  as  the  attacks  of  paralysis 
(hemiplegia  or  paraplegia)  sometimes  supervene  from  the  commencement 
of  the  disease.  Hysteria  may  simulate  insular  sclerosis  ;  it  may,  indeed, 
be  associated  with  it. 

etiology. — The  setiology  of  insular  sclerosis  is  very  obscure.  It  is 
chiefly  seen  in  adults,  but  it  is  not  rare  in  children.  The  infectious  diseases 
(variola,  scarlatina,  typhoid  fever,  diphtheria,  dysentery,  and  pneumonia) 
appear  to  act  as  a  determining  cause.  As  Jaccoud  has  shown,  these  diseases 
are,  as  a  matter  of  fact,  capable,  of  causing  the  symptoms  of  insular  sclerosis, 
but  we  must  wait  for  further  cases,  followed  by  post-mortem  examination, 
before  we  can  say  that  they  may  produce  the  disease. 


IX.  ACUTE  MYELITIS  IN  GENERAL. 

Before  describing  the  different  varieties  of  acute  myelitis,  it  mil  be  well  to  discuss 
these  affections  in  general  terms.  As  regards  localization,  we  find  cases  of  diffuse 
myelitis,  in  which  the  lesions  are  scattered,  attacking  both  the  grey  and  the  white 
matter.  In  some  forms  of  myelitis  the  lesions  confine  themselves  more  to  the  grey 
matter,  especially  to  the  anterior  comua.  They  are  called  "  poliomyelitis  "  (TroXtos, 
grey).  Other  forms  of  myelitis  confine  themselves  to  the  white  matter,  and  are  called 
"  leucomyeUtis  "  {XevKos,  white). 

As  regards  pathogenesis,  myelitis  is  divided  into  two  great  classes — myeUtis  due  to 
infectious  or  toxi-infectious  agents  (and  we  must  mention  here  aU  the  infections — typhoid 
fever,  influenza,  diphtheria,  cholera,  coU  bacillus,  streptococcia,  staphylococcia,  gonor- 
rhoea, syphilis,  and  tuberculosis),  and  myelitis  due  to  toxic  substances  (alcohol,  lead, 
ergot,  pellagra,  arsenic,  etc.).  We  shall  see  how  these  questions  in  human  pathology 
have  been  cleared  up  by  experiments. 


1292  TEXT-BOOK  OF  MEDICINE 

Myelitis  due  to  Infection. 

Experiments. — Myelitis  has  been  produced  by  Charrin  with  the  BaciUu-s  pyocyaneus  ; 
by  Roux  and  Yersin  with  the  diphtheria  tosine  ;  by  Grancher,  Martin,  and  Leroux- 
Rebard  with  avian  tubercle  bacilh ;  by  Gilbert  and  Lion  with  human  tubercle 
bacilli ;  by  Thoinot  and  Massehn  with  the  Staphylococcxis  aureVrS  ;  by  Gilbert  and  Lyon 
with  the  B.  coli  ;  by  Vincent  with  the  B.  typhosus  ;  by  Roger,  Bourges,  Widal,  and 
Besancon  with  the  streptococcus  ;  by  Marinesco  with  the  tetanus  toxine. 

These  cases  of  experimental  myelitis  may  be  produced  either  by  injecting 
into  the  bloodvessels  the  microbes  themselves  or  their  toxines.  When  the 
experiment  is  made  with  h^ing  cultures,  the  pathogenic  microbes  may  be 
found  m  the  spinal  lesions.  Thoinot  and  Massehn  found  the  Bacillus  coli 
and  the  staphylococcus.  On  the  other  hand,  they  did  not  find  the  strepto- 
coccus. The  presence  or  the  colonization  in  situ  of  a  microbe  is  not  therefore 
an  essential  condition  for  the  determination  of  the  lesions.  It  has,  indeed, 
been  proved  that  most  of  the  pathogenic  microbes  act  by  means  of  their 
toxines,  as,  for  example,  in  the  special  lesions  provoked  by  the  pyocyanic 
toxine  (Charrin),  by  the  diphtheritic  toxine  (Enriquez  and  Haillon),  and 
by  the  streptococcic  toxine  (Manfredi  and  Traversa).  The  pathogenic 
microbe  may  have  disappeared,  and  its  toxine  may  still  persist.  The 
microbe  may  have  been  cultivated  in  a  spot  remote  from  the  spinal 
cord,  and  its  toxine  may  nevertheless  poison  the  bulbo-spinal  axis 
(diphtheria). 

Paralytic  troubles  occur  in  experimental  animals  at  indefinite  periods ; 
they  may  be  early  or  late.  The  paralysis  is  sometimes  the  first  manifesta- 
tion of  the  infection,  the  animal  appearing  to  be  in  no  wise  afiected  by  the 
infectious  agents  with  which  it  has  been  inoculated.  Events  usually 
take  this  course  in  the  human  being.  The  paralytic  troubles  may  be  con- 
temporary with  the  infectious  disease,  or  may  not  appear  till  later,  so  that 
the  infection  having  passed  unnoticed,  the  myehtis  appears  to  be  an  essential 
or  spontaneous  disease. 

The  medullary  troubles  vary  greatly  in  the  experimental  animals. 
One  animal  has  flaccid  paraplegia  ;  another  one  has  spasmodic  paraplegia, 
with  permanent  or  paroxysmal  contracture.  In  one  animal  the  paralytic 
lesions  remain  confined  to  the  hind-quarters  ;  in  another  one  they  invade  all 
the  limbs,  becoming  general,  hke  Landry's  ascending  paralysis ;  or  else  they 
may  assume  a  hemiplegic  type.  Sometimes  the  muscles  remain  normal ; 
at  other  times  they  are  atrophied  (amyotrophia).  These  various  types  do 
not  depend  solely  on  the  nature  of  the  infective  agent,  since  in  the  animals 
under  experiment  the  streptococcus,  for  example,  may  produce  the  flaccid  or 
spasmodic,  paraplegic  or  general,  amyotrophic  or  non-amyotrophic,  varieties 
of  paralysis.  The  same  fact  is  observed  in  human  pathology.  The  same 
provoking  agent  (typhoid  fever,  influenza,  streptococcia,  infection  by  the 


DISRASE8  OF  THE  SPINAL  CORD  1293 

Bacillus  coli)  may  cause  various  medullary  lesions,  and  consequently  diverse 
symptoms. 

h\  the  animals  experimented  on,  the  duration  and  the  severity  of  the 
troubles  are  very  variable — transient  and  curable  paralysis,  rapid  and  fatal 
complications,  or  slow  and  chronic  evolution  of  the  disease.  Here  again 
chnical  medicine  is  in  agreement  with  experimental  research. 

The  medullary  lesions  in  animals  present  many  forms.  Sometimes  we 
find  no  lesion  in  the  nerve  centres,  the  nerves,  or  the  muscles.  This  apparent 
absence  of  lesions,  in  spite  of  severe  sjTnptoms,  has  been  noticed  by  Charrin 
and  Babinski  in  paralyses  caused  by  infection  with  the  Bacillus  pyocyaneus, 
and  by  Gilbert  and  Lion  in  paralyses  caused  by  infection  with  a  bacillus 
obtained  from  a  case  of  endocarditis.  Similar  conditions  may  exist  in  the 
human  being,  but  as  a  rule  the  medullary  lesions  found  in  animals  "  are 
concentrated  in  an  almost  exclusive  manner  in  the  gangUon  cells  of  the 
grey  matter,  and  particularly  in  the  large  cells  of  the  anterior  cornua  " 
(Vaillard).  Granular  degeneration,  changes  in  the  protoplasm  and  in  the 
nucleus,  vacuolar  condition  of  the  cell,  atrophy  of  the  cell  and  of  its  prolonga- 
tions are  seen.  The  disaggregation  of  the  chromatophile  elements  is  said  to 
be  the  first  change  in  the  nerve  cell,  the  chromatolysis  being  either  peripheral, 
perinuclear,  or  diffuse  (Marinesco).  It  is  said  to  be  accompanied  by  lesions 
of  the  achromatic  substance,  which  shows  molecular  disintegration,  has  a 
vitreous  aspect,  and  stains  readily.  The  white  matter  of  the  spinal  cord 
presents  less  constant  and  less  characteristic  changes.  Nevertheless  in 
rabbits  infected  with  the  streptococcus  the  white  columns  are  attacked,  the 
cyhnder-axis  is  changed,  and  the  nerve  fibres  are  atrophied  (Widal  and 
Besan9on).  In  rabbits  infected  with  the  Bacillus  coli  the  white  matter  is 
also  affected  (Thoiuot  and  Masselin). 

The  neuroglia  is  almost  always  free.  The  bloodvessels  show  no  lesion 
in  their  walls,  although  they  are  dilated  and  cause  haemorrhage.  These  dif- 
ferent changes  are  generally  disseminated  throughout  the  entire  length  of 
the  spinal  cord,  being  more  pronounced  at  the  medullary  swelhngs. 

These  cases  of  experimental  myeUtis  have  the  greatest  analogy  with 
acute  infective  myeUtis  in  the  human  being.  The  infection  and  the  toxi- 
infection  are  the  proved  or  disguised  cause  of  myeHtis,  whether  the  myeHtis 
is  produced  by  a  specific  pathogenic  agent  or  by  pathogenic  agents  acting  as 
a  secondary  infection.  Sometimes  the  microbe  is  still  present  in  the  medul- 
lary lesions,  as  in  the  cases  of  Curschmann  and  Vaillard,  due  to  the  Bacillus 
typhosus,  and  the  cases  of  Auche  and  Hobbs,  due  to  streptococcal  infection 
from  the  spinal  cord  of  smallpox  patients.  Most  frequently,  it  is  true,  the 
pathogenic  microbes  have  not  reached  the  cord,  or  they  may  have  dis- 
appeared, and  it  is  their  toxines  that  have  provoked  the  lesions.  In  chnical 
medicine,  as  in  experimental  research,  the  infection  may  cause  acute  diffuse 


1294  TEXT-BOOK  OF  MEDICINE 

myelitis,  with  disseminated  lesions  (white  and  grey  matter),  or  with  localized 
lesions  (pohomyehtis).  In  chnical  medicine,  as  in  the  animals  experimented 
on,  the  infection  of  the  cord  may  show  several  forms,  with  or  without  amyo- 
trophy, contractures,  and  sensory  troubles.  The  symptomatic  picture 
may  be  very  varied,  although  the  disease  is  due  to  the  same  pathogenic 
agent,  as  in  three  cases  quoted  by  Mosse  of  influenzal  myehtis  and  poly- 
neuritis, the  disease  running  a  difierent  course,  according  to  the  soU  in 
which  the  infection  developed. 

We  now  have  some  idea  of  the  aetiology  and  pathogenesis  of  certain 
obscure  forms  of  myehtis,  which  were  formerly  called  essential,  spontaneous, 
or  a  jrigore — not  that  cold  is  not  an  important  agent,  of  which  count  must 
be  taken,  but  it  is  an  agent  incapable  'per  se  of  provoking  an  infection.  Such 
must  be  certain  cases  of  myehtis  attributable  to  the  Bacillus  coli,  and  super- 
vening in  infections  due  to  this  germ  (enteritis,  diarrhoea,  cystitis,  pyelitis), 
and  in  streptococcal  infections. 

Although  the  known  infectious  agents  have  but  httle  tendency  to  produce 
chronic  myehtis  from  the  outset,  it  is  none  the  less  true  that  the  acute 
infective  process  may  be  transformed  into  a  slow  process,  which  finally 
becomes  chronic. 

Myelitis  from  Intoxication.— The  history  of  myehtis  due  to  toxic 
substances  is  less  extensive  and  less  interesting  than  that  of  infective 
myelitis,  but  nevertheless  it  comprises  certain  developments  wliich  are 
referred  to  under  the  Intoxications  (ergotism,  pellagra,  etc.). 

X.  INFANTILE  POLIOMYELITIS— ATROPHIC  SPINAL  PARALYSIS 

OF  CHILDHOOD. 

Description. — Infantile  pohomyehtis  (infantile  paralysis)  occurs  chiefly 
in  children  from  one  to  three  years  of  age.  It  begins  with  fever  and  para- 
lysis, and  terminates  in  a  chronic  stage  with  atrophy.  The  onset  is  quite 
insidious.  One  child  is  taken  ill  with  severe  or  shght  fever,  lasting  a  few 
hours  or  a  few  days ;  another  child  has  con\Tilsions  ;  and  yet  another  has 
gastro -intestinal  troubles,  and  the  case  is  thought  to  be  one  of  simple  indis- 
position, because  other  symptoms  capable  of  giving  a  clue  to  the  diagnosis 
are  absent.  In  some  cases  we  fijid,  as  initial  symptoms,  pains  in  the  spine, 
the  trunk,  or  the  hmbs ;  hypersesthesia  or  anaesthesia.  The  child  complains, 
but  as  it  is  unable  to  state  precisely  the  seat  and  the  nature  of  the  pain, 
the  physician  perhaps  suspects  rheumatism.  Sometimes  from  the  com- 
mencement we  notice  contractures,  especially  in  the  muscles  which  are 
paralyzed  later. 

A  few  days  after  this  obscure  onset — sometimes,  indeed,  the  next  day — 
paralysis  appears.     It  does  not  assume  the  progressive  form,  but  rapidly 


PTSEASER  OF  THE  SPINAL  CORD  1295 

strikes  all  the  parts  vvliicli  are  to  be  attacked.  The  paralysis  rarely  affects 
all  four  limbs.  Sometimes  it  is  limited  to  a  le<T  or  an  arm.  It  moat  often 
assumes  the  form  of  parajilegia.     It  aflects  a  radicular  topography. 

The  physician  who  on  the  previous  evening  considered  the  child  to  be 
suffering  from  simple  indisposition,  rheumatic  pains,  or  a  chill,  is  told  next 
day  :  "  The  child  is  paralyzed,  and  cannot  move  his  legs.  He  can  scarcely 
rise  up  in  bed  on  account  of  the  paralysis  in  the  arms."  As  a  matter  of 
fact,  the  paralysis  is  obvious  in  the  legs  ;  and  will  soon  reach  some  of  the 
muscles  of  the  arm.  The  muscles  of  the  trunk  and  of  the  neck  may  be 
involved,  and  the  child's  head  wobbles  in  all  directions.  In  a  case  that  I 
attended  with  Joffroy  these  symptoms  were  accompanied  for  several  days 
with  fits  of  suffocation  and  continuous  and  paroxysmal  dyspnoea,  that  caused 
us  the  greatest  anxiety.  The  bulbar  nuclei  were  doubtless  involved.  The 
affection  sometimes  extends  to  the  nuclei  in  the  medulla  and  pons,  causing 
double  paralysis  of  the  external  oculo-motor  muscles. 

The  tendon  reflexes  are  diminished,  but  the  sphincters  are  intact. 
Electrical  examination  from  the  first  gives  the  following  results  :  Increased 
reaction  to  the  galvanic  current,  and  reaction  of  degeneration  in  the  muscles 
which  are  to  remain  paralyzed ;  rapid  disappearance  of  galvanic  excitabiUty 
in  these  same  muscles.  The  persistence  of  Faradic  contractility  after  a 
fortnight  is  a  good  sign. 

The  paralytic  period  is  followed  by  a  kind  of  slow  remission.  From  two 
to  six  months  after  the  commencement  of  the  disease  the  paralysis  leaves 
certain  muscles  and  becomes  limited  usually  to  the  extensor  longus  digi- 
torum,  the  peronei,  and  the  tibialis  anticus.  It  is  Hkewise  observed  in 
the  triceps  femoralis,  the  serratus  magnus,  the  infraspinatus,  the  rhomboids, 
etc.  When  the  paralysis  persists  in  the  upper  Hmbs,  the  deltoid  is  usually 
attacked. 

The  period  of  atropby  then  commences.  The  atrophy,  which  may 
appear  from  the  first  month,  involves  the  paralyzed  muscles.  Trophic 
troubles  also  affect  the  osseous  system.  Certain  bones — the  femur  or  tibia — 
are  arrested  in  their  development,  and  remain  thinner  and  shorter  than  those 
on  the  healthy  side,  thus  giving  rise  to  a  hmp.  There  is  no  relation  between 
the  change  in  the  bones  and  that  in  the  muscles.  The  bone  may  be  affected 
in  the  segment  of  a  limb  without  any  lesion  in  the  muscular  system,  and 
vice  versa,  just  as  if  the  bones  and  the  muscles  had  different  trophic  centres. 
In  the  paralyzed  and  atrophied  hmb,  marked  coldness  (Charcot)  and  a 
diminution  in  the  cahbre  of  the  bloodvessel  have  been  noticed.  These 
partial  atrophies  are  followed  by  deformity  of  the  limbs.  The  overaction 
of  the  antagonistic  muscles  that  have  remained  healthy  causes  vicious 
positions,  such  as  club-foot,  especially  equino-varus,  forcing  the  patient  to 
walk  on  the  outer  edge  of  the  foot.     When  the  atrophic  lesion  is  more 


1296  TEXT-BOOK  OF  MEDICINE 

extensive,  the  legs  become  slender  and  deformed,  the  unfortunate  patients 
being  obliged  to  drag  themselves  on  their  ischia.  In  the  upper  limbs  we 
meet  with  club-hand ;  and  in  the  trunk,  with  scoliosis.  The  arrested  de- 
velopment of  the  bones  on  one  side  causes  limping.  The  prognosis  of  this 
disease  is  not  dangerous  as  regards  the  life  of  the  patient,  but  incurable 
infirmities  are  the  consequence. 

Diagnosis. — The  tender  age  of  the  patients  explains  the  difficulty  of 
the  diagnosis  at  the  commencement  of  the  affection.  Several  diseases  may- 
simulate  infantile  paralysis.  We  find  infantile  cerebral  hemiplegia,  with 
paralysis  and  atrophy  of  both  hmbs  on  the  same  side ;  but  infantile  paralysis 
is  flaccid,  while  contracture  is  present  in  the  case  of  cerebral  paralysis. 
Infantile  pseudo -paralysis  of  syphilitic  origin,  like  spinal  paralysis,  may 
affect  one  limb  or  several  limbs,  but  this  syphilitic  pseudo -paralysis  is  due 
to  the  separation  of  the  diaphysis  from  the  epiphysis  (Parrot,  Troisier). 
It  is  recognized  by  sharp  pains  on  movement,  and  by  the  swelling  of  the 
joints,  accompanied  or  not  by  crepitus. 

Obstetrical  paralyses,  due  to  the  application  of  the  forceps,  have  a  special 
locaKzation  to  the  deltoid,  infraspinatus,  biceps,  brachialis  anticus,  supinator 
longus,  and  coraco -brachialis.  Hysteria  with  atrophy  is  very  rare  in 
very  young  children.  The  diagnosis  can  be  made  by  remembering  that 
the  tendon  reflexes  are  normal  and  the  electrical  reactions  are  preserved  in 
hysteria. 

etiology. — The  aetiology  of  infantile  paralysis  is  most  obscure,  and  the 
various  causes  invoked — cold,  dentition,  etc. — are  anything  but  proved. 
The  disease  generally  appears  in  children  between  the  first  and  the  third 
year.  In  some  cases  it  has  followed  infectious  conditions  (measles,  scarla- 
tina, etc.).  Everything  leads  us  to  beheve  that  infantile  poHomyeHtis  is 
the  result  of  an  infection.  It  has  a  febrile  onset,  accompanied  by  general 
symptoms,  and  it  sometimes  appears  in  epidemics  (Marie).  As  a  matter  of 
fact,  the  accounts  of  several  epidemics  have  been  pubhshed.  In  1885 
Cordier  saw  within  a  few  months  thirteen  cases  of  infantile  paralysis  at 
Sainte-Foy-l'Argentiere,  in  a  population  of  1,500  inhabitants.  In  1888 
Medin  noted  in  six  months  forty-four  cases  of  infantile  paralysis  in  the  same 
district.  In  1890  Leegard  reported  eight  cases  of  infantile  paralysis  in  a 
small  Norwegian  town  where  the  disease  had  hitherto  been  unknown. 
Finally,  Pasteur  saw  infantile  paralysis  attack  seven  children  of  the  same 
family  in  three  weeks.     Cerebro-spinal  meningitis  has  been  arraigned. 

Pathological  Anatomy. — The  lesions  of  infantile  paralysis  closely 
resemble  those  of  progressive  muscular  atrophy,  except  that  the  former 
are  acute  and  the  latter  chronic.  The  atrophy  of  the  muscles  is  most  often 
a  simple  atrophy,  with  or  without  fatty  infiltration. 

The  foci  of  myelitis  are  often  multiple  ;  they  may  be  3  or  4  inches  in 


DISKASKS  OK  TIIK  SPINAL  (JOflD  1207 

longlli.  Tlic  appearanci!  of  tlic  focus  varies  aecordiiij;  as  the  post-mortem 
examination  is  made  in  the  ueuie  or  in  the  elironie  in-riod.  Tn  Mie  acute 
stage  we  hud  iulhimmatory  softening.  It  is  a  systematic  anterior  myelitis, 
which  appears  limited,  or  nearly  so,  to  the  anterior  cornua  of  the  grey 
matter,  although  it  is  not  easy  to  explain  why  an  aj)parcntly  identical 
lesion  should  at  one  time  produce  isolated  muscular  atrophy  (progressive 
muscular  atrophy)  and  at  another  muscular  atrophy  preceded  by  paralysis 
and  accompanied  by  atrophy  of  bone  (spinal  paralysis  of  childhood). 

The  lesion  of  the  anterior  cornua  consists  in  atrophy  of  the  large  motor 
cells,  with  prohferation  of  the  connective  tissue.  The  cells  are  invaded 
en  bloc,  and  are  not  picked  one  by  one,  as  in  progressive  muscular  atrophy. 
The  nerve  fibres  running  in  the  grey  matter  of  the  anterior  cornua  are 
attacked.  The  bloodvessels  are  thickened  and  dilated.  Marie  thinks  that 
the  arterioles  are  responsible  for  the  foci  of  pohomyelitis  :  "It  seems  that 
the  central  artery  of  the  anterior  cornua  is  most  frequently,  if  not  exclu- 
sively, affected  by  the  process."  In  some  cases  the  foci  are  also  found  in  the 
bulb  or  the  brain,  but  then,  according  to  the  localization  of  the  lesions,  and 
according  to  the  symptomatic  aspect,  the  affection  ends  in  infantile  cerebral 
hemiplegia,  in  idiocy,  or  in  epilepsy. 

The  anterior  roots  of  the  nerves  are  even  more  afiected  than  in  pro- 
gressive muscular  atrophy.  When  the  examination  of  the  spinal  cord  is 
made,  not  at  the  time  of  the  acute  lesions,  but  many  years  later,  the  focus 
of  softening  is  replaced  by  corresponding  atrophy,  which  does  not  stop  at 
the  anterior  cornua,  but  also  attacks  the  antero -lateral  columns,  the  posterior 
columns,  and  even  the  posterior  cornua.  The  inflammatory  focus  of  the 
acute  condition  is  replaced  by  a  fibrillary  tissue  of  a  neurogUal  nature. 

This  atrophic  paralysis  of  childhood  has  the  greatest  affinity  with  pro- 
gressive muscular  atrophy,  with  acute  spinal  paralysis  of  adults,  and  with 
anterior  spinal  general  paralysis.  The  proof  of  the  affinity  of  these  various 
afiections  of  medullary  origin  is  found  in  that  patients  who  in  their  infancy 
have  had  an  attack  of  atrophic  paralysis  have  later  sufiered  from  spinal 
paralysis,  from  progressive  muscular  atrophy,  from  all  three  diseases,  or 
from  anterior  spinal  general  paralysis.  Other  analogous  cases  have  been 
published.  One  of  my  cases,  who  had  suffered  from  infantile  paralysis, 
subsequently  had  nine  attacks  of  transient  paraplegia. 

Treatment. — As  soon  as  the  period  of  retrogression  begins,  if  not  before, 
slowly-interrupted  currents  should  be  employed;  they  form  the  most 
rational  method  of  treatment.  The  treatment  must  be  carried  out  with 
care  and  perseverance.  Massage,  salt  baths,  and  a  cure  at  Salies  should 
also  be  employed. 


1298  TEXT-BOOK  OF  MEDICINE 

XI.  POLIOMYELITIS  IN  THE  ADULT— ACUTE  SPINAL 
PARALYSIS  IN  THE  ADULT. 

Acute  poliomyelitis  in  the  adult — that  is  to  say,  myelitis  with  a  tendency  to  limit 
itself  in  the  region  of  the  anterior  cornua  (ttoAios,  grey) — does  not  form  as  well-marked 
a  morbid  entity  as  infantile  poUomyelitis.  Some  writers  question  whether  many  cases 
of  spinal  paralysis  in  adults  are  nothing  but  polyneuritis.  I  am  of  the  opinion  that 
poljTneuritis  must  claim  some  cases  formerly  considered  to  be  spinal  paralysis.  I  also 
think  that  it  is  sometimes  difificult  to  classify  the  spinal  paralyses  of  adults,  the  disease 
being  often  curable,  and  the  post-mortem  examination  being  then  lacking ;  but  it  is 
none  the  less  true  that  the  spinal  paralyses  of  adults  rest  on  a  group  of  pathological 
and  clinical  facts  which  assures  their  autonomy.  This  autonomy  is  rightly  claimed  by 
Grasset,  who  quotes  in  its  favour,  not  only  former  researches,  but  the  much  more  recent 
writings  of  men  like  Franz  Miiller  in  1880,  of  Blocq  and  of  Marinesco,  and  the  publica- 
tions of  Blocq,  referring  to  two  incontestable  post-mortem  examinations  made  by 
Schultze  and  Rissler.  Blocq  is,  furthermore,  quite  positive  in  his  conclusions.  "  It  is 
permissible,"  says  he,  "  after  the  recent  example  of  Raymond  and  Marie,  according  to 
the  teaching  of  Charcot,  and,  relying,  moreover,  on  demonstrative  cases,  to  admit  the 
existence  of  an  acute  spinal  paralysis  in  adults  chnically  and  anatomically  similar  to 
infantile  paralysis." 

1.  Acute  Spinal  Paralysis  of  Adults. 

A  form  of  paralysis  very  similar  to  infantile  poKomyelitis  may  develop 
in  adults.     It  is  called  acute  spinal  paralysis. 

Duclienne  was  the  first  to  describe  it.  "  I  have  long  thought,"  says  he, 
"  that  the  symptomatology  of  the  atrophic  paralysis  of  childhood  would  not 
be  met  with  in  the  adult,  but  having  sometimes  seen  this  same  symptoma- 
tology in  the  adult,  I  have  naturally  concluded  that  the  paralysis  must  be 
produced  by  a  similar  anatomical  lesion.  This  consideration  induced  me, 
therefore,  to  call  it  acute  anterior  spinal  paralysis  of  adults,  due  to  atrophy 
of  the  anterior  cells." 

The  disease  commences  with  diffuse  pains  in  the  hmbs,  rigidity,  mus- 
cular contractures,  and  gastro-intestinal  troubles.  Rapid  and  more  or  less 
extensive  paralysis  then  appears.  After  a  few  days  atrophy  appears  in 
some  of  the  muscles,  and  becomes  locahzed  in  them,  whilst  the  paralysis 
disappears.  The  sphincters  of  the  bladder  and  of  the  rectum  are  intact. 
The  tendon  reflexes  are  diminished  or  abohshed.  The  sensory  troubles  are 
more  marked  than  in  infantile  paralysis  ;  they  are  due  to  lesions  of  the  pos- 
terior cornua  and  of  the  commissures,  in  addition  to  the  essential  lesion  in 
the  anterior  cornua. 

The  electrical  reactions  (loss  of  faradic  reaction)  are  seen  here,  as  in  the 
child.  One  single  factor  distinguishes  the  disease  in  the  adult  from  that  in 
the  child — viz.,  in  the  adult  the  deformities  are  less  frequent  and  less 
marked  than  in  the  child,  because  growth  has  finished  when  the  disease 
occurs. 

The  diagnosis  from  Landry's  disease  (acute  ascending  paralysis)  is  the 


DISEASES  OF  THE  SPINAL  CORD  1209 

more  difl&cult  in  that  this  affection  specially  involves  the  anterior  cornua  ; 
but  acute  spinal  paralysis  has  a  much  slower  course,  and  the  atrophy  follows 
closely  on  the  paralysis,  confining  itself  to  a  few  muscles. 

2.  Anterior  Spinal  General  Paralysis. 

Uiuler  this  name  Duchenne  has  described  a  distinct  morbid  entity  with 
the  following  characteristics  :  An  individual,  without  appreciable  cause,  is 
seized  with  paralysis,  commencing  in  the  lower  hmbs,  and  becoming  general 
in  all  the  muscles  of  the  body,  except  those  of  the  face.  The  paralysis  is 
flaccid,  without  contractures  ;  the  sphincters  are  normal ;  sensation  is  intact ; 
the  tendon  reflexes  are  abohshed,  and  the  apphcation  of  the  faradic  current 
has  practically  no  effect.  The  muscular  atrophy  appears  during  the  course 
of  the  paralysis.  It  is  very  marked,  and  affects  all  the  muscles  without 
distinction,  so  that  the  patient  is  confined  to  his  bed,  and  incapable  of  making 
the  shghtest  movement.  After  a  few  weeks  the  movements  gradually 
reappear,  and  the  atrophy  in  turn  diminishes.  This  disease  is  usually  slow 
in  its  course,  and  Duchenne  therefore  called  it  subacute.  The  charac- 
teristic of  this  affection  is  that  it  terminates  by  a  restoration  to  health.  The 
paralysis  and  the  atrophy  disappear  completely  without  leaving  any  trace. 

The  anatomical  lesion  is  seated  in  the  motor  cells  throughout  the  entire 
length  of  the  spinal  cord.  It  remains  confined  to  these  cells,  but  this  myelo- 
pathy is  of  a  special  nature,  and  does  not  end  in  irremediable  lesions,  lil.u 
the  myelopathies  of  atrophic  paralysis  of  childhood.  Landouzy  and 
Dejerine,  in  a  remarkable  monograph,  have  reported  several  cases.  I  give 
a  summary  of  two  of  them  : 

Case  1. — A  man,  fifty-five  years  of  age,  was  taken  ill  with  paralysis  and  atrophy 
affecting  all  the  muscles  of  the  body,  except  those  of  the  face.  The  principal  features 
of  this  case  were :  Rapid  evolution  of  the  paralysis  and  of  the  muscular  atrophy ;  old 
deformity  of  the  left  leg,  due  to  infantile  paralysis ;  abohtion  of  the  tendon  reflexes  in 
all  the  diseased  muscles ;  reaction  of  degeneration ;  marked  exaggeration  of  the  idio- 
muscular  contractility ;  integrity  of  the  general  and  special  sensibUity ;  integrity  of  the 
sphincters  ;  complete  cure  of  the  paralysis  and  of  the  muscular  atrophy  after  a  duration 
of  ten  months.  The  patient  died  of  miliary  tuberculosis.  At  the  post-mortem  examina- 
tion the  spinal  cord  showed  the  following  lesions  :  An  old  focus  of  infantile  paralysis  in 
the  lumbar  swelling  on  the  left  side  ;  shght  changes,  and  probably  of  recent  date,  in  the 
anterior  grey  matter  of  the  rest  of  the  spinal  cord  ;  integrity  of  the  anterior  and  posterior 
roots ;  integrity  of  the  intramuscular  peripheral  nerves. 

Case  2. — A  woman,  thirty  years  of  age,  was  taken  ill  with  paralysis  and  atrophy 
of  all  the  muscles  of  the  body,  the  disease  having  commenced  with  temporary  paralysis 
of  the  left  facial  nerve,  abohtion  of  the  patellar  reflex,  alteration  of  the  faradic  con- 
tractility, integrity  of  sensibihty,  integrity  of  the  sphincters  and  of  the  nutrition  of  the 
skin,  paralysis  and  atrophy  of  rapid  evolution,  ending  in  recovery  after  seven  months. 
No  return  of  the  disease  four  years  later. 

Discussion — Diagnosis. — We  may  notice,  therefore,  in  adults  spinal 
paralysis  of  acute  or  subacute  course,  producing  muscular  paralysis  ^itb 


1300  TEXT-BOOK  OF  MEDICINE 

more  or  less  general  atrophy,  not  causing  the  death  of  the  patient,  recovering 
completely  in  some  cases,  and  sometimes  leaving  indelible  stigmata  of 
muscular  atrophy.  These  cases  have  a  tendency  to  confine  themselves  to 
the  anterior  grey  matter  of  the  spinal  cord.  They  are  cases  of  pohomyehtis. 
Although  their  infective  origin  is  not  clearly  proved,  we  may  readily  admit 
it,  and  the  systematization  of  the  spinal  lesions  is  certainly  due  to  the 
selective  action  of  the  toxi-infection  for  the  anterior  grey  matter  (Marie). 

The  diagnosis  between  acute  spinal  paralysis  and  polyneuritis  presents 
great  dijB&culties.  Confusion  has  often  arisen  between  polyneuritis  and  acute 
pohomyehtis.  I  would  even  say  that  in  many  cases  it  is  almost  unavoidable, 
because  the  two  diseases,  polyneuritis  and  acute  pohomyehtis,  may  difier 
very  shghtly.  As  a  general  rule,  such  is  not  the  case.  A  neurologist  will 
find  sufficient  to  distinguish  with  a  degree  of  certainty  between  polyneuritis 
and  anterior  pohomyehtis,  and  I  cannot  do  better  than  take  as  my  guide 
the  admirable  lectures  given  by  my  colleague  Raymond  at  La  Salpetriere. 

The  manner  of  the  onset  and  of  the  evolution  of  the  disease  presents 
certain  distinct  features.  In  acute  anterior  pohomyehtis  the  motor  para- 
lysis commences  in  the  root  of  the  hmbs.  It  is  far  from  being  symmetrical, 
and  it  may  confine  itself  to  one  hmb  (monoplegia)  or  to  a  single  segment. 
Furthermore,  it  reaches  its  maximum  in  a  few  days.  It  then  ceases  to 
extend.  In  the  first  phase  the  muscles  are  simply  paralyzed,  and  not 
atrophied.  In  this  paralytic  phase,  however,  electrical  tests  will  show 
which  of  the  paralyzed  muscles  will  later  be  atrophied.  Atrophy  wiU  invade 
those  muscles  which  have  lost  from  the  first  their  faradic  excitabihty. 
Furthermore,  the  diminution  of  the  faradic  excitabihty  is  proportionate  to 
the  degree  of  paralysis. 

In  polyneuritis  the  onset  is  much  less  sudden  ;  even  the  course  of  events 
is  slower.  The  paralysis  spreads  from  the  periphery  towards  the  centre — 
that  is  to  say,  from  the  extremities  of  the  hmbs  to  their  roots.  It  shows 
its  maximum  of  intensity  at  the  extremities  (feet,  hands).  The  hands  and 
feet  therefore  drop.  Polyneuritis  is  ushered  in  with  numbness  and  tinghng 
in  the  toes  and  fingers.  It  is  also  announced  by  painful  twitchings  of  the 
hmbs.  In  this  phase  the  polyneuritis  may  extend  to  the  areas  supphed  by 
the  cranial  nerves,  giving  rise  to  alarming  symptoms — paralysis  of  the 
phrenic  nerve  (fits  of  suffocation  and  death  from  paralysis  of  the  diaphragm), 
paralysis  of  the  vagus  nerve  (tachycardia,  death  from  cardiac  paralysis). 
During  the  second  phase  of  these  two  diseases  the  dominant  symptom  is 
muscular  atrophy,  which  behaves  differently  according  as  it  depends  on 
anterior  pohomyehtis  or  on  polyneuritis. 

In  acute  anterior  poliomyelitis  the  atrophy  strikes  en  masse  the  muscles 
which  have  lost  their  faradic  excitabihty,  and  respects  the  neighbouring 
muscles,  whether  paralyzed  or  not.     In  places  where  it  is  severe,  it  is  pro- 


DISEASES  0¥  THE  SPINAL  CORD  l.iOl 

portionatc  to  the  degree  of  the  paralysis.  It  is  irremediable,  and  causes  a 
kind  of  muniniitic'iition  in  the  atropliied  parts.  At  an  advanced  period 
the  atrophied  segments  of  the  hmbs  show  a  Hvid  tint  and  a  lowering  of  the 
local  temperature. 

In  polyneuritis  the  atroj)hy  almost  always  accompanies  the  motor 
paralysis,  but  it  is  generally  later.  It  never  strikes  en  masse  a  group  of 
muscles  to  the  exclusion  of  the  neighbouring  ones.  It  always  affects  a 
character  of  diffusion,  contrasting  with  the  distribution  of  the  atrophy  in 
poliomyeUtis.  It  invades  the  muscles  which  have  preserved  their  faradic 
excitability  at  the  onset  of  the  first  phase.  Finally,  it  is  curable,  in  spite  of 
the  paralysis. 

Other  differential  characters  require  notice.  Thus,  in  pohomyelitis  the 
abohtion  of  the  tendon  reflexes  is  constant  in  the  paralyzed  and  atrophied 
limbs.  Exaggeration  of  the  cutaneous  reflexes  is  never  seen.  In  poly- 
neuritis the  tendon  reflexes  may  be  preserved  and  the  cutaneous  reflexes 
may  be  exaggerated. 

In  pohomyelitis  the  sensory  troubles  play  a  very  minor  part.  In  poly- 
neuritis, independently  of  the  early  paraesthesias,  we  notice  diffuse  pains, 
often  of  myosalgia.  The  compression  of  the  nerve  trunk  and  of  the  muscles 
is  always  painful.  This  last  sign  is  of  great  diagnostic  value.  The  same 
may  be  said  of  the  cutaneous  hyperaesthesia,  of  the  anaesthesia,  and  of  the 
delayed  sensation,  which  are  far  from  being  constant.  Lowering  of  the 
temperature  in  the  paralyzed  parts  may  also  be  noticed,  as  well  as  herpetic, 
bullous,  and  eczematous  eruptions,  alopecia  or  hypertrophy  of  the  hair, 
deformity  or  shedding  of  the  nails,  but  especially  subcutaneous  peri- 
articular oedema,  which,  being  associated  with  the  pains,  may  lead  to  a 
suspicion  of  articular  rheumatism. 

In  anterior  poliomyeUtis  paralyses  of  the  cranial  nerves  are  quite  excep- 
tional ;  the  absence  of  psychical  troubles  is  the  rule.  In  polyneuritis 
paralyses  of  the  cranial  nerves  are  relatively  frequent.  The  same  may  be 
said  of  the  intellectual  troubles,  which  in  some  circumstances  assume  the 
triple  character  of  amnesia,  intellectual  weakness,  and  delirium  (Korsakoff's 
polyneuritic  psychosis). 

Finally,  acute  pohomyelitis  is  not  subject  to  relapses,  but  it  always 
leaves  irreparable  traces.  Polyneuritis,  essentially  a  curable  affection,  is 
subject  to  recurrences. 

Such  are  the  distinctive  characters  of  acute  pohomyeUtis  and  poly- 
neuritis. I  have  verified  their  value  and  their  correctness  in  a  patient 
with  polyneuritis  whom  I  saw  with  Raymond. 

M.  X.,  a  cavahy  officer,  was  a  powerful  man.  In  his  history,  as  far  as  morbid 
conditions  were  concerned,  we  only  found  traumatic  arthritis  of  the  right  knee,  with 
muscular  atrophy  of  the  quadriceps  extensor.     The  arthritis  and  the  atrophy  were 

^^'  83 


1302  TEXT-BOOK  OF  MEDICINE 

both  cured.  During  the  May  manoeuvres  M.  X.  was  seized  with  violent  rigors,  fever, 
and  lassitude.  The  doctor  found  an  influenzal  condition,  with  high  fever  (104^  P.). 
Four  days  afterwards  the  patient  noticed  a  weakness  in  his  lower  limbs  ;  twenty-four 
hours  later  the  weakness  invaded  the  upper  limbs.  At  the  same  time  the  pains  in  the 
lumbar  region  had  disappeared.     Xothing  abnormal  in  regard  to  the  sphincters. 

The  febrile  condition  gradually  passed  away,  the  appetite  came  back,  and  the 
patient,  though  almost  completely  paralyzed,  was  brought  back  to  Paris.  At  our 
first  visit  the  general  condition  was  good.  We  found  total  paralysis  of  the  four  limbs, 
but  the  patient  could  abduct  the  right  arm  by  a  snake-like  movement.  The  paralysis 
wa-s  Hmited  to  the  hmbs.  At  this  period  the  muscular  atrophy  was  scarcely  apparent. 
On  the  other  hand,  pressure  at  the  points  of  exit  of  the  nerves  caused  pain.  Xo  hyper- 
sesthesia  and  no  anaesthesia  of  the  skin.  By  eztending  and  raising  the  legs  vigorously, 
sharp  pains  were  felt  along  the  sciatic  nerves.  The  reaction  of  degeneration  was  present 
in  most  of  the  muscles.  The  reflexes  were  completely  abohshed.  The  functions  of  the 
sphiacters  were  normal. 

In  spite  of  appropriate  treatment,  the  patient  was  unable  for  several  months  to 
perform  the  shghtest  movement.  The  muscular  atrophy  was  extremely  pronounced. 
Improvement  gradually  supervened ;  less  pain,  less  marked  reaction  of  degeneration. 
Tonic  treatment  with  strychnine,  phosphate  of  hme,  arsenic,  etc.,  was  associated  with 
carefully  applied  electrification  and  massage.  Six  months  after  the  commencement  of 
the  disease  the  patient  was  weU  on  the  road  to  recovery. 

The  foregoing  discussion  proves  that  in  many  instances  we  can  distin- 
guish between  acute  poliomyelitis  and  polyneuritis.  Too  absolute  a  divi- 
sion must  not,  however,  be  attempted  between  these  different  nervous 
localizations  of  infectious  diseases.  While  iti  certain  cases  the  toxi- 
infection  afiects  the  nerves  or  the  spinal  cord  exclusively,  in  other  cases 
the  process  involves  the  spinal  cord  and  the  peripheral  nervous  system 
successively  or  simultaneously.  Pohomyehtis  is,  then,  associated  with 
polyneuritis,  and  their  symptoms  blend.  This  association  of  polyneuritis 
and  pohomyehtis  has  been  noticed  by  Grasset,  Lepine,  Mosse  and  Dastarac, 
and  by  Mosse  in  an  interesting  study  of  influenzal  paralyses. 


XII.  ACUTE  DIFFUSE  MYELITIS. 

The  forms  of  myehtis  already  described,  irisular  sclerosis  excepted,  tend 
to  limit  themselves  to  a  system  of  fibres  or  cells  (posterior  column,  anterior 
cornua),  and  their  respective  symptoms  (locomotor  ataxy,  progressive 
muscular  atrophy,  atrophic  paralysis  of  iniancy,  acute  spinal  paralysis  of 
adults)  lend  themselves  to  chnical  types  that  are  almost  constant.  This  is 
not  the  case  in  diffuse  myehtis,  which  strikes  indifferently  the  various  parts 
of  a  medullarv  segment,  grey  matter  or  white  columns,  while  the  meninges 
are  alwavs  involved.  It  invades  the  spinal  cord  in  its  various  regions,  and 
consequently  offers  a  very  variable  symptomatology. 

Pathological  Anatomy. — Diffuse  and  interstitial  acute  myehtis  forms 
foci  of  variable  dimensions  (focal  myehtis).  It  sometimes  extends  to  an 
entire  region  of  the  spinal  cord.     When  it  is  superficial,  the  meninges  are 


DISEASES  OF  THE  SPINAL  COllD  1303 

always  invaded.  In  some  cases  it  is  limited  to  the  grey  matter  of  the  spinal 
cord  (central  myehtis).  Post  mortem  we  find  changes  varying  according 
to  the  age  and  the  acutencss  of  the  morbid  process.  The  spinal  cord  is 
generally  softened.  In  some  cases  it  is  tiuctuating  and  converted  into  a  pulp 
of  varying  consistency  and  colour.  It  often  happens  that  the  lesion  is 
much  less  advanced,  and  even  so  httle  apparent  that  it  can  only  be  recog- 
nized by  histological  examination. 

In  the  first  period  the  myehtis  is  characterized  by  congestion,  swelUng 
of  the  invaded  portion,  and  sero-fibrinous  exudate  into  the  connective  tissue. 
The  vessels  are  dilated  and  tilled  with  blood  ;  the  lymphatics  are  blocked 
with  red  corpuscles  and  with  leucocytes  that  have  emerged  by  diapedesis. 
The  axis-cyhnder  is  very  much  swollen  ;  the  nerve  ceU  is  enlarged,  and  the 
connective  tissue  is  undergoing  prohferation. 

In  the  second  period  we  meet  with  abundant  embryonic  cells  formed  by 
the  neurogha,  and  on  the  second  or  third  day  the  inflamed  part  becomes 
softened.  This  softening  is  at  first  red,  becoming  yeUow  or  white  from 
alteration  of  the  colouring  matter  of  the  blood,  and  from  the  addition  of 
new  elements.  Granulo-fatty  bodies  are  formed  in  this  focus  of  softening. 
These  granulo-fatty  bodies,  with  which  the  leucocytes  become  charged,  are 
in  part  derived  from  the  myeline  of  the  nerve  fibres.  Haemorrhages  are 
not  uncommon  in  these  foci  of  softening  ;  they  are  secondary  haemorrhages, 
primary  haemorrhages  of  the  spinal  cord  being  quite  exceptional. 

In  the  third  period  we  find  yellow  or  white  softening,  and  the  various 
terminations  of  the  anatomical  process — the  passage  of  the  myehtis  into  the 
chronic  state,  cicatrization  of  the  focus,  or  progressive  extension  of  the 
lesion. 

Symptoms. — Acute  myelitis  is  characterized  bymotor,  sensory,and  trophic 
troubles  of  varying  degree.  Let  us  take  as  our  type  myehtis  of  the  dorso- 
lumbar  region.  Eigors  and  fever  open  the  scene.  The  patient  complains 
of  pain,  formication,  and  cramps  in  the  legs.  Girdle  pains  are  marked,  and 
exploration  of  the  spine  with  the  hand  or  with  a  sponge  soaked  in  hot  water 
often  causes  pain  in  the  dorso-lumbar  region.  Weakness  of  the  lower 
limbs,  accompanied  or  not  by  contractures,  immediately  appears,  and 
increases  to  such  a  degree  that  walking  soon  becomes  impossible  (paraplegia). 
In  some  cases  the  loss  of  movement  in  the  lower  Hmbs  is  absolute.  The 
reflex  movements  are  increased  in  the  initial  period,  and  disappear  later ; 
the  electrical  reactions  undergo  the  same  changes  as  the  reflex  movements. 
Sensation  is  affected  or  lost  in  the  parts  below  the  lesion. 

Incontinence  of  urine  (paralysis  of  the  vesical  sphincter)  is  generally 
preceded  by  retention  (paralysis  of  the  detrusor).  The  urine  rapidly  be- 
comes ammoniacal,  blood-stained,  and  purulent.  Retention  and  incon- 
tinence of  the  faeces  are  also  observed. 

83—2 


1304  TEXT-BOOK  OF  MEDICINE 

The  trophic  and  vasomotor  troubles  are  numerous,  and  early  eschars 
appear  on  the  scrotum,  over  the  malleoli,  and  the  sacral  region.  The  sacral 
eschar  (decubitus  acutus)  quickly  increases  in  depth  and  extent.  To  the 
same  period  belong  oedema,  transient  rise  in  temperature,  and  later  con- 
siderable fall  of  the  temperature  in  the  legs.  Copious  sweatings  of  the 
upper  hmbs  have  also  been  noted  (Mannkofi). 

Dorso -lumbar  myeUtis  may  kill  in  a  few  days  (apoplectiform  myehtis). 
Death  often  supervenes  in  the  second  to  the  fourth  week.  When  the  issue 
is  to  be  fatal,  respiratory  troubles  make  their  appearance,  and,  the  patient, 
plunged  in  marasmus  and  coma,  is  generally  carried  ofi  by  asphyxia.  Acute 
myehtis  is  rarely  cured.  I  have,  however,  seen  one  case  of  a  complete  cure 
in  a  patient  with  acute  non- syphilitic  myehtis.  It  sometimes  passes  into 
the  chronic  condition. 

Varieties. — Acute  myelitis  of  the  dorso-lumbar  region  is  themostcommon 
variety,  but  myelitis  may  affect  other  parts  of  the  spinal  cord.  When  it 
involves  the  brachio- spinal  region,  from  the  fifth  cervical  to  the  sixth  dorsal 
vertebra,  the  upper  limbs  show  motor  and  sensory  troubles  analogous  to 
those  of  the  lower  Hmbs,  and  the  patient  often  experiences  gastric  pain 
and  vomiting,  which  resemble  the  gastric  crises  of  ataxy.  The  pupils  are 
sometimes  dilated  and  the  eyeballs  are  prominent,  but  these  symptoms  of 
excitation  are  transient,  and  constriction  of  the  pupil  follows  the  dilatation. 

Myelitis  of  the  cervical  region  shows  itself  by  special  symptoms — pains 
in  the  nuchal  region,  contractures  of  the  muscles  of  the  neck,  trismus, 
paralysis  of  the  four  limbs  or  of  the  arms  alone,*  pain  and  oedema  in  the 
upper  limbs,  dysphagia,  slowing  or  quickening  of  the  pulse,  syncope  and 
apoplectiform  troubles,  hiccough,  dyspnoea,  and  attacks  of  suffocation. 

Optic  neuritis  is  seen  in  acute  myelitis.  It  is  usually  bilateral,  and  it 
precedes  or  accompanies  the  onset  of  the  myelitis.  It  may  affect  the  retro- 
bulbar type — ^that  is  to  say,  it  gives  rise  to  a  central  scotoma,  with  slight  or 
no  ophthalmoscopic  signs.     Kecovery  is  possible. 

Acute  myehtis  does  not  always  remain  confined  to  the  region  primarily 
invaded.  It  may  commence  in  the  dorso-lumbar  region,  and  spread  up  to 
the  cervical  region.  Acute  ascending  paralysis  (Landry)  is  probably  an 
ascending  myelitis.  I  say  probably,  for  side  by  side  with  cases  in  which 
the  lesions  are  indisputable  there  are  others  in  which  the  histological 
examination  has  not  shown  anything  (Vulpian).  Some  cases  are  simply 
polyneuritis.     Widal  and  Le  Sourd  have  described  a  case  of  acute  ascending 

*  In  order  to  explain  the  paralysis  of  the  upper  limbs  before  that  of  the  lower  ones 
Brown-Sequard  points  out  that  the  motor  tracts  of  the  upper  hmbs  are  more  superficial 
than  the  motor  tracts  of  the  lower  ones.  But  why  not  admit,  says  Hallopeau,  that  the 
lesion  first  destroys  the  grey  nuclei  of  the  upper  hmbs,  prior  to  attacking  the  lateral 
columns,  which  contain  the  motor  tracts  of  the  lower  limbs  ? 


DISEASES  OF  THE  SPINAL  CURD  IMO," 

paralvsis,  fharacft'ii/iMl  fnmi  the  histolnificul  point  of  view  hy  an  innanuna- 
tion  exclusively  limited  to  the  anterior  roots,  without  meningeal  (Oianges 
and  without  lymphocytosis  of  the  cerel)ro-spinal  fluid.  Landry's  di.seaae 
may  be  ver)^  ra})id  or  alow.  It  is  apyretic,  and  presents,  as  it  were,  super- 
posed from  the  lumbar  to  the  cervical  region,  the  syriipfoms  just  described 
under  the  various  forms  of  myelitis. 

iEtiology-  -Duration. — Acute  myelitis  is  primary  or  secondary.  Cold 
is  a  very  rare  cause  of  myelitis.  Secondary  myelitis  is  at  times  due  to  the 
spread  of  a  neighbouring  lesion,  such  as  Pott's  disease.  It  may  also  super- 
vene in  chronic  myelitis.  Sometimes  it  is  consecutive  to  an  irritation  of 
the  peripheral  nerves  (ascending  neuritis).  This  morbid  process  has  been 
produced  experimentally  (Hayem),  but  clinically  we  do  not  always  meet 
with  the  lesion  intermediate  between  myelitis  and  the  supposed  provoking 
organ.  In  the  majority  of  cases  acute  myelitis  is  due  to  toxi-infectious 
agents,  and  belongs,  therefore,  to  the  class  of  infectious  diseases.  This 
setiological  and  pathogenic  question  w^as  fully  discussed  in  Section  IX. 

The  course  and  duration  of  acute  myelitis  are  not  subject  to  any  fixed 
rule.  Apoplectiform  myelitis  is  fatal  in  four  or  five  days,  and  the 
suddenness  of  the  events  is  due  to  various  causes.  Thus  at  the  post-mortem 
examination  we  find  a  haemorrhagic  focus  or  an  inflammatory  lesion  which 
from  the  outset  involves  a  large  part  of  the  spinal  cord.  Sometimes,  on  the 
contrary,  we  find  lesions  that  have  followed  an  ascending  course,  and  are 
not  well  marked,  as  if  they  had  not  had  time  to  evolve.  In  some  cases 
the  myelitis  is  of  the  recurrent  type  ;  in  others  it  runs  a  subacute  or  chronic 
course  ;  and  in  a  few  exceptional  cases  recovery  may  occur. 

Epidemic  Paraplegia. — About  twenty  years  ago  a  form  of  epidemic 
paraplegia  was  described  in  Spain.  It  was,  up  to  a  certain  point,  com- 
parable with  epidemic  cerebro-spinal  meningitis.  This  acute  or  chronic 
disease  was  characterized  by  incomplete  paraplegia,  with  much  pain,  incon- 
tinence of  urine,  and  conservation  of  the  electro -muscular  contractility. 
Similar  cases  have  been  met  with  in  France. 

XIII.  CHRONIC  DIFFUSE  MYELITIS. 

Pathological  Anatomy. — The  history  of  chronic  diffuse  myelitis  in 
part  blends  with  that  of  acute  diffuse  myelitis.  The  pathological  anatomy 
of  the  lesion  is  summed  up  in  two  words— sclerosis  or  softening.  The 
softening  is  most  often  the  last  stage  of  an  acute  myehtis,  and  the  sclerosis 
realizes  the  most  common  change  in  chronic  myeUtis.  Prohferation  of  the 
neuroglia  leads  to  progressive  sclerosis.  The  connective  network  and  the 
wall  of  the  vessels  become  thickened,  the  nerve  fibres  diminish  in  size, 
the  myeline  becomes  segmented  and  separates  out,  the  nerve  cells  lose  their 


1306  TEXT-BOOK  OF  MEDICINE 

processes   and  become   atrophied.     The   spinal  cord  becomes  indurated, 
assumes  a  grejdsh  tint,  and  stains  readily  with  carmine. 

This  sclerosis  (induration  of  the  connective  tissue,  and  consequent 
atrophy  of  the  nerve  elements)  is  not  always  irregularly  diffused.  It  some- 
times occupies  a  well-defined  segment  of  the  spinal  cord,  affecting  either 
the  whole  (transverse  myehtis)  or  only  one-half  of  the  spinal  cord  (hemi- 
lateral  myehtis — Brown-Sequard).  It  takes  the  form  of  a  ring,  the  meninges 
being  affected  while  the  grey  matter  is  free  (annular  sclerosis — Vulpian). 
It  surrounds  the  ependymal  canal,  which  becomes  constricted  or  dilated 
(periependymal  sclerosis — Hallopeau),  and  invades  various  regions  in 
succession  (ascending  or  descending  myehtis — Hallopeau)  ;  but  aU  these 
varieties  are  exceptions,  and  in  the  most  common  form  the  inflammation 
predominates  in  the  antero-lateral  parts  of  the  cord  on  a  level  with  the 
dorso-lumbar  enlargement,  and  gives  rise  to  chronic  paraplegia.  Chronic 
myelitis  often  provokes  secondary  ascending  or  descending  scleroses,  which 
at  length  complicate  the  initial  picture  of  the  disease.  The  causes  are 
those  of  acute  myelitis,  to  which  heredity  may  be  added. 

Description. — Aside  from  cases  in  which  the  symptoms  of  excitation 
(acute  phase)  open  the  scene,  the  disease  commences  with  disturbance  of 
locomotion. 

The  patient  soon  becomes  fatigued,  the  legs  feel  heavy,  walking  is 
painful,  and  especially  difficult  when  plantar  ansesthesia  is  also  present 
(walking  on  down).  Later  the  patient  can  only  walk  with  a  stick  or  other 
support.  His  feet  hardly  leave  the  ground  ;  he  gUdes  rather  than  walks, 
'  and  in  the  end  locomotion  becomes  impossible  and  the  paraplegia  complete. 
The  reflex  movements,  which  were  at  first  increased,  persist  as  long  as  the 
grey  matter  of  the  spinal  cord  is  not  destroyed. 

The  reproductive  functions  are  generally  abolished.  Troubles  of  the 
bladder  and  of  the  rectum  (retention  and  incontinence)  are  not  early,  unless 
the  genito-crural  enlargement  is  invaded.  Retention  of  urine  precedes 
incontinence,  because  paralysis  of  the  detrusor  precedes  paralysis  of  the 
sphincter ;  but  "  the  function  of  the  sphincters  sometimes  remains  intact, 
in  spite  of  the  existence  of  cervico-dorsal  lesions,  provided  they  are  super- 
ficial, whence  it  may  be  inferred  that  the  cerebro-vesical  cord  occupies  in 
the  anterior  system  of  the  spinal  cord  a  deeper  position  than  the  cords  of 
the  lower  Hmbs  "  (RoUet). 

In  conclusion,  paraplegia,  accompanied  by  paralysis  of  the  sphincters, 
forms  the  common  picture  of  chronic  dorso-lumbar  myehtis ;  but  it  is  not 
uncommon  for  this  picture  to  be  modified  by  the  appearance  or  by  the 
predominance  of  some  new  symptom,  such  as  pain  (lesion  of  the  posterior 
cords),  ansesthesia  (lesions  of  the  grey  and  posterior  white  matter),  con- 
tractures (primary  or  descending  lesions  of  the  lateral  cords),  muscular 


DTREASES  OF  THE  SPINAL  CORD  l.SOT 

atrophy  (lesions  of  the  anterior  cornua).  The  average  duration  of  chronic 
myeUtis  is  six  years.  Deatli  is  due  either  to  the  extension  of  the  paralysis 
or  to  complications,  such  as  cystitis,  phthisis,  or  pneumonia. 

Varieties. — I  have  already  indicated,  under  Acute  Myelitis,  the  diversity 
of  the  symptoms,  according  as  the  lesion  is  in  the  lumbar,  dorsal,  or  cervical 
regions.  I  shall  now  describe  certain  rare  varieties  in  which  the  myelitis 
is  hemilateral,  central,  or  cortical. 

1.  Hemilateral  Myelitis.— When  one-half  of  the  cord  is  affected  by 
traumatism,  compression,  tumour,  or  sclerosis,  we  see  certain  special  symp- 
toms, well  described  by  Brown-Sequard.  The  salient  features  are  as  follows  : 
(1)  paralysis  on  the  side  of  the  body  corresponding  to  the  lesion  in  the 
spinal  cord  (hemiparaplogia)  ;  (2)  anaesthesia  of  the  side  of  the  body  opposite 
to  the  lesion  (crossed  hemianaesthesia).  The  dissociation  of  these  two 
symptoms,  one  of  which  is  direct  and  the  other  crossed,  is  due  to  the  fact 
(Brown-Sequard)  that  the  motor  fibres  have  already  crossed  in  the  bulb. 
The  higher  the  lesion  is  in  the  spinal  cord,  the  more  extensive  are  these 
symptoms. 

2.  Central  Myelitis. — In  this  variety  of  periepend}Tnal  myelitis  the  grey 
matter  is  especially  attacked  in  front  of  the  central  canal  of  the  spinal  cord. 
The  S}Tiiptoms  consist  in  paralysis,  followed  by  muscular  atrophy  and 
diminution  of  the  electrical  contractility.  This  variety  of  myelitis  closely 
resembles  syringomyelia. 

Blisters,  cauterization,  and  the  use  of  electricity  sum  up  the  treatment 
of  chronic  myelitis.  Iodide  of  potassium,  in  large  doses,  and  mercurial 
preparations  must  always  be  tried  when  syphilis  is  proved  or  suspected. 


XIV.  SYPHILITIC  MYELITIS. 

etiology. — Syphihs  of  the  spinal  cord  independent  of  any  other  lesion 
in  the  nerve  centres  is  not  very  frequent.  In  1,085  cases  of  syphiKtic 
lesions  of  the  nerve  centres,  we  find  416  cases  of  cerebro-spinal  s}'^liilis,  and 
only  77  cases  of  pure  medullary  syphilis  (Fournier,  Boulloche).  The  time 
of  the  syphilitic  infection  is  of  great  importance.  The  spinal  cord  may  be 
attacked  from  the  commencement  of  the  disease.  In  fifty-eight  cases  of 
early  medullary  syphilis  (Moinet),  myehtis  was  rare  before  the  third  month, 
fairly  common  from  the  third  to  the  tenth  month,  and  frequent  in  the  sixth 
month.  In  two-thirds  of  the  cases  (Fournier)  myehtis  is  seen  from  the 
third  to  the  tenth  year  of  the  syphiUtic  infection.  It  is  very  rare  in  women, 
but  frequent  in  men  between  twenty  and  forty  years  of  age.  As  contribu- 
tory causes,  alcoholism,  venereal  excesses,  traumatism,  and  overwork  may 
be  mentioned. 

Does  syphilis,  if  not  treated,  predispose  to  myehtis  ?     Fournier's  answer 


1308  TEXT-BOOK  OF  MEDICINE 

is  affirmative  ;  Mauriac's  answer  is  negative.  Severe  syphilis  is  often  ac- 
companied by  acute  and  early  myelitis. 

Pathological  Anatomy.— The  lesions  difier  in  acute  and  in  chronic 
syphihtic  myehtis.  Acute  syphihtic  myehtis  presents  the  same  lesions  as 
ordinary  acute  myehtis.  In  the  spinal  cord  we  find  one  or  more  foci  of 
softening,  usually  in  the  middle  regions  of  the  spinal  cord.  The  lesions  are 
difiuse,  attacking  the  white  and  the  grey  matter.  The  meninges  frequently 
participate  in  the  process  which  reahzes  the  diffuse  embryonic  meningo- 
myehtis  of  Gilbert  and  Lyon.  In  these  cases  of  acute  myelitis  with  a  sudden 
onset  the  vascular  lesions  predominate,  phlebitis  and  arteritis  representing 
the  initial  element  of  the  inflammatory  process.  There  is  a  true  syphilitic 
arteritis,  analogous  to  cerebral  arteritis,  followed  by  vascular  obliteration, 
with  softening  of  a  more  or  less  extensive  area  of  the  spinal  cord. 

When  medullary  syphilis  is  subacute  or  chronic,  we  also  find  lesions  of 
meningitis,  embryonic  infiltration  of  the  meninges  and  of  their  prolonga- 
tions, gummata,  hyperaemia,  and  dilatation  of  the  bloodvessels.  The 
degenerated  parenchyma  sometimes  becomes  sclerotic,  and  the  disease 
incurable.  Myehtis  is  sometimes  accompanied  by  cerebral  changes, 
especially  meningitis  of  the  base  of  the  interpeduncular  region  and  of  the 
chiasma.  Medullary  syphihs  in  some  cases  affects  the  entire  length  of  the 
spinal  cord.  Most  often,  however,  it  is  limited  to  the  dorso-lumbar 
region. 

Symptoms. — Syphilitic  myehtis  shows  so  many  clinical  types  that  its 
description  must  be  separated  into  the  acute  and  chronic  forms  and  a  rare 
form. 

Acute  Myelitis. — The  acute  form  of  meduUary  syphihs  is  almost  always 
an  early  trouble.     This  form  usually  commences  very  suddenly. 

In  one  patient,  twenty-seven  years  of  age,  the  myelitis  announced  itself  nine  months 
after  the  chancre  by  formication  in  both  legs,  with  umisnal  weakness.  Next  day  the 
patient  could  not  even  stand.  He  also  had  complete  retention  of  urine,  abohtion  of 
the  patellar  reflexes,  total  anaesthesia  of  the  lower  limbs,  and  sUght  pain  in  the  lumbar 
region.  These  symptoms  had  appeared  within  thirty-six  hours  with  the  suddermess 
which  seems  to  be  the  principal  characteristic  of  this  acute  and  early  form.  Ten  days 
later  incontinence  of  urine  followed  the  retention,  and  at  the  end  of  a  fortnight  incon- 
tinence of  faeces  appeared.  The  patient  was  submitted  to  a  very  active  treatment 
(inunction  of  90  grains  of  mercurial  ointment  and  240  grains  of  iodide  a  day).  Three 
weeks  later  movement  reappeared  in  the  legs.  In  ten  weeks  the  patient  left  the  hospital 
cured,  never  having  had  either  trophic  troubles  or  contractures. 

The  termination  of  acute  syphihtic  myehtis  is  far  from  being  always 
as  favourable  as  in  the  preceding  case.  With  Hammonic,  I  attended  a 
man  of  fifty-five  who  was  taken  iU,  a  year  after  the  chancre,  with  such 
rapid  syphihtic  myelitis  that  death  supervened  in  six  weeks. 

In  its  acute  and  early  form  syphihtic  myehtis  presents  the  clinical 


DISEASES  OF  THE  SPINAL  COKD  1309 

picture  of  transverse  meriingo-myelitis :  onset  with  sensor)''  troubles, 
formication,  numl)ness  of  the  lower  Hmhs,  and  girdle  pains,  followed  by 
motor  troubles,  weakness  of  the  legs,  paresis,  paraplegia  with  or  without 
contractures,  retention  and  incontinence  of  urine  and  of  faeces,  trophic 
troubles,  bed-sores,  and  general  svmptoms. 

Chronic  Myelitis. — This  form  may  be  chronic  from  the  outset  or  may 
follow  on  acute  or  subacute  myelitis.  In  the  form  which  is  chronic  from 
the  first  the  onset  is  very  different  from  that  of  subacute  myelitis.  It  is 
much  slower,  and  the  functional  impotence  comes  on  gradually. 

In  ono  of  ray  patients,  twenty-two  years  of  age,  the  myelitis  declared  itself  three 
years  after  the  chancre  with  incontinence  of  urine,  formication  in  one  leg,  and  muscular 
spasms  when  the  foot  touched  the  ground.  In  a  short  while  the  legs  grew  stiff  and  pain- 
ful, and  in  three  months'  time  walking  was  impossible.  Contracture  was  accompanied 
by  exaggeration  of  the  patellar  reflexes  and  by  the  phenomenon  of  spinal  tremor.  Sensi- 
bihty  was  intact.  After  active  treatment  (inunction  of  90  grains  of  mercurial  ointment 
and  2-40  grains  of  iodide  a  day)  the  improvement  was  progressive.  A  sacral  bed-sore 
which  had  appeared  a  few  days  after  the  patient's  admission,  and  which  had  led  me  to 
fear  a  fatal  termination,  healed  rapidly.  The  pains  disappeared.  Walking  was  possible 
after  three  weeks,  but  the  leg  remained  somewhat  stiff,  as  the  contracture  had  not 
completely  ceased. 

I  have  just  described  the  common  symptoms  of  syphilitic  myelitis,  but 
in  some  forms,  which  are  very  much  rarer,  medullary  syphilis  resemble.^ 
sclerosis  of  the  antero-lateral  cords,  progressive  muscular  atrophy,  insular 
sclerosis,  or  Brown-Sequard's  paralysis  (paralysis  of  one  limb  and  anaesthesia 
of  the  other). 

Under  the  name  of  syphilitic  spinal  paralysis  Erb  has  descri])ed  a  variety 
of  chronic  medullary  s}^hilis,  characterized  by  incomplete  spastic  para- 
plegia of  progressive  course.  The  disease  commences  with  pains  in  the  legs, 
weakness,  and  muscular  rigidity.  It  takes  months  and  years  to  end  in 
spastic  paresis  of  the  lower  limbs,  and  hardly  ever  goes  on  to  complete 
paraplegia.  The  patients  continue  to  walk,  but  they  have  a  spastic  gait, 
with  exaggeration  of  the  tendon  reflexes  and  ankle-clonus.  The  sensory 
troubles  consist  in  numbness,  formication,  and  anaesthesia.  The  bladder 
troubles  consist  in  retention  or  incontinence  of  urine,  with  urgent  desire  to 
urinate.     The  genital  functions  are  weakened. 

Trophic  troubles  are  absent ;  no  amyotrophy  and  no  bed-sores.  This 
form  may  remain  stationary  for  an  indefinite  period.  Specific  treatment, 
if  early  applied,  may  lead  to  good  results.  In  spite  of  its  relatively  benign 
appearance,  this  variety  of  chronic  myehtis  may  be  complicated  by  multiple 
lesions  of  the  spinal  cord  or  of  the  brain,  which  render  the  prognosis  more 
serious.  This  form  of  syphiUtic  spinal  paralysis  is  frequent.  It  does  not, 
as  a  rule,  appear  at  as  early  a  period  as  acute  s}'phiUtic  myelitis  ;  it  supervenes 
nevertheless  in  the  first  few  years  of  the  syphihtic  infection.     The  absence 


1310  ■  TEXT-BOOK  OF  MEDICINE 

of    post-mortem  examinations  lias  prevented  our  tracing  its  pathological 
anatomy.     It  is  certainly  a  transverse  myelitis  of  tlie  dorso-lumbar  region. 

Early  or  late  syphilitic  myehtis  is  often  accompanied  by  syphihtic 
manifestations  in  other  regions  (cerebro-spinal  syphihs  and  bnlbo-spinal 
syphilis). 

I  saw  with  Foumier*  a  remarkable  case  of  syphilitic  myehtis  simulating  acute  tabes. 
A  man  who  had  been  syphihtic  for  about  ten  years  was  taken  ill  with  heaviness  in  the 
legs,  difficulty  in  walking,  and  the  foUowing  symptoms :  ptosis  of  the  left  eye,  patches 
of  ansesthesia  on  the  buttock,  diminution  of  the  patellar  reflexes,  paresis  of  the  bladder, 
impotence,  and  Komberg's  sign.  All  these  symptoms  disappeared  in  two  months  and 
a  half,  through  active  specific  treatment. 

Diagnosis. — The  diagnosis  must  be  promptly  made  in  order  that  treat- 
ment can  be  commenced  at  once.  If  a  man  is  suddenly  seized  with  para- 
plegia, contracture  of  the  lower  hmbs,  and  incontinence  or  retention  of 
urine,  we  must  think  of  syphihs.  Careful  examination  will  at  times  enable 
us  to  recognize  characteristic  cicatrices,  specific  eruption,  cutaneous  gum- 
mata,  enlarged  glands,  violent  headache,  etc.  We  can  then  have  no 
doubt  as  to  the  syphilitic  nature  of  the  affection.  This  is  the  true  manner 
of  making  a  diagnosis,  because  to  differentiate  in  any  other  manner  between 
syphihtic  myehtis  and  the  diseases  most  resembling  it  (insular  sclerosis, 
tabes,  and  transverse  myehtis)  is  often  a  very  difficult  matter. 

Cyto-diagnosis  of  the  cerebro-spinal  fluid  gives  interesting  results  in 
syphihtic  meningo -myehtis.  It  is  clearly  positive  with  pronounced  l5nnpho- 
cytosis  (Sicard  and  Monod),  whereas  it  is  often  negative  in  Pott's  disease 
with  chronic  pachymeningitis  (Widal  and  Le  Sourd). 

The  prognosis  of  untreated  syphihtic  myehtis  is  grave.  In  the  acute 
form  death  has  been  noticed  eighteen  times  in  fifty-eight  cases  in  conse- 
quence of  the  myehtis.  In  seven  cases  there  was  shght  improvement,  in 
seventeen  cases  marked  improvement,  and  only  sixteen  cases  of  cure.  In 
the  chronic  forms  death  is  not  so  common,  but  recoveries  are  rare,  because 
the  treatment  is  often  delayed.  Too  often  the  syphihs  passes  unnoticed,  and 
the  most  energetic  medication  cannot  then  remove  the  lesions  of  sclerosis. 

Hereditary  Spinal  Syphilis. — Hereditary  s}^hihs  of  the  spinal  cord 
had  untU  recently  been  httle  studied.  This  lacuna  has  been  filled  by 
GiUes  de  la  Tourette,  whose  conclusions  I  quote  verbatim. 

Hereditary  syphihs  may  attack  the  spinal  cord  during  the  first  years 
of  hfe  (heredo-syphihs),  during  intra-uterine  hfe  (early  congenital  heredo- 
syphihs),  during  adolescence  and  adult  age  (late  heredo-syphihs). 

When  syphihs  attacks  the  infant  before  birth,  the  accouchement  is  often 
premature.     The  chUd  may  be  stillborn  or  ahve.     If  the  child  is  stUlborn, 

*  Dieulafoy  and  Fournier,  "  Accidents  SyphiUtiques  Cerebro-spinaus  de  Forme 
Tabetique  "  (Societe  de  Dermatologie,  1890). 


DISEASES  OF  THE  SPTNAL  CORD  l.'-ll 

or  if  il  rapidly  succurabs,  we  cannot  with  certainty  attribute  death  to  ilio 
spinal  lesion,  because  we  find  in  almost  every  case  fatal  lesions  in  the  viscera. 
The  clinical  signs  are  tluMi  completely  absent,  fn  sufh  a  case  the  lesions 
of  the  spinal  cord  consist  in  a  diffuse  embryonic  mcniiigo-inyelitiB,  analogous 
to  the  interstitial  hepatitis  of  congenital  syphilis.  Congestion  with  leuco- 
cytic  stasis  is  never  absent,  and  may  attain  an  extreme  degree,  leading 
even  to  rupture  of  the  vessels  (Gasne). 

If  the  child  survives  the  congenital  lesions,  symptoms  appear,  but  they 
blend  in  part  with  the  symptoms  of  cerebral  sclerosis.  Anatomically,  the 
lesions  end  in  sclerosis.  The  symptoms  reveal  themselves,  as  far  as  the 
spinal  cord  is  concerned,  by  spasmodic  paralysis.  When  hereditary  sy|)hilis 
attacks  the  spinal  cord  in  childhood  or  in  youth,  the  brain  may  also  partici- 
pate in  the  process  (cerebro-spinal  sjrphilis),  but  the  spinal  lesion  is  especially 
associated  with  lesions  of  the  mesencephalon.  In  these  cases  of  early  or  late 
hereditary  syphiUs  the  chnical  types  are  more  varied  than  in  congenital 
spinal  syphilis.  In  fact,  as  the  patient  advances  in  years,  the  tissues  be- 
come more  and  more  differentiated,  and  take  on  a  more  marked  functional 
i?idividuality.  The  spinal  cord,  the  meninges,  and  the  vessels  seem  to  be 
more  individually  affected.  The  embryonic  infiltration  collects  more  readily, 
in  order  to  end  in  perivascular  or  meningeal  gumma.  The  clinical  field 
becomes  enlarged,  and,  leaving  the  general  tendency  to  become  cerebro- 
spinal on  one  side,  early  or  late  hereditary  syphilis  does  not  sensibly  differ 
from  the  numerous  expressions  of  acquired  spinal  or  cerebro-spinal  syphihs. 
At  times  it  causes  brachial  monoplegias,  with  flaccid  paralysis  and  consequent 
muscular  atrophy  of  an  amyotrophic  form  (Raymond). 

Treatment. — Medullary  syphihs  demands  very  active  treatment.  For 
a  fortnight  or  three  weeks  I  give  daily  mercurial  injection  of  90  grains  of 
Neapohtan  ointment,  or,  better  still,  injections  of  biniodide  of  mercury. 
Large  doses  of  iodide  of  potassium  are  also  given.  By  these  active  measures 
I  have  cured  three  patients,  and  owing  to  the  precautions  taken  (incessant 
cleansing  of  the  mouth  and  of  the  teeth  with  chlorate  of  potash,  and  the 
same  drug  taken  internally),  I  have  never  seen  any  complication  arise. 
The  utihty  of  this  energetic  treatment  is,  in  my  opinion,  proved,  for  two  of 
my  three  patients  had  been  taking  mercury  and  iodide  of  potassium  for 
months,  but  in  too  small  doses. 

XV.  AFFECTIONS  OF  THE  CAUDA  EQUINA  AND  OF  THE 
FILUM  TERMINALE. 

The  spinal  cord  terminates  below  the  lumbar  enlargement  in  a  conical 
extremity,  the  filum  terminale,  which  is  threadhke,  and  descends  as  far  as 
the  coccyx.     From  the  lumbar  enlargement  the  lumbar  and  sacral  nerves 


1312  TEXT-BOOK  OF  MEDICINE 

arise,  and  follow  a  long  course  in  the  spinal  canal  before  traversing  the 
conjugate  foramina.  These  nerves,  disposed  like  a  fan  (the  lumbar  nerves 
being  external  to  the  sacral  nerves),  form  the  cauda  equina,  surrounding 
the  filum  terminale.  The  lesions  of  these  regions,  studied  in  France  by 
Raymond  and  by  Dufour,  give  rise  to  very  curious  symptoms. 

Pathological  Physiology.— If  the  exit  of  the  third  pair  of  sacral  nerves 
is  considered  as  the  upper  hmit  of  the  cauda  equina  (Raymond),  the  lesions 
of  this  region  provoke  the  following  symptoms :  Paralysis  of  the  bladder,  with 
integrity  of  the  involuntary  sphincter  ;  sjiidrome  of  paradoxical  ischuria, 
comprising  retention  of  urine,  followed  by  incontinence  through  over- 
flowing ;  paralysis  of  the  anal  sphincter ;  anaesthesia  of  the  urethra,  of  the 
perineum,  of  the  anus,  of  the  inner  surfaces  of  the  buttocks,  and  of  the 
postero-superior  region  of  the  thigh ;  hyposesthesia  of  the  penis  and  of  the 
scrotum,  or  of  the  labia  majora  ;  incomplete  paralysis  of  the  gluteus  maxi- 
mus,  of  the  plantar  muscles,  and  of  the  posterior  surface  of  the  leg  ;  power  of 
erection,  but  diminution  of  voluptuous  sensation  from  ansesthesia  of  the 
urethra  ;  slowness  of  ejaculation. 

If  the  lesion  is  higher  in  the  lumbar  swelling  or  in  the  roots  of  the  cauda 
equina,  we  find  total  suppression  of  erection,  complete  paralysis  of  the 
sphincter  of  the  bladder,  with  incontinence,  and  paralysis  of  the  gluteus 
medius  and  minimus  (Dufour).  If  the  lesion  is  seated  in  the  lowest  portion, 
or  filum  terminale,  there  is  paralysis  of  the  bladder  and  of  the  rectum,  or 
of  only  one  of  these  viscera  (Lachmann). 

etiology. — Trauma  is  the  most  frequent  cause  of  these  affections. 
Direct  injury  (crushing  or  gunshot  wounds  of  the  lumbar  region)  and  in- 
direct trauma  (falls  on  the  feet,  buttocks,  chest  or  hips,  fracture  and  luxa- 
tion of  the  lumbo-sacral  column)  are  often  present.  I  must  likewise  mention 
hydatid  cysts  either  extra-  or  intraspinal,  tumours  (epithehoma,  sarcoma, 
neuroma,  or  gummata),  and  syphihtic  or  tubercular  spinal  meningitis. 
Injuries  are  especially  met  with  in  men,  and  hydatid  cysts  in  women. 

Pathological  Anatomy. — The  lesions  are  due  to  the  medullary  haemor- 
rhage and  to  the  compression.  The  cauda  equina  is  flattened.  The  white 
columns  and  the  grey  axis  may  disappear  completely.  Histologically,  we 
find  atrophy  of  the  cells  of  the  grey  cornua,  presence  of  granular  bodies, 
disappearance  of  the  myeline  of  the  nerve  fibres,  perivascularitis,  with 
thickening  of  the  sheaths  and  of  the  bloodvessels.  The  roots  present 
identical  lesions.  Above  and  below  the  point  attacked  Wallerian  degenera- 
tion takes  place,  with  all  its  consequences. 

Symptoms. — Sensation  is  always  affected.  Pains  are  never  absent. 
They  usually  involve  the  lumbar  or  sacro-coccygeal  region,  and  radiate 
into  the  lower  limbs,  the  groins,  the  buttocks,  the  knees,  and  the  ankles, 
often  corresponding  with  the  distribution  of  the  sciatic  nerve.     The  pains 


DISEASES  (»K  THE  SPINAL  COIID  i:il:; 

may  be  spontaneous  or  provoked  by  percussion  of  the  sacro-Iumbar  region, 
walking,  and  flexion  of  the  leg.  The  sacrum,  the  coccyx,  the  legs,  and  the 
feet,  often  present  zones  of  hyperaosthesia.  Anaesthesia  is  the  rule  ;  it 
varies  from  the  slightest  hyi)oa?sthesia  to  complete  loss  of  sensation.  Its 
distribution  admits  of  four  categories,  which  are  important  in  diagnosis 
(Dufour) : 

(1)  Anaesthesia  of  the  ano-rectal  and  vesico-urethral  mucosae;  anaes- 
thesia of  the  perineum,  of  the  scrotum,  of  the  penis,  of  the  inferior  and 
internal  half  of  the  buttocks,  and  of  the  posterior  part  of  the  thighs  (the 
anaesthesia  affects  a  triangular  form,  with  the  apex  pointing  downwards). 
(2)  Anaesthesia  of  the  skin  suppHed  by  the  sciatic  nerve,  \vith  or  without 
participation  of  the  perineo-scrotal  and  visceral  branches.  The  persistence 
of  sensation  on  the  internal  edge  of  the  foot  and  at  the  root  of  the  big  toe 
is  of  much  diagnostic  value.  (3)  Anaesthesia  of  the  anterior  and  internal 
regions  of  the  thigh  and  of  the  leg.  (4)  Anaesthesia  of  the  entire  lower  limb, 
of  the  bladder,  and  of  the  rectum.  The  testicles  are  always  sensitive 
to  pressure. 

Paralysis  with  muscular  atrophy  attacks  the  region  of  the  buttocks, 
the  posterior  muscles  of  the  thigh,  the  muscles  of  the  legs,  and  the  muscles 
of  the  perineum  ;  in  rare  cases  the  quadriceps  and  the  adductors  of  the 
thigh.  I  have  already  referred  to  the  importance  of  the  muscles  attacked 
as  regards  the  localization  of  the  lesions.  The  paralysis  is  always  flaccid  ; 
it  explains  the  disturbance  of  equilibrium,  of  walking,  and  of  movements. 
The  reflexes  are  diminished  or  abolished. 

Of  all  the  trophic  troubles,  the  most  frequent  are  bed-sores  on  the 
buttocks,  sacrum,  and  trochanters.  The  spidrome  of  paradoxical  ischuria 
(retention  of  urine  with  incontinence)  and  obstinate  constipation,  with  or 
^vithout  involuntary  passage  of  faeces,  make  up  the  vesical  and  rectal  troubles. 
The  genital  functions  are  aboKshed  ;  most  frequently  desire  and  sensation 
are  weakened.  The  erections  continue,  but  ejaculation  does  not  occur, 
the  ejection  of  the  semen  being  hindered  by  the  paralysis  of  the  muscles 
of  the  perineum. 

The  onset  and  the  course  of  the  disease  depend  essentially  on  the  cause. 
In  the  case  of  traumatism,  pains  and  paralysis  are  sudden  ;  improvement 
and  cure  are  possible.  The  only  complications  arise  from  the  infection  of 
the  bladder  and  from  the  bed -sores.  In  the  case  of  tumour  the  course  is 
progressive,  and  whether  the  timiour  is  malignant  or  benign,  it  causes 
death  in  the  absence  of  surgical  intervention. 

Diagnosis. — Toxic  neuritis  (lead,  alcohol,  oxide  of  carbon,  etc.)  is  dis- 
tinguished from  affections  of  the  cauda  equina  and  of  the  filum  terminale 
by  the  predominance  of  the  paralysis  in  the  antero-external  muscles  of  the 
leg,  and  by  its  symptoms.     Double  sciatica  may  lead  to  confusion,  but 


1314  TEXT-BOOK  OF  MEDICINE 

careful  examination  of  tlie  patient,  analysis  for  glycosuria,  tlie  presence  of 
a  neoplasm  in  the  pelvis,  or  of  a  prostato-pelvic  carcinoma  (Guy on),  will 
clear  up  tlie  diagnosis.  The  same  remark  applies  to  dorso-lumbar  rheu- 
matic arthritis,  muscular  lumbago,  amyotrophia  (Charcot-Marie's  type), 
and  all  the  spinal  affections  that  have  some  analogy  with  those  of  the  cauda 
equina.  The  position  of  the  lesion  as  regards  height  has  been  discussed 
under  the  Pathological  Physiology. 

Treatment. — The  pains  must  be  reheved  by  analgesics,  such  as  anti- 
pyrin  and  pyramidon.  If  syphilis  is  suspected,  immediate  recourse  must  be 
had  to  injections  of  biniodide  of  mercury.  In  the  case  of  tumours  and  of 
traumatism,  surgical  intervention  is  indicated.  Several  cases  of  success 
fully  justify  it  (Thorburn,  Renn,  Schaw,  and  Busch). 

XVI.  H^MATOMYELIA. 

Ollivier  of  Angers  in  1827  applied  the  term  haematomyelia  to  haemor- 
rhage into  the  spinal  cord. 

etiology. — According  as  the  hsemorrhagic  rupture  occurs  in  healthy 
or  diseased  tissue,  the  hsematomyeha  is  primary  or  secondary.  Secondary 
hsematomyeha  is  met  with  in  acute  myehtis,  in  meningo-myeUtis  consequent 
on  Pott's  disease  (Raymond),  in  abscesses  of  the  spinal  cord,  and  in  softening 
by  thrombosis  or  emboHsm.  We  may  also  note  the  share  of  syphilis 
(Siemerhng),  of  syringomyeha,  of  ghomata,  of  myxomata,  and  of  sarcomata. 

Primary  heematomyeha  may  follow  on  fracture,  dislocation,  or  violent 
movements  of  the  vertebral  column,  exaggerated  flexion  of  the  head  back- 
wards (Thorburn),  and  elongation  of  the  spinal  cord  by  the  appHcation  of 
the  forceps.  Concussion  is  an  undoubted  cause  of  slight  haematomyelia. 
In  the  genesis  of  so-caUed  spontaneous  haematomyelia  we  always  meet  with 
strain,  fits  of  whooping-cough,  poisoning  by  tetanus  or  strychnine,  stoppage 
of  the  menstrual  flow,  cold  (Hochhaus),  and  the  vascular  changes  of  syphiUs 
and  alcohohsm. 

I  must  mention  as  a  more  singular  and  interesting  cause  sudden  decom- 
pression in  divers.  The  caissons  used  for  sinking  piles  are  certainly  the  most 
dangerous  of  these  apparatus.  The  accidents  always  happen  at  the  moment 
of  decompression,  when  the  divers  are  about  to  leave  the  water.  "  They 
only  pay  on  leaving  "  (Pol  and  Watelle).  In  sudden  decompression  the 
spinal  lesions  are  due  to  the  Liberation  of  the  nitrogen  which  under  pressure 
has  accumulated  in  excess  in  the  blood,  and  which  is  then  set  free  (Bert). 
Decompression  is  harmless  if  care  is  taken  to  make  it  last  several  minutes 
for  each  atmosphere.  Several  causes  generally  unite  to  produce  hsemato- 
myeUa,  and  it  seems  that  the  vascular  system  of  the  spinal  cord  must  have 
a  "  relative  fragiUty  "  (J.  Lepine). 


DISEASES  OF  THE  SPINAL  CORD  1315 

Pathogenesis.— J.  Lepino  has  caused  experimental  haeiuatomyelia  by 
various  means.  Injection  of  blood  into  the  posterior  columns  in  the  neij^li- 
bourhood  of  the  centre  of  the  spinal  cord  spreads  the  huemorrhage  upwards 
in  the  grey  matter  and  the  central  canal.  The  nerve  tissue  becomes  partially 
softened.  Punctures  of  the  spinal  cord  are  accompanied  by  myelitis,  with 
vascular  dilatations  and  capillary  extravasations  in  the  grey  matter.  Spinal 
concussion  is  followed  by  intense  congestion  of  the  injured  region,  leading  to 
haemorrhage.  Later  it  may  provoke  myehtis.  It  is  a  curious  fact  that 
animals  can  be  accustomed  to  spinal  concussion  (J.  Lepine).  By  placing 
rabbits  and  guinea-jiigs  in  a  large  autoclave,  under  a  pressure  of  ten  atmo- 
spheres, and  decompressing  them  in  a  few  seconds,  J.  Lepine  found  in 
the  spinal  cords  gaseous  emboli,  hsemorrhagic  infarcts,  and  primary  haemor- 
rhages due  to  rupture  of  the  vessels.  The  vascular  distension  is  due  to  the 
hberation  of  the  gases  of  the  blood  in  situ,  and  to  the  great  afflux  of  the  blood 
in  the  abdomen,  driven  out  by  the  gaseous  distension  of  the  intestines. 

Pathological  Anatomy. — The  grey  matter  is  the  seat  of  election  for 
medullary  haemorrhages,  because  it  is  much  more  vascular  than  the  white 
matter.  The  capillaries  of  the  branches  of  the  anterior  spinal  artery  supply 
the  anterior  cornu,  Clarke's  column,  and  the  most  anterior  portion  of  the 
posterior  cornu.  The  remainder  of  this  cornu  is  supplied  by  capillaries 
coming  from  the  posterior  radicular  arteries,  which  send  prolongations 
forward  as  far  as  Clarke's  column.  This  column  also  receives  the  branches 
of  the  artery  in  the  posterior  sulcus.  I  have  considered  it  right  to  dwell 
on  this  intensive  vascularization,  as  it  is  in  part  responsible  for  the  localiza- 
tion of  the  haemorrhage.  I  must  also  mention  the  existence  of  septa  which 
limit  the  effusions  of  blood  to  exact  regions  of  the  grey  matter  (Goldscheider 
and  Flatan). 

The  medullary  haemorrhages  are  capillary  or  focal.  The  former  are 
punctiform,  of  the  size  of  a  pin's  head,  and  close  to  the  vessels  of  the  grey 
matter.  The  latter  are  composed  of  a  clot  broken  up  into  several  secondary 
clots,  separated  by  more  or  less  torn  nerve-tissue.  The  grey  matter  is 
destroyed  in  Clarke's  column,  in  the  posterior  grey  commissure,  and  in  part 
of  the  posterior  cornu  ;  the  anterior  cornua  may  be  immune.  The  central 
haemorrhages  are  elongated,  and  known  as  tubular  haematomyehtis  (Levier). 
When  the  lesions  have  time  to  evolve,  softening  follows  the  haemorrhage, 
which  is  ehminated,  causing  a  lacunar  condition,  and  sometimes  ascending 
degenerations.  At  a  more  advanced  stage  haematomyelia  may  give  rise 
to  syringomyeHa,  according  to  Minor,  Raymond,  and  Brissaud.  Certain 
forms  of  haematomyeha  produce  symptoms  of  syringomyeha. 

Symptoms.— The  onset  of  traumatic  haematomyeha  is  instantaneous. 
The  paraplegia  is  complete,  sudden,  and  associated  with  corresponding 
anaesthesia.    In  spontaneous  hsmatomyeha  the  onset  is  more  or  less  suddea 


1316  TEXT-BOOK  OF  aiEDICINE 

and  the  disease  is  establislied  in  a  few  hours,  without  pain  or  fever.  Sensa- 
tion in  the  lower  limbs  and  in  the  trunk  is  completely  lost.  The  paraplegia 
is  total,  and  often  accompanied  by  paralysis  of  the  abdominal  muscles. 
Incontinence  of  urine  and  of  fseces  is  often  preceded  by  retention.  The 
reflexes  are  abolished.  A  shght  tendency  to  collapse,  with,  a  lowering  of  the' 
central  temperature,  is  sometimes  noticed.  After  a  few  hours  or  a  few 
days  the  symptoms  improve  ;  sensation  reappears,  the  abdominal  muscles 
regain  the  power  of  movement,  and  the  reflexes  reappear.  We  hope  for 
recovery,  but  it  is  only  relative,  the  improvement  ceasing  after  a  few  weeks. 
"  The  affection  becomes  fixed  "  (Jean  Lepine),  and  leaves  behind  a  pareto- 
spasmodic  condition  of  the  lower  limbs,  with  atrophy  and  sensory  troubles. 
Slight  incontinence  is  almost  the  rule  as  regards  the  sphincters.  Eecovery 
is,  however,  possible.  Acute  decubitus,  consecutive  myehtis,  and  urinary 
infection  may  cause  death.  Early  death  depends  on  the  abundance  of  the 
heemorrhage  and  on  its  locaUzation  in  the  cervical  cord,  near  the  bulb. 

Central  haematomyelia  (Minor)  reveals  itself  by  shght  motor  troubles 
and  by  important  sensory  signs.  The  syringomyehc  dissociation  of  the 
sensibility  is  constant,  and  persists  after  the  more  or  less  complete  return 
of  the  motor  functions. 

Haematomyelia  with  Brown -Sequard's  syndrome  is  not  often  accom- 
panied by  zones  of  hj-persesthesia  ;  the  syndrome  is  almost  always  incom- 
plete. Cervical  heematomyeha,  according  to  its  localization,  provokes 
either  diplegia  of  the  upper  limbs,  with  muscular  atrophy,  pseudo-h}-per- 
trophy,  vasomotor  troubles,  and  arrest  of  development  (Raymond), 
paralysis  of  the  diaphragm,  or  complete  paralysis  of  the  brachial  plexus. 
Recovery  is  exceptional.     Death  supervenes  in  a  few  hours  or  in  a  few  days. 

HsematomyeHa  of  the  filum  terminale  is  characterized  by  integrity  of 
the  mobihty  in  the  lower  hmbs,  ansesthesia  of  the  inferior  region  of  the 
buttocks  and  of  the  middle  portion  of  the  posterior  surface  of  the  thigh, 
anesthesia  and  vesico-rectal  paralysis,  disturbance  of  the  genital  functions. 

The  diagnosis  must  be  made  from  the  apoplectiform  affections — haema- 
torrhachis,  consequent  on  gunshot  wounds  ;  Pott's  disease  with  sudden 
bending,  rapid  syringomyeUa,  acute  apoplectiform  myehtis,  and  traumatic 
hysteria.  The  difficulties  are  often  very  great,  and  the  ^etiological  data 
must  always  be  borne  in  mind. 

The  treatment  depends  on  the  cause.  In  cases  of  fracture,  dislocation, 
or  Pott's  disease,  surgicah intervention  may  be  successful.  Care  must  be 
taken  to  avoid  the  use  of  counter-irritants,  because  they  may  produce  a 
deep,  incurable,  and  even  fatal  bed-sore  (Brissaud). 


DISEASES  OF  Till':  SPINAL  CORD  1:'.I7 


XVIT.  COMPRESSION  OF  THE  SPINAL  CORD. 

Does  compression  exist  ?  And  if  so,  what  is  the  nature  of  this  com- 
pression ?  Is  the  spinal  cord  deeply  or  superficially  affected,  or  is  it  simply 
inhibited  ?  Where  is  the  seat  of  the  compression  1  Must  we  intervene 
surgically  ? 

The  positive  diagnosis  of  medullary  compression  rests  on  the  following 
symptoms  :  Girdle  pains,  pains  in  the  lower  limbs  ;  paraplegia,  which  is 
generally  spastic  ;  vesical  and  rectal  troubles  ;  sensory  disturbances  ;  trophic 
phenomena  ;  deformity  of  the  vertebrae ;  and  radiography  of  the  suspected 
region. 

Meningo-myelitis,  whether  toxic,  infective,  influenzal,  syphilitic,  etc., 
from  the  fact  that  it  especially  affects  the  meninges,  may  exercise  some 
compression  on  the  parenchyma  of  the  spinal  cord  ;  but  this  is  not,  properly 
speaking,  compression  of  the  cord,  especially  from  the  surgical  point  of 
view.  The  most  frequent  causes  of  compression  are  fractures  or  disloca- 
tions of  the  spine,  having  their  seat  of  election  at  the  twelfth  dorsal  and  the 
first  lumbar  vertebrae.  Next  come  meningeal  and  extrameningeal  tumours 
(sarcomata,  fibromata,  myxomata,  hydatid  cysts,  tubercles,  etc.),  vertebral 
tumours,  and  Pott's  disease. 

The  diagnosis  of  compression  being  made,  we  must  next  ascertain  how 
far  the  cord  is  afiected.  Are  the  pyramidal  tracts  degenerated  ?  This 
problem  is  of  interest,  and  it  is  sometimes  a  difficult  problem  to  solve. 
The  question  must  be  divided  ;  the  case  is  sometimes  one  of  sudden  com- 
pression, at  other  times  one  of  slow  compression. 

Sudden  Compression. — This  variety  is  due  to  falls,  injuries,  or  bullet- 
wounds,  and  the  paraplegia  appears  suddenly.  If  a  few  days  after 
the  onset  of  paraplegia  we  find  trophic  phenomena  (vasomotor  troubles), 
important  sensory  troubles,  retention  of  urine,  and  fever,  it  may  be  said 
that  the  spinal  cord  is  seriously  afiected.  When  under  these  conditions 
the  paraplegia  remains  indefinitely  flaccid,  with  complete  loss  of  the  reflexes 
and  absolute  superficial  and  deep  anaesthesia,  complete  division  of  the 
spinal  cord  must  be  diagnosed.  The  spinal  cord  cannot  become  regenerated, 
and  the  lesion  is  irremediable.  The  patient  soon  dies  from  extensive  bed- 
sores and  urinary  infection.  Intervention  is  useless  in  this  case,  as  will  be 
readily  understood.  It  would  only  put  a  quicker  end  to  the  patient's  life 
by  fresh  traumatic  shock. 

If,  on  the  contrary,  after  the  accident,  more  or  less  pronounced  paresis 
alone  persists,  with  exaggeration  of  the  tendon  reflexes  and  slight  sensory 
and  trophic  troubles,  the  spinal  cord  is  compressed  rather  than  destroyed. 
Intervention  is  indicated,  and  the  patient  may  recover. 

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1318  TEXT-BOOK  OF  MEDICINE 

Slow  Compression. — In  the  case  of  slow  compression  the  severity  of 
the  paresis,  and  especially  of  the  objective  sensory  symptoms,  the  trophic 
phenomena,  the  reflex  movements  of  defence,  rather  than  the  spastic  features 
and  the  exaggerations  of  the  reflexes,  will  indicate  the  gravity  of  the  spinal 
lesion. 

In  the  long  run  slow  compression,  provided  it  is  progressive,  may  lead 
to  complete  section  of  the  spinal  cord.  In  this  case,  do  the  clinical  symptoms 
vary  ?  Authorities  do  not  agree  on  this  point,  and  the  entire  discussion 
(Limoges  Congress,  1901)  turns  on  the  condition  of  the  tendon  reflexes. 
The  classical  theory  of  Charcot  states  that  even  in  complete  section  there  is 
always  an  exaggeration  of  the  reflexes  below  the  lesion.  Bastian's  theory 
denies  this  opinion.  According  to  Bastian,  Bruns,  and  Borolby,  there  is 
certainly  contracture  and  exaggeration  of  the  reflexes  when  the  lesion  of  the 
spinal  cord  is  not  complete ;  but  as  soon  as  this  section  is  complete,  the 
paralysis  becomes  flaccid  and  the  reflexes  are  abolished.  The  importance 
of  this  discussion  from  the  surgical  point  of  view  will  be  understood. 

When  surgical  intervention  has  been  deemed  necessary,  we  look  for 
the  signs  that  will  localize  the  situation  and  extent  of  the  compression. 
Notice  must  be  taken  of  pain  on  percussion  over  a  vertebra,  of  the  promin- 
ence or  the  deformity  of  certain  spinous  processes,  and,  in  some  cases,  of 
radiography.  Nothing,  however,  can  replace  the  study  of  the  upper  limit 
of  the  anaesthesia.  To  it  our  final  appeal  must  be  made.  We  know,  for 
example,  that  a  band  of  anaesthesia  through  the  umbilicus  corresponds  with 
the  eighth  dorsal  root,  and  if  we  remember  that  this  root  arises  at  the  level 
of  the  eighth  dorsal  vertebra,  we  can  immediately  map  out  the  exact  seat  of. 
the  lesion. 

Regarding  the  relations  between  the  spines,  the  bodies  of  the  vertebrae, 
and  the  spinal  nerve  roots,  Chipault  says  :  "  In  the  cervical  region  it  is  always 
necessary  to  add  one  to  the  mimber  of  the  spine  determined  by  palpation 
to  find  the  number  of  the  roots  which  arise  at  its  level ;  in  the  dorsal  region 
we  must  add  two  ;  in  the  inferior  dorsal  region,  three.  The  lower  part  of 
the  eleventh  dorsal  vertebra  and  the  subjacent  interspinous  space  corre- 
spond to  the  last  three  lumbar  pairs.  The  twelfth  dorsal  spine  and  the 
subjacent  interspinous  space  correspond  to  the  sacral  roots."  The  lesion 
having  been  thus  mapped  out,  laminectomy  may  be  performed. 

XVIII.  SPINAL  MENINGITIS. 

Spinal  meningitis  is  acute  or  chronic.  Amongst  its  causes  I  would  mention  lesions 
in  the  neighbourhood,  vertebral  caries,  tumour,  abscesses,  and  bed-sores  of  the  sacrum. 
Tubercular  spinal  meningitis  is  allied  to  cerebral  meningitis  of  the  same  nature.  I  may 
eay  the  same  of  pneumonic  spinal  meningitis.  To  complete  this  section,  the  one  on 
Cerebro-spinal  Meningitis  must  be  studied.     It  will  then  be  seen  how  the  infection  of 


DISEASES  OF  THE  SPINAL  CORD  l.ilO 

tho  moningos  takes  place,  and  what  are  the  causes  of  this  infection.  This  general  survey 
of  spinal  meningitis  leaves  much  to  be  desired.  I  shall  deal  with  a  few  generalities,  but 
as  regards  tho  description  of  tho  various  forms  of  meningitis,  1  refer  the  reader  to  tho 
respective  sections  in  which  they  are  described. 

Pathological  Anatomy. — The  inflammation  affects  all  the  meninges, 
and  principally  the  pia  mater,  which  is  thickened  and  infiltrated  with 
fibrino-purulent  deposits,  while  the  subarachnoid  space  is  invaded  by  a 
flaky  or  purulent  sero-fibrinous  liquid.  When  the  meningitis  is  chronic, 
there  are,  furthermore,  adhesions  between  the  meninges  and  the  spinal  cord, 
amounting  in  some  cases  to  meningo-medullary  sclerosis.  The  spinal  cord 
is  sclerosed  at  its  periphery,  principally  in  its  posterior  columns  (Vulpian). 

Description. — (1)  Acute  Meningitis. — The  phenomena  of  pain  and  of 
contracture  may  be  attributed  to  the  excitation  of  the  nerve  roots  emerging 
from  the  spinal  cord  (Jaccoud)  and  to  the  excitation  of  the  nerves  of  the 
meninges,  the  pia  mater  being  richly  supplied  (Vulpian).  Moderate  fever 
first  appears,  and  is  accompanied  later  by  spinal  and  girdle  pains,  pains  m 
the  limbs,  cutaneous  hypersesthesia,  and  cramps,  which  vary  in  situation 
with  the  localization  of  the  meningitis. 

Meningitis  of  the  cer\'ical  region  is  at  times  accompanied  by  opisthotonos, 
and  meningitis  of  the  dorso-lumbar  region  may  in  its  fiist  period  cause 
retention  of  urine  and  of  faeces  from  the  contraction  of  the  sphincters  of  the 
bladder  and  rectum.  The  reflex  movements  and  the  muscular  contractility 
are  normal. 

For  some  years  past  the  study  of  meningitis  has  been  aided  by  new 
signs — Kernig's  sign,  lumbar  puncture,  and  cyto-diagnosis.  These  signs 
will  be  discussed  under  Cerebro- Spinal  Meningitis.  Kernig's  sign  is  as 
follows  :  As  long  as  the  patient  is  in  the  dorsal  decubitus,  the  legs  may  be 
extended,  and  will  remain  extended,  without  the  least  muscular  resistance. 
If  the  patient  is  made  to  sit  down  (this  is  sometimes  painful  on  account  of 
the  stifiness  in  the  nuchal  and  dorsal  muscles),  the  legs  are  flexed  on  the 
thighs  and  the  thighs  on  the  trunk  ;  in  other  words,  whilst  he  is  being  placed 
in  a  sitting  position  the  patient  draws  his  legs  and  his  thighs  towards  him. 
Lumbar  puncture  consists  in  making  a  puncture  in  the  subarachnoid  space, 
between  the  laminae  of  the  third  and  fourth  lumbar  vertebra.  Cyto-diagnosis 
gives  the  cellular  formula  of  the  cerebro -spinal  fluid. 

The  early  phenomena  of  excitation,  which  last  thirty-six  to  forty-eight 
hours,  are  succeeded  by  diminution  of  the  pains  and  by  paretic  symptoms. 
The  prognosis  is  very  grave.  The  meningitis  may  be  cured  or  pass  into  the 
chronic  state.     If  it  attacks  the  cervical  region,  the  patient  dies  of  asphyxia. 

Acute  Spinal  Perimeningitis. — Cases  have  been  reported  in  which 
trauma  produced  spinal  perimeningitis,  not  meningitis.  The  inflamma- 
tion is  primarily  limited  to  the  perimeningeal  cellular  tissue,  without  the 

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1320  TEXT-BOOK  OF  MEDICINE 

dura  mater  being  involved,  and  a  phlegmon  develops.  The  symptoms  are 
not  those  of  meningitis,  but  rather  those  of  myelitis  due  to  compression 
and  softening  of  the  spinal  cord, 

(2)  Chronic  Meningitis  is  usually  primary ;  it  also  presents  a  phase  of 
excitation  and  a  phase  of  paralysis.  The  phenomena  of  excitation  are 
hypersesthesia,  cramps,  and  pains  throughout  the  limbs  and  the  spine.  These 
pains  are  not  as  severe  as  those  of  acute  meningitis,  and  simulate  rather 
rheumatic  pains.  The  phenomena  of  paralysis  are  symmetrical  and  appear 
slowly.  Most  frequently  chronic  cortical  myelitis  develops  and  the  troubles 
of  myelitis  appear. 

Chronic  meningitis  has  a  predilection  for  the  cervical  region  (cervical 
pachymeningitis).  The  primary  change  affects  the  dura  mater,  which 
becomes  dense  and  fibrous.  It  subsequently  invades  the  cervical  cord,  and 
chronic  meningo- myelitis  is  the  result,  the  entire  thickness  of  the  cord 
undergoing  the  changes  of  diffuse  transverse  myelitis.  The  disease  com- 
mences with  pain  and  terminates  with  paralysis.  To  the  painful  period 
belong  the  pains  in  the  neck,  head,  and  upper  limbs,  mth  rigidity  and  con- 
tracture simulating  Pott's  disease.  To  the  paralytic  period  belong  the 
increasing  paralysis  of  the  upper  limbs  and  their  muscular  atrophy  (lesions 
of  the  anterior  cornua).  The  contracture  of  the  lower  limbs  (descending 
sclerosis  of  the  lateral  columns)  is  a  late  symptom.  The  disease,  though 
very  grave,  may  end  in  recovery. 

Myelitis  and  spinal  meningitis  have  many  signs  in  common,  and  the 
former  is  often  complicated  by  the  latter.  Nevertheless  to  myelitis  belong 
the  early  paralytic  troubles,  anaesthesia,  and  trophic  troubles,  which  we 
do  not  find  in  meningitis. 

The  treatment  of  meningitis  consists  in  local  blood-letting,  counter- 
irritants  to  the  affected  region,  the  administration  of  calomel,  subcutaneous 
injections  of  morphia,  etc. 


CHAPTER  II 
POLIOENCEPHALITIS 

DISEASES  OF  THE  PONS  AND  BULB 

Anatomy. — Before  describing'  polioencephalitis  (ttoAioj,  grey),  I  shall  luentii^n  bi-iefly 
Ihe  (listribntiou  of  tlie  grey  nuclei  in  the  l)ulb  and  pons. 

When  tlie  spinal  cord  passes  into  the  bulb,  it  opens  out  posteriorly,  and  its  central 
canal,  having  become  superficial,  spreads  out  and  continues  to  form  the  floor  of  the 
fourth  ventricle.  The  result  of  this  expansion  of  the  spinal  cord  is  that  the  parts  which 
were  posterior  in  the  cord  become  external  in  the  bulb.  Accordingly,  the  nuclei  of  the 
motor  nerves  in  the  bulb  (which  are  the  upward  continuation  of  the  spinal  motor  nerves) 
are  situated  along  the  median  Une  imder  the  floor  of  the  fourth  ventricle,  while  the  nuclei" 
of  the  mixed  nerves  are  situated  a  Uttle  more  outside.  The  bulbar  motor  nuclei  include 
the  nuclei  of  the  hypoglossus  below  and  the  nuclei  of  the  facial  and  of  the  sixth  nerves 
above. 

Higher  still  in  the  pons  are  the  nucleus  of  the  fourth  pair  (pathetic  nerve)  and  the 
superposed  nuclei  of  the  third  pair  (common  oculo-motor).  The  mixed  nuclei  are  those 
of  spinal  accessory,  pneumogastric,  glosso -pharyngeal,  and  the  motor  portion  of  the 
trifacial  nerves.  Let  us  add  the  nucleus  of  the  auditory  nerve.  In  short,  all  these 
nuclei  are  grouped,  some  around  the  central  canal  of  the  spinal  cord  when  it  passes  into 
the  bulb,  others  in  the  ventricular  floor  near  Flourens'  vital  node.  The  accumulation 
of  these  nuclei  in  such  a  restricted  space,  and  the  extreme  importance  of  the  organs 
which  the  nerves  supply,  explain  the  invading  course  of  the  symptoms  and  the  gravity 
of  the  lesions  in  this  region. 

The  nuclei  of  the  oculo-motor  nerves  in  the  pons  and  the  nuclei  of  the  motor  nerves 
in  the  bulb  represent  the  prolongation  of  the  anterior  comua  of  the  grey  matter  of  the 
spinal  cord.  Systematic  degeneration  of  the  anterior  grey  column  of  the  spinal  cord 
(anterior  poHomyeUtis)  causes  in  its  chronic  form  progressive  muscular  atrophy 
(Duchenne- Aran's  type).  If  the  lesion,  instead  of  first  affecting  the  anterior  comua  of 
the  cord,  attacks  the  grey  nuclei  in  the  bulb,  we  observe  the  sjTnptoms  of  labio-glosso- 
laryngeal  paralysis.  Similarly,  if  the  lesion,  instead  of  first  affecting  the  spinal  or 
bulbar  column,  attacks  the  grey  matter  in  the  pons,  the  symptoms  of  ophthalmoplegia 
develop. 

Chronic  progi-essive  ophthalmoplegia  is,  therefore,  in  the  case  of  the  pons  the  equiva- 
lent of  labio-glosso-laryngeal  paralysis  in  the  bulb  and  of  progressive  muscular  atrophy 
in  the  spinal  cord — that  is  to  say,  the  expression  of  a  systematic  change  limited  to  the 
eeUs  of  the  grey  motor  sub.stauce  in  one  of  these  three  regions.  As  the  gi'ey  motor 
column  may  be  affected  throughout  its  entire  length  in  the  spinal  cord,  in  the  bulb, 
and  in  the  pons  (polioencephalo-myelitis),  thus  causing  at  the  same  time  progi-essive 
muscular  atrophy,  labio-glosso-pharyngeal  paralysis,  and  progressive  external  ophthal- 
moplegia, so,  too,  may  one  of  these  tlu-ee  segments  be  affected  separately.  Thus,  by 
analogy  with  poliomyelitis,  where  a  lesion  involves  the  anterior  comua  of  the  spinal 

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1322  TEXT-BOOK  OF  MEDICINE 

cord,  Wernicke  proposes  to  call  tlie  corresponding-  affection  of  the  bulbar  and  of  tlie 
pontiae  nuclei  polioencephalitis  (ttoXios,  grey).  He  distinguishes  two  varieties — 
superior  pohoencephahtis,  the  lesion  being  in  the  nuclei  of  the  oculo-motor  nerves,  and 
causing  ophthalmoplegia  ;  and  inferior  pohoencephahtis,  the  lesion  beuig  in  the  bulbar 
nuclei,  and  giving  rise  to  labio-glosso-laryngeal  paralysis.  Pohoencephahtis,  hke  poho- 
myehtis,  may  have  an  acute,  subacute,  or  chronic  course. 


Fig.  59. — Fotjeth  Ventricle  and  Nuclei  of  the  Cranial  Nerves. 

GP,  Pmeal  gland ;  Q A,  anterior  quadrigemmal  body ;  QP,  posterior  quadrigeminal  body ; 
CG,  external  geniculate  body  ;  Pes,  superior  peduncle  of  cerebellum  ;  Pci,  inferior 
peduncle  of  cerebellum ;  RR,  Reil's  band ;  III-XII,  nuclei  of  cranial  nerves ; 
4^  V^,  fourth  ventricle. 

I.  GLOSSO-LABIO-LARYNGEAL  PAEALYSIS— INFERIOR 
CHRONIC  POLIOENCEPHALITIS. 

Glosso-labio-laryngeal  paralysis,  described  in  1864  by  DucJienne  with 
the  exactness  found  in  all  the  descriptions  of  this  keen  observer,  com- 
mences insidiously  without  fever  and  without  pain,  and  progressively 
invades  the  tongue,  the  lips,  the  velum  palati,  and  the  larynx.  After 
having  destroyed  the  functions  of  deglutition  and  of  phonation,  it  often 
ends  in  asphyxia  or  syncope. 

The  following  typical  case  occurred  under  my  care  : 

A  man,  aged  seventy-three  years,  had  preserved  his  understanding,  although  he  was 
unable  to  speak  a  word.  His  speech  was  reduced  to  a  mumbhng  of  inarticulate  sounds. 
Deglutition  was  practicaUy  impossible,  the  hps  were  wide  open,  and  the  sahva  drooled 
away.  The  velum  palati  was  flaccid,  and  the  tongue,  flattened  against  the  floor  of  the 
mouth,  was  motionless.  The  extrinsic  muscles  of  the  larynx  were  paralyzed.  The 
condition  was  bulbar,  and  not  pseudo -bulbar.  Against  the  hypothesis  of  pseudo- 
bulbar paralysis  we  had  the  progressive  course  of  the  disease  without  any  stroke,  and 
the  absence  of  paralysis  in  the  hmbs.  The  absence  of  any  nervous  trouble  ehminated 
the  hypothesis  of  any  previous  affection  of  the  nervous  system,  such  as  tabes,  syringo- 
myeha,  or  amyotrophic  lateral  sclerosis.  The  condition  in  this  case  was  rather  that  due 
to  a  primary  lesion  in  the  bulb. 


rOLTOEXrEPTTALITIS  1323 

The  trouble  had  comraoncod  oigh((>en  montlis  before  with  some  difTiculty  in  mastica- 
tion and  deglutition.  As  treatment  was  futile,  and  the  man  was  doomed  to  die  of 
himgor,  I  advised  gastrostomy,  which  gave  a  fair  measure  of  relief. 

1.  Paralysis  of  the  Tongue. — Glosso-labio-laryngeal  paralysis  generally 
commences  in  the  toiigne,  the  superior  lingualis  being  the  first  muscle 
attacked,  just  as  in  progressive  muscular  atrophy  the  abductor  of  the  thumb 
is  first  affected.  The  muscles  of  the  tongue  being  paralyzed  (nerve  supply 
from  the  hypoglossus  and  the  facial),  difficulties  in  pronunciation  and  in 
deglutition  result.  The  patient  pronounces  t  and  d  like  ch,  on  account  of 
the  paralysis  of  the  superior  lingual  muscle,  which  normally  raises  and 
presses  the  tip  of  the  tongue  against  the  upper  teeth.  As  the  tongue  has 
lost  its  lateral  movement  and  cannot  be  applied  to  the  palate,  the  first 
phase  of  deglutition  is  much  impeded,  and  the  saliva  is  swallowed  with 
difficulty.  It  accumulates  in  the  mouth,  and  drools  away.  At  a  more 
advanced  period  the  movements  of  the  tongue  are  completely  abolished, 
and  it  appears  fixed  to  the  floor  of  the  mouth.  When  the  atrophy  is  fairlv 
considerable,  the  tongue  is  wrinkled. 

2.  Paralysis  of  the  Velum  Palati  increases  still  more  the  difficulties  in 
pronunciation  and  deglutition.  B  and  p  are  articulated  like  m  for  the  follow- 
ing reasons  :  In  the  normal  condition  the  letters  h  and  p  are  formed  by  the 
column  of  expired  air,  which  suddenly  separates  the  lips  and  causes  them  to 
vibrate.  WTien  the  velum  is  paralyzed,  the  column  of  expired  air  loses  its 
force  by  being  separated  into  two  parts  :  one  gently  separates  the  lips,  and 
only  succeeds  in  producing  m,  wliile  the  other  passes  into  the  nasal  fossae, 
where  it  gives  rise  to  a  nasal  intonation.  The  patient  can  remedv  this 
inconvenience  by  pinching  his  nose.  Deglutition,  already  impeded  by  the 
paralysis  of  the-  tongue,  becomes  still  more  difficult.  In  fact,  the  stage 
of  deglutition  when  the  bolus  is  passing  from  before  backwards  between  the 
tongue  and  the  palate  can  only  be  carried  out  properly  when  the  velum, 
being  made  tense  by  the  tensor  palati  (fifth  pair),  is  drawn  downwards  by 
the  palato-glossi  (facial  nerve),  and,  finally,  when  the  floor  of  the  mouth  is 
stretched  by  the  mylohyoid  muscles  (mylohyoid  branch  of  the  inferior 
dental  nerve),  which,  acting  like  a  girth,  press  the  base  of  the  tongue  firmly 
against  the  velum.  As  most  of  these  conditions  are  abolished  in  glosso- 
labio-pharyngeal  paralysis,  the  dysphagia  is  excessive,  and,  in  spite  of 
every  efltort  on  the  part  of  the  patient,  the  lightest  meal  becomes  a  painful 
and  laborious  operation,  and  deglutition  is  often  accompanied  by  the  passage 
of  food  into  the  nasal  fossae  or  into  the  larynx,  which  causes  fits  of  suffoca- 
tion and  of  asphyxia.  Paralysis  of  the  velum  also  betrays  itself  by  other 
symptoms,  such  as  impossibility  of  sucking,  of  gargling,  etc. 

3.  Paralysis  of  the  Lips. — When  the  lips  are  paralyzed,  the  patient 
can  neither  whistle  nor  pronounce  the  vowels  o  and  u.  [This,  of  course,  is  the 


1P,24  TEXT-BOOK  OF  MEDICINE 

Frencli  u. — Translator.]  The  paralysis  of  the  orbicularis  allows  the  over- 
action  of  the  motor  muscles  of  the  commissures.  The  mouth  becomes 
widened  ;  the  physiognomy  is  that  of  a  crying  child  ;  the  food  is  held  in  the 
mouth  with  difficulty,  and  the  saliva  flows  incessantly. 

4.  Paralysis  of  the  Pterygoid  Muscles. — These  muscles  (supplied  by 
the  trigeminal  nerve)  preside  over  the  grinding  movements  of  the  jaw  (move- 
ments for  grinding  the  food).  The  paralysis  of  these  muscles  is  generally 
the  precursor  of  grave  trouble  (Duchenne). 

Paralyses  of  the  tongue,  of  the  velum,  of  the  lips,  and  of  the  pterygoid 
muscles  combine  to  abolish  (1)  phonation,  (2)  deglutition.  At  length  degluti- 
tion becomes  extremely  difficult,  and  speech  is  merely  an  unintelligible  growl 
with  a  nasal  tone.  As  these  paralyses  are  symmetrical,  they  do  not  cause 
deviation  of  the  mouth,  of  the  tongue,  or  of  the  uvula.  The  other  muscles 
of  the  face  are  not  affected  (superior  facial  branch),  and  the  intelligence 
remains  intact,  but  other  troubles  are  soon  added  to  those  already  described. 

5.  Laryngeal  Troubles. — Anaesthesia  and  loss  of  the  reflex  excitability 
of  the  mucosse  of  the  pharynx,  larynx,  and  trachea  may  exist  from  the  com- 
mencement of  the  disease  (Krishaber),  The  muscles  of  the  larynx  are  some- 
times attacked  by  incomplete  paralysis.  The  voice  is  weakened,  but  not 
extinguished. 

6.  Respiratory  Troubles. — ^At  an  advanced  period  of  the  disease  the 
respiration  is  compromised,  and  the  least  effort  causes  breathlessness. 
Expiration  is  incomplete  and  coughing  is  difficult.  The  mucus  accumulated 
in  the  bronchi  is  brought  up  with  difficulty.  Furthermore,  the  mildest 
bronchitis  may  cause  grave  complications.  This  respiratory  insufficiency, 
which  Duchenne  attributes  to  paralysis  of  the  bronchial  muscles,  is  com- 
plicated by  attacks  of  dyspnoea,  which  become  more  frequent  as  the  disease 
progresses. 

7.  Cardiac  Troubles. — Cardiac  troubles  also  supervene  at  an  advanced 
stage  of  the  disease.  The  patient  complains  of  a  feeling  of  faintness,  with 
angina  and  palpitations,  and  fatal  syncope  often  ends  the  scene. 

Course — Prognosis. — Glosso-labio-laryngeal  paralysis  commences  in- 
sidiously and  without  fever.  It  attacks  successively  the  tongue,  the  soft 
palate,  the  orbicularis  oris,  the  pterygoid  muscles,  the  larynx,  the  respiratory 
muscles,  and  the  heart,  and  after  a  duration  varying  from  a  few  months  to 
three  years  the  patient  is  carried  off  rapidly  or  slowly  by  various  complica- 
tions. Sudden  death  supervenes  from  syncope  or  asphyxia.  It  is  also 
caused  by  the  passage  of  food  into  the  trachea,  or  by  some  intercurrent 
disease,  such  as  bronchitis  or  pneumonia.  Slow  death  is  due  to  the  wasting 
from  which  the  patient  would  suffer  unless  fed  with  the  oesophageal  tube. 
Respiratory  and  cardiac  complications  mark  the  second  phase  of  the  disease. 
They  are  generally  preceded  by  paralysis  of  the  pterygoid  muscles,  which 


rOTJOEXrEPHAUTIS  1  ?.2.' 

seems  to  indicate  that  the  bulbar  lesion  spreads  from  the  motor  nucleus 
of  thf  fiftli  nerve  to  tlio  nucleus  of  the  vagus. 

Diagnosis  and  Varieties. — Cases  in  which  the  tongue,  the  lips,  and  the 
soft  palate,  are  separately  paralyzed  must  not  be  confounded  with  glosso- 
labio-larvngeal  paralysis.  Simultaneous  paralysis  of  the  facial  nerves  has 
some  symptoms  in  common  with  glosso-labio-laryngeal  paralysis  ;  the  dif- 
ference lies  in  the  paralysis  of  the  muscles  of  the  upper  part  of  the  face. 
Diphtheritic  paralvsis  of  the  soft  palate  is  distinguished  by  the  previous 
existence  of  croup  or  angina,  by  the  sudden  onset  of  the  trouble,  and  by  the 
integrity  of  the  movements  of  the  tongue  and  of  the  lips.  General  paralysis 
presents  amongst  its  symptoms  hesitation  in  speech  and  peculiar  tremor  of 
the  lips,  which  have  nothing  in  common  with  the  initial  troubles  of  phona- 
tion  seen  in  glosso-labio-laryngeal  paralysis. 

I  have  so  far  described  the  primary  form  of  glosso-labio-laryngeal  para- 
lvsis, but  the  disease  is  often  secondary  to  progressive  muscular  atrophy, 
insular  sclerosis,  and  amyotrophic  sclerosis.  It  may  even  be  said  that  in 
many  cases  it  forms  such  an  integral  part  of  these  diseases  that  the  idio- 
pathic form  of  glosso-labio-laryngeal  paralysis  is  doubted  by  some  writers. 
When  it  is  associated  with  the  different  affections  just  enumerated,  it  be- 
comes joined  to  the  symptoms  peculiar  to  each  of  these  morbid  conditions, 
and  we  have  the  bulbo-spinal  form  (Hallopeau). 

In  certain  cases  the  syndrome  of  glosso-labio-laryngeal  paralysis  has 
supervened  suddenly,  consequent  on  haemorrhage  or  softening  of  the  bulb. 
In  this  case  the  appearance  of  the  glosso-labio-laryngeal  paralysis  coincided 
with  sudden  death  (embolism  of  the  vertebral  artery — Hayem),  or  with 
hemiplegia  and  recovery. 

The  syndrome  of  glosso-labio-laryngeal  paralysis  may  also  find  its  cause, 
not  in  a  bulbar,  but  in  a  cerebral  lesion.  This  has  been  described  under  the 
name  of  pseudo-bulbar  paralysis  of  cerebral  origin.  The  cases  of  Lepine 
and  those  published  later  prove  that  there  really  exists  a  glosso-labio- 
laryngeal  paralysis  of  cerebral  origin.  Oppenheim,  ha\'ing  found  sKght 
bulbar  lesions  associated  with  cerebral  lesions  in  several  post-mortem 
examinations,  has  described  a  mixed  form,  to  which  he  has  given  the  name 
of  paralysis  of  cerebro-bulbar  origin.  No  matter  how  we  may  regard 
Oppenheim's  cases,  the  pseudo-bulbar  form  with  a  cerebral  locahzation  really 
exists.  In  which  region  are  we  to  locahze  the  cerebral  lesion  ?  A  prioin,  it 
seems  that  the  lesion  ought  to  be  bilateral,  and  that  it  ought  to  affect  the 
centre  for  the  movements  of  the  hps  (inferior  facial  nerve),  which  is  situated 
in  the  lower  part  of  the  ascending  frontal  convolution,  the  centre  for  move- 
ment of  the  tongue  (hypoglossal  nerve),  and  the  centre  for  the  muscles  of 
mastication  (motor  branch  of  the  fifth  nerve),  which  are  all  close  together. 
It  seems  that  the  lesion  ought  hkewise  to  affect  the  centre  for  the  move- 


1326  TEXT-BOOK  OF  MEDICINE 

ments  of  deglutition,  wMcli  is  near  the  foot  of  the  ascending  frontal  con- 
volution, and  the  cortical  centre,  which  probably  hes  at  the  junction  of  the 
foot  of  the  ascending  frontal  and  the  foot  of  the  third  frontal  convolutions. 
And,  as  a  matter  of  fact,  in  several  cases  of  pseudo-bulbar  paralysis  the 
cortical  or  subcortical  lesions  were  seated  in  the  above-mentioned  cerebral 
region.  A  bilateral  lesion  of  the  optic  thalamus  and  corpus  striatum,  and  a 
cortical  lesion  of  the  right  hemisphere,  with  a'lesion  in  the  left  thalamus  and 
corpus  striatum,  or  vice  versa,  also  give  a  similar  syndrome  (Halipre). 

The  interpretation  of  these  pseudo-bulbar  paralyses,  however,  is  more 
difficult  when  the  cerebral  lesion  is  situated  in  the  external  segment  of  the 
lenticular  nucleus.  Sometimes,  even,  there  is  no  symmetry  of  the  lesions. 
In  such  a  case,  for  instance,  there  is  a  focus  of  softening  in  the  head  of  the 
nucleus  on  the  right  side,  and  another  focus  in  the  white  matter  of  the  middle 
lobe  of  the  left  hemisphere.  These  facts,  though  difficult  to  interpret,  have 
been  ingeniously  explained  by  Halipre  and  Brissaud.  In  any  event,  glosso- 
labio-laryngeal  paralysis  of  cerebral  origin  is  distinguished  from  the  bulbar 
form  by  the  absence  of  atrophy  in  the  paralyzed  muscles,  and  by  the 
preservation  of  the  reflex  movements,  which  spares  the  patient  the  troubles 
in  respiration  and  circulation  that  are  always  a  source  of  danger  in  true 
bulbar  paralysis. 

Asthenic  bulbar  paralysis  (Erb's  syndrome)  closely  resembles  Du- 
cheime's  glosso-labio-laryngeal  paralysis,  but  distinctive  features  are  not 
wanting.  The  constancy  of  ptosis,  of  paresis  of  the  muscles  of  mastication 
and  of  the  nape  of  the  neck,  the  alternation  of  periods  of  remission  and 
aggravation,  the  myasthenic  electrical  reaction  (JoUy),  form  the  principal 
characteristics  of  Erb's  spidrome,  and  furnish  the  points  for  diagnosis. 

Pathological  Anatomy. — It  was  first  believed  that  glosso-labio-laryngeal 
paralysis  is  not  accompanied  by  muscular  atrophy.  It  is  true  that  paralysis 
is  the  chief  feature,  but  there  is  also  atrophy  of  the  muscles,  which  is  some- 
times visible  with  the  naked  eye,  and  always  under  the  microscope.  This 
atrophy,  often  well  marked  in  the  tongue,  is  similar  to  that  described  under 
Progressive  Muscular  Atrophy. 

The  atrophy  of  some  of  the  bulbar  nerves  has  been  noticed,  but  the 
initial  lesion  of  the  disease  is  seated  in  the  bulbar  nuclei  of  these  nerves 
(Charcot),  just  as  the  initial  lesion  of  progressive  muscular  atrophy  is  seated 
in  the  anterior  cornua  of  the  spinal  cord.  The  organs  of  phonation,  of  de- 
glutition, of  respiration,  and  of  circulation,  which  are  progressively  invaded 
by  the  disease,  are  suppUed  by  the  hypoglossal,  facial,  trigeminal,  spinal 
accessory,  and  pneumogastric  nerves.  The  initial  lesion  of  the  disease 
must,  therefore,  be  sought  in  the  nuclei  of  these  nerves. 

The  lesion  in  the  nuclei  consists  in  atrophy  of  the  nerve  cells,  with  or 
without  pigmentary  degeneration.     It  is  analogous  with  the  lesion  in  the 


POLIOENCEPHALITIS  1327 

anterior  cornua  of  tlic  sj)iiuil  cord  in  progressive  muscular  atrophy.  The 
bulbar  nuclei  are  unequally  affected  by  the  atrophy  ;  tiie  nucleus  of  the 
hypoglossal  nerve  is  the  most  affected  (Joflroy),  and  in  a  section  of  the 
bulb  we  find  the  large  cells  of  this  nucleus  replaced  by  some  deformed 
cells. 

II.  CHEONIC  SUPERIOR  POLIOENCEPHALITIS. 

Ophthalmoplegia  is  called  external  or  internal,  according  as  the  paralysis 
affects  the  motor  muscles  of  the  eyeball  or  the  internal  musculature  of  the 
eye  (iris  and  ciliary  muscle).  AU  the  ocular  paralyses  must  not,  however, 
be  classed  under  this  rubric,  even  though  they  are  of  nuclear  origin.  It 
is  useful  to  distinguish  from  ophthalmoplegia,  and  to  classify  separately — 
(1)  the  classical  paralyses  of  each  of  the  nerves  of  the  eye  (paralysis  of  the 
third,  fourth,  and  sixth  pair) ;  (2)  associated  paralyses  which  affect  in  both 
eyes  the  muscles  producing  similar  movements. 

External  ophthalmoplegia  is  a  special  clinical  type,  due  to  paralysis 
of  all  the  motor  muscles  of  the  eye,  and  characterized  in  typical  cases  by 
absolute  immobility  of  the  eyes.  "  When  however,  the  paralysis  of  the  third 
pair  is  coexistent  with  that  of  the  sixth  pair,  and  when  the  superior  oblique 
only  is  intact  (fourth  pair),  the  slight  movement  in  a  downward  and  out- 
ward direction  scarcely  changes  the  clinical  picture.  On  the  other  hand, 
when  the  third  and  fourth  pairs  are  paralyzed,  it  is  very  rare  for  the  sixth 
pair  to  be  absolutely  free.  For  these  reasons,  the  term  '  external  ophthal- 
moplegia '  may  also  be  applied  to  cases  in  which  the  muscles  supphed  by 
two  different  nerves  in  the  same  eye  are  paralyzed,  one  of  them  being  con- 
stantly the  common  oculo -motor  nerve  "  (Sauvineau). 

Internal  ophthalmoplegia  is  paralysis  of  the  entire  internal  musculature 
of  the  eye. 

These  two  forms,  when  present  in  the  same  eye,  constitute  mixed  or 
total  ophthalmoplegia.  Each  one  of  these  three  forms  may  be  unilateral 
or  bilateral. 

Ophthalmoplegia  may  be  divided  according  to  the  situation   of  the 

lesion  in  the  course  of  the  fibres  from  the  cerebral  cortex  to  the  orbital 

branches  of  the  motor  nerves  of  the  eye.     These  varieties  will  be  described 

under  the  Paralyses  of  the  Motor  Muscles  of  the  Eye.     We  are  only  concerned 

at  present  with  ophthalmoplegia  of  nuclear  origin — that  is  to  say,  arising 

from  a  progressive  change  in  the  nuclei  of  the  motor  nerves  of  the  eye.     A 

short  account  of  these  nuclei  will  lead  to  a  better  understanding  of  the 

subject. 

Anatomy. — The  common  oculo -motor  nerve  arises  in  the  grey  column  under  the 
floor  of  the  aqueduct  of  Sylvius.  This  column  forms,  not  a  single  nucleus,  but  a  series 
of  distinct  nuclei  (Hensen  and  Valkers,  Kahler  and  Pick,  Westphal).     Each  one  of 


1328  TEXT-BOOK  OF  MEDICINE 

these  little  nuclei  constitutes  a  motor  centre  corresponding  to  one  of  the  terminal 
branches  of  the  oculo-motor  nerve,  and  corresponding,  therefore,  to  one  of  the  muscles 
of  the  eye  supplied  by  the  third  pair.  This  grey  column  under  the  aqueduct  of  Sylvius 
forms  the  principal  part  of  the  oculo-motor  nucleus.  It  comprises  five  separate  nuclei, 
which  control  the  four  extrinsic  muscles  supphed  by  the  third  pair  and  the  levator 
muscle  of  the  eyeUd. 

In  front  of  the  principal  portion  of  this  nucleus  there  exists  another  smaller  portion, 
formed  of  smaller  nerve  cells.  It  is  not  under  the  aqueduct  of  Sylvius,  but  under  the 
floor  of  the  third  ventricle,  and  a  httle  separated  from  the  median  Mne.  It  com- 
prises two  nuclei  for  the  sphincter  of  the  iris  and  the  cihary  muscle. 

As  regards  the  disposition  of  the  nuclei,  the  scheme  proposed  by  Kahler  and  Pick  is 
generally  followed : 


Median 
side. 


1.  Cihary  muscle. 

2.  Sphincter  of  the  iris.  I     Lateral, 

3.  Internal  rectus.  5.  Levator  palpebrae.  y  or  external 
6.  Superior  rectus.  side. 

4.  Inferior  rectus.  7.  Inferior  oblique,    j 

The  nucleus  of  the  fourth  nerve  is  just  below. 
Lower  still  the  nucleus  of  the  sixth  nerve  is  found. 

Symptoms. — The  onset  of  ophthalmoplegia  is  insidious,  and  the  muscles 
are  affected  one  after  the  other  without  regular  order. 

When  the  ophthalmoplegia  is  complete,  the  physiognomy  of  the  patient 
has  a  special  character,  known  as  Hutchinson's  facies.  The  eyeUds  are  half 
closed,  so  that  the  patient  appears  to  be  asleep  ;  they  partially  cover  the 
cornea.  As  the  patient  tries  to  remedy  this  blepharoptosis  by  contraction 
of  the  frontalis  muscle,  the  brow  is  wrinkled  and  the  eyebrows  are 
arched.  If  the  upper  eyelids  are  raised,  the  eyeballs  are  immovable,  "  as 
though  formed  of  wax  "  (Benedickt).  When  the  paralysis  affects  all  the 
external  muscles,  the  eyes  are  directed  straight  forwards.  The  look  is, 
however,  somewhat  vague,  because  the  optical  axes  are  not  absolutely 
parallel. 

If  the  patient's  head  is  held  so  that  he  cannot  make  up  for  the  absence  of 
movement  in  the  eyes  by  moving  the  neck,  and  if  he  tries  to  fix  an  object 
and  to  foUow  it  upwards,  downwards,  outwards,  and  inwards,  we  find  that 
the  eye  remains  absolutely  immovable.  The  ophthalmoplegia,  however,  is 
not  always  so  complete,  and  more  or  less  limited  movements  may  be  per- 
formed in  the  direction  of  the  action  of  one  or  of  several  of  the  muscles  of 
the  eye.  In  order  to  be  more  certain,  we  may  have  recourse  to  the  examina- 
tion of  the  field  of  fixation. 

Diplopia  only  shows  itself  when  there  is  a  considerable  difierence  in  the 
paralysis  of  the  various  motor  muscles. 

The  nuclear  affection  most  frequently  remains  limited  to  the  extrinsic 
muscles,  the  internal  musculature  being  unaffected.  The  sphincter  of  the 
iris  and  the  ciliary  muscle  respectively  continue  to  react  to  light  and  to 
accommodation. 


POLIO  KNCKPHALITLS  1321i 

Kiiiall\ ,  let  us  notice  the  absence  of  vertigo,  of  Iiciidjirlio,  and  of  every 
cerebral  reaction. 

Su(^h  is,  in  broad  outline,  the  asjtect  ol  a  patient  sulTering  from  external 
ophthalmoplegia. 

The  features  of  interiuil  o|)hthalmoplegia  are  as  follows  :  the  puf)il  is 
moderately  dilated  ;  it  does  not  react  to  light  or  to  accommodation.  The 
ciliary  muscle  is  also  paralyzed.  The  patient  can  no  longer  accommodate, 
the  punctum  proximum  being  brought  forward  and  confounded  with  the 
punctura  remotum.  Internal  ophthalmoplegia  may  be  primary  and  exist 
alone,  being  later  accompanied  by  external  ophthalmoplegia.  It  may  be 
secondary  to  the  latter.  Finally,  it  may  appear  at  the  same  time  as  external 
ophthalmoplegia. 

Course — Prognosis. — The  course  of  nuclear  ophthalmoplegia,  in  its 
chronic  form,  varies.  It  sometimes  remains  stationary  for  years  ;  some- 
times, on  the  contrary,  it  follows  a  progressive  course.  The  course  varies 
according  to  the  nuclear  region  in  which  the  lesion  starts,  and  whether 
the  lesion  remains  confined  to  these  nuclei  or  extends  farther. 

In  the  first  case  the  ophthalmoplegia,  which  is  purely  external,  becomes 
complicated  with  internal  ophthalmoplegia.  The  ophthalmoplegia  becomes 
total.  The  inverse  course  (which  commences  in  the  intrinsic  muscles  of  the 
eye)  is  far  less  common.  The  affection  may  not  remain  limited  to  the  nuclei 
of  the  oculo-motor  nerves,  but  may  also  attack  the  other  nuclei  (motor  and 
sensory  nuclei  of  the  fifth  nerve),  the  vasomotor  centres  (glycosuria,  albu- 
minuria, polyuria),  the  bulbar  nuclei  (labio-glosso-laryngeal  paralysis),  and 
even  the  anterior  spinal  cornua  (progressive  muscular  atrophy). 

In  other  cases  we  see  that  ophthalmoplegia  complicates  a  spinal  or 
cerebro -spinal  afie'ction.  It  will  be  understood  that  the  prognosis  will  vary 
in  the  different  forms. 

Diagnosis. — Hutchinson's  facies  is  characteristic,  and  cannot  be  con- 
founded  with  the  bulbar  or  the  myopathic  facies.  The  difficulty  consists 
in  establishing  the  nuclear  origin  of  the  ophthalmoplegia  and  in  distin- 
guishing it  from  the  supranuclear  and  cortical,  basal,  orbital,  and  peri- 
pheral varieties  of  ophthalmoplegia.  Slow  and  gradual  abolition  of  the 
movements  of  the  eyes,  affecting  progressively,  without  regular  order,  the 
motor  muscles  of  the  eyeballs  ;  special  paresis  less  pronounced  (at  least  at 
the  commencement)  after  a  night's  rest  ;  incomplete  ptosis  ;  absence  of 
cerebral  phenomena ;  integrity  of  the  pupil  reflexes  and  of  accommodation, 
are  the  classical  characteristics  of  nuclear  external  ophthalmoplegia,  and 
tiU  recently  nuclear  ophthalmoplegia  was  synonymous  vnth  external  oph- 
thalmoplegia (Elanc).  Nevertheless,  the  existence  of  internal  ophthalmo- 
plegia accompanying  an  external  ophthalmoplegia  must  not  lead  us  to  reject 
the  diagnosis  of  a  nuclear  lesion.     On  the  contrary,  internal  ophthalmo- 


1330  TEXT-BOOK  OF  MEDICINE 

plegia  can  hardly,  in  the  present  condition  of  our  knowledge,  and  leaving 
an  orbital  lesion  or  a  peripheral  cause  out  of  the  question  (reflex  paralysis), 
be  attributed  to  anything  else  than  to  a  nuclear  lesion  of  the  nuclei  sub- 
jacent to  the  third  ventricle  (Sauvineau). 

The  preceding  characteristics  allow  us  to  distinguish  ophthalmoplegia 
from  paralyses  which  are  also  of  nuclear  origin,  but  are  due  to  other  causes, 
such  as  traumatism,  haemorrhage,  tumour,  or  acute  polioencephalitis. 

Eeferring  to  cases  of  ophthalmoplegia  that  are  independent  of  a  lesion 
in  the  nuclei,  they  present  special  characters  which  generally  allow  them  to 
be  distinguished  from  cases  of  nuclear  ophthalmoplegia. 

External  ophthalmoplegia  has  been  seen  with  muscular  atrophy  and 
with  polyneuritis.  The  existence  of  some  intoxication,  as  a  cause  and  the 
favourable  course  of  events  are  in  favour  of  polyneuritis.  Ophthalmo- 
plegia has  also  been  found  in  certain  forms  of  leprosy.  Finally,  external 
ophthalmoplegia  has  been  met  with  in  exophthalmic  goitre  (Ballet),  and  in 
hysteria  (Raymond).  In  external  ophthalmoplegia,  due  to  neurosis,  the 
paralysis  only  afEects  the  voluntary  muscles,  and  spares  the  automatic 
movements  and  the  reflexes.  The  lesion  of  the  nuclei  of  the  third,  fourth 
and  sixth  nerves  in  ophthalmoplegia  consists  in  an  atrophy  of  the  motor 
cells.  On  microscopic  examination,  the  cells  are  found  to  be  small,  rounded, 
and  deprived  of  processes. 


III.  SYPHILITIC  POLIOENCEPHALITIS  OF  THE  BULB 

AND  PONS. 

Clinical  Case.* — On  iN'ovember  10,  1907,  a  man  aged  29  years  was  admitted  under  my 
care.  His  appearance  was  striking.  Even  through,  kis  clothes  his  right  shoulder 
looked  flat.  The  upper  eyelids  drooped,  partially  hiding  the  eyeballs  (third  nerve 
paralysis).  At  times  he  ti'ied  to  correct  the  hlepharoptosis  by  contracting  the 
frontalis ;  the  forehead  wrinkled  up,  and  the  eyebrows  became  arched,  but  the  lids  did 
not  move.  Instinctively  (especially  when  walking),  he  held  his  head  backwards  to 
allow  the  Light  to  enter  the  eyes  below  the  lids. 

On  raising  the  lids,  the  eyeballs  were  fixed  in  the  position  of  external  strabismus. 
All  the  motor  muscles  of  the  eye  were  paralyzed  with  the  exception  of  the  external 
rectus,  which  held  the  ball  in  the  position  of  external  strabismus. 

In  short,  all  the  symptoms  of  external  ophthalmoplegia  were  present.  But  the 
patient  also  had  internal  ophthalmoplegia,  because  his  pupils  did  not  react  to  light  or 
to  accommodation  (paralysis  of  the  sphincter  iridis  and  of  the  ciliary  muscle).  His 
ophthalmoplegia  was  total  and  bilateral,  except  for  the  external  rectus.  It  had  been 
progressive  in  nature,  being  at  first  limited  to  the  left  levator  palpetrag,  next  involving 
the  right  levator,  and  finally  affecting  the  external  and  internal  musculature  of  both 
eyes.     The  ophthalmoscope  revealed  nothing  abnormal,  and  the  sight  was  perfect. 

A  double  question  demanded  solution  :  What  was  the  cause  of  the  ophthalmoplegia, 

*  Dieulafoy,  Clinique  Medicate  de  VKotd-Dieu,  6^  volume  1909,  quatrieme  et 
cinquieme  le9ons. 


rOLIOENCKPHALITIS  1331 

and  ill  \vlia<  n-jf  ion  was  tljo  provokinjr  losiou  ?  "Wa«  it  due  to  taburi  ?  Tho  frequonoy 
of  DiMiliir  jiiil.sii's  in  tubes  is  wnU  known  ;  tliey  nuij-  appoiir  in  tli(>  pre-ataxic  as  wt-ll  as 
in  tin?  <'<>ntirniiMl  stiip<  of  this  inulud}'.  T}i(»  patiimt  wrtainly  lia<l  not  tabes.  Tlut 
oplithaliuopK'iria  was  of  eijrht  months'  standing',  and  yet  htt  showed  no  sti^fiuata  of 
tabes:  no  li^'liiiiinj^'-pains,  no  visceral  t-risos,  no  Argyll-ilobei'tsou's  pupil,  no  llem- 
berjr's  sign,  lie  had  no  sensory  disturbances,  no  changes  in  his  gait ;  and  lastly,  all 
his  reflexes  were  normal. 

Was  tlie  ophtlialmoplepia  of  diabetic  orij^'in  ?  Ocular  palsies  may  occur  in  mild  as 
well  as  in  sevei-e  diabetes  * ;  at  times,  indeed,  i)aralysis  of  an  oculo-motor  nerve  may 
appear  suddenly  and  be  the  tirst  sijru  to  call  attention  to  diabetes  as  the  cause.  As  a 
general  rule,  when  we  are  looking  for  the  cause  of  an  ocular  palsy,  we  must  always 
think  of  diabetes  mellitus.  I  have  collected  seventy-four  cases  of  ocular  paralysis  in 
diabetes ;  forty-live  cases  of  paralysis  of  the  sixth  nerves ;  seventeen  of  paralysis  of 
the  third  nerves ;  six  of  paralysis  of  the  fourth  nerves ;  five  cases  of  external  ophthalmo- 
plegia, and  one  case  of  progressive  ophthalmoplegia  with  fatal  bulbar  symptoms. 
Diabetes  is,  therefore,  an  important  cause  of  ocular  paralysis ;  failure  to  recognize 
this  fact  has  led  to  serious  errors  in  diagnosis  and  prognosis.  In  this  case  there  was 
no  suggestion  of  diabetes. 

Among  the  causes  of  ocular  paralysis,  syphilis  stands  in  front  rank.  It  shows  a 
preference  for  the  third  nerve.  While  it  induces  partial  or  isolated  paralysis  of  tho 
third,  fourth,  and  sixth  nerves,  it  may  also  induce,  by  various  mechanisms  associated, 
ocular  palsies  which,  to  some  extent,  come  xmder  the  heading  of  ophthalmoplegia. 
The  patient  was  certainly  syphilitic  ;  six  years  previously  he  had  suffered  from  a 
chancre,  followed  by  secondary  symptoms,  and  shortly  before  the  appearance  of  the 
ophthalmoi)legia  he  had  been  under  treatment  for  a  tertiary  \ilcer  of  the  velum  palati. 

It  was,  therefore,  logical  to  suppose  that  the  ophthalmoplegia  was  syphilitic  in 
origin;  in  what  region,  then,  was  the  lesion?  Ophthalmoplegia  may  result  from 
periostitis  of  the  sphenoidal  fissure  ;  since  the  three  motor  nerves  of  the  eye  i^ass 
through  this  fissure,  an  osteo-syphiloma  of  the  orbit  may  aft'ect  these  nerves,  causing 
ophthalmoplegia.  In  such  a  case,  however,  the  paralysis  is  unilateral.  And  again,  the 
ophthalmic  branch  of  the  fifth  nerve  passes  throiigh  this  fissure,  and  may  be  affected 
by  an  osteo-syphiloma  of  the  sphenoidal  region  ;  when  such  is  the  case,  sensory 
troubles,  such  as  anjethesia  of  the  frontal  and  nasal  regions,  are  present  in  addition  to 
ophthalmoplegia.  In  the  present  case,  there  was  no  disturbance  of  sensation  in  the 
areas  supjilied  by  the  ophthalmic  nerve,  and,  moreover,  the  paralysis  was  bilateral,  a 
very  different  matter. 

Could  we  attiibute  the  ophthalmoplegia  to  a  syphiletic  lesion  at  the  base  of  the 
brain?  Syphilis  has  a  liking  for  the  basilar  region,  where  it  gives  rise  to  many 
lesions,  such  as  pachj-meningitis,  aneurysms  of  the  circle  of  WilUs,  centres  of  soften- 
ing, and  gummata  of  varying  numbers  and  dimensions.  If  the  syphiloma  develops 
at  the  posterior  part  of  the  interpeduncular  space  or  in  the  region  of  the  pons  and 
bulb,  and  especially  if  the  gummata  are  multiple,  several  of  the  oculo-motor  nerves  may 
be  affected  on  one  or  both  sides,  thereby  causing  associated  ocular  paralysis,  which  to 
some  extent  comes  under  the  heading  of  ophthalmoplegia. 

Had  we  sufficient  reasons  in  the  present  case  to  localize  the  lesion  at  the  base  of 
the  brain  ?  And,  moreover,  could  Ave  compare  the  ophthalmoplegia  in  tliis  case  with 
the  somewhat  incomplete  forms  of  ophthalmoplegia  originating  from  syphilitic 
basilar  lesions  ?  No.  On  analysing  the  recorded  cases  of  syi)hilitic  lesions  at  the  base 
of  the  brain  (lesions  foiind  2)oiit- mortem),  we  find  that  the  ocular  palsies  rarely  affect 
the  grouping  that  merits  the  name  of  ophthalmoplegia.  Furthennore,  they  are  always 
associated  with  other  conditions  ;    thus,  the  limbs  ai-e  affected  with  paralysis,  hemi- 


♦  Dieulafoy,  CUnique  Medicale  de  VHotel-Dieu,  lyotJ,  o^  volume,  8«  le9on. 


1332  TEXT-BOOK  OF  MEDICINE 

plegia,  contracture,  etc.,  sliowiug-  tliat  the  basilar  lesiou.  causing  tlie  ocular  paralysis, 
is  so  situated  that  it  has  also  compromised  the  pyramidal  tract  in  its  course  through 
the  peduncle,  the  pons,  or  the  bulb. 

The  case  in  question  was  quite  different.  In  the  first  place  the  ophthalmoplegia 
■was  complete  and  bilateral,  a  condition  not  met  with  in  syphilitic  lesions  of  the  base. 
In  the  second  place,  when  the  patient  was  first  examined,  the  ophthalmoplegia  had 
lasted  for  nine  months  without  any  trace  of  hemiplegia,  without  contracture,  without 
Babinski's  sign,  and  without  any  indication  of  a  lesion  in  the  pyi'amidal  tract. 

For  these  reasons  I  eliminated  the  hypothesis  of  a  lesion  at  the  base  of  the  brain, 
and  put  the  ophthalmoplegia  down  to  a  lesion  of  the  grey  nuclei  of  the  pons,  which 
are  the  true  origin  of  the  oculo -motor  nerves.  In  short,  my  diagnosis  was  polioen- 
cephalitis. It  was  easy  to  follow  the  course  of  events.  The  nuclear  masses  which 
supply  the  levatores  palpebrarum  (third  nerves)  were  involved  some  weeks  apart.  The 
masses  supplying  the  external  musculatui-e  of  the  eye  (third  and  f  oui-th  nerves)  were 
next  affected.  The  nuclei  of  the  sixth  pair  were  not  involved  and,  therefore,  the  eye- 
baU.-j  were  fixed  in  the  position  of  external  sti'abismiis. 

We  have,  so  far,  comsidered  only  the  ophthalmological  syndrome  ;  that  is,  only  one 
side  of  the  question,  because  the  patient  was  not  suffering  from  polioencephalitis 
limited  to  the  grey  nuclei  of  the  pons,  but  from  a  condition  which  had  also  invaded 
the  bulb.  Before  the  onset  of  the  ocular  paralysis  he  had  been  troubled  with  marked 
polyuria  and  polydipsia,  indicating  that  the  nucleus  in  the  bulb,  which  controls 
urination,  had  been  involved  before  the  nuclei  for  the  movements  of  the  eyes.  The 
polyuria  was  simple,  glycosuria,  phosphatui-ia,  and  azoturia  being  absent.  About  this 
time  severe  dy.sphagia  appeared,  and  an  ulcerating  gumma  was  found  on  the  right  side 
of  the  velum  palati  :  an  injection  of  grey  oil  was  given  every  week  and  the  ulcer 
healed.     Intense  headache  with  insomnia,  anorexia  and  wasting  was  present. 

The  situation  became  worse,  and  in  May,  1907,  the  patient  was  admitted  under 
Caussade.  The  ocular  symptoms  now  appeared:  injections  of  benzoate  of  mercury 
were  given.  At  the  end  of  June  it  was  clear  that  the  mischief  had  attacked  the  nuclei 
of  the  facial  and  glosso-pharyngeal  nerves  in  the  bulb.  The  velum  palati  was  para- 
lyzed, the  voice  became  nasal,  and  the  food  regurgitated  through  the  nose.  The  food- 
bolus  stuck  in  the  pharynx  because  the  consti-ictors  were  paralyzed,  and  a  most  painful 
feeling  of  strangulation  was  present.     It  was  necessary  to  pass  an  oesophageal  tube. 

As  a  tendency  to  syncope,  vertigo  and  vomiting  were  present,  it  was  thought  that 
the  nucleus  of  Deiters  was  involved.  The  patient  was  confined  to  his  bed  ;  he  was  fed 
with  the  tube  ;  he  could  not  hold  his  urine  or  his  fteces  ;  the  wasting  was  marked  and 
the  prognosis  most  grave.     An  injection  of  calomel  was  given  every  week. 

In  August  he  left  the  hospital,  feeling  better.  On  August  10,  Caussade  sent  him 
to  the  Hotel-Dieu.  On  admission,  ophthalmoplegia,  constant  thirst,  urine  6  to  7 
litres  in  the  day,  palato-pharyngeal  paralysis  present,  dysphagia,  regurgitation  of  food 
through  the  nose. 

Further  examination  revealed  glosso-Iabial  paralysis.  The  tongue  was  pushed  over 
to  the  right,  and  its  right  half  was  markedly  ati'ophied  (lesion  in  the  hypoglossal 
nucleus).  The  mouth  was  di-awn  over  to  the  left ;  whistling  or  blowing  out  a  candle 
impossible  (lesion  in  the  nucleus  of  the  facial  nerve). 

Marked  atrophy  of  the  upper  part  of  the  right  trapezius  showed  a  lesion  of  the 
spinal  accessory  nucleus.  The  right  shoulder  was  flattened  and  had  lost  its  firmness. 
Examination  of  the  muscles  showed  diminished  reaction  to  the  galvanic  current.  Such 
was  the  man's  condition  on  admission ;  not  a  brilliant  outlook.  For  reasons  already 
given,  my  diagnosis  was  bixlbo-pontine  polioencephalitis.  A  prognosis  was  also  neces- 
sary, since  polioencephalitis  is  not  without  danger.  "Was  the  patient  on  the  road  to 
tabes  ?  Was  he  threatened  with  amyotrophy,  or  with  progressive  muscular  ati-ophy  ? 
Had  he  not  to  fear  a  disastrous  retiu-n  of  giosso-labio-laryngeal  palsy  ? 


rOLIOENCKPHALTTIS  1333 

etiology-  Treatment.— Was  the  poliooncoplialiLis  in  this  caso 
syi»liilitic  ?  'llmt  the  patient  was  sypliiliLic,  was  certain.  Six  years 
beluie  ho  had  a  chancre  Ibllowecl  by  secondary  symptoms,  and,  later,  when 
the  ophthalmoplegia  appeared,  ho  had  suffered  from  tertiary  ulceration 
of  the  velum  palati.  And  again,  bearing  in  mind  the  remarkable  results 
obtained  by  specific  treatment,  the  natural  conclusion  was  that  the  lesion 
was  syphilitic. 

Indeed,  when  we  remember  the  usual  and  practically  fatal  course  of 
labio-glosso-laryngeal  paralysis,  as  described  in  the  classical  text-books,  it 
was  somewhat  surprising  that,  at  a  given  moment,  the  bulbo-pontine 
lesion  in  this  case  should  be  arrested  in  such  a  striking  manner;  this 
excellent  result  was  doubtless  attributable  to  the  treatment  employed. 

It  is  true  that  mercurial  treatment  was  not  at  first  successful,  and  that 
in  spite  of  injections  of  grey  oil,  of  calomel,  and  of  benzoate  of  mercury, 
the  malady  continued  its  course.  Notwithstanding,  Caussade  persisted 
with  the  treatment,  giving  further  injections  of  calomel,  until  at  the  end 
of  July  some  improvement  was  manifest;  the  headache  diminished,  the 
dysphagia  was  less  marked,  the  vomiting  became  less  frequent,  and 
strength  was  gradually  regained,  so  that  on  August  23  the  patient  left  the 
hospital.  During  September  and  October  twenty  inunctions  of  mercury 
were  given  ;  the  weight  increased  by  some  30  lbs. ;  but  the  bulbo-pontine 
syndrome  did  not  show  the  same  progress. 

When  the  patient  was  admitted  to  the  Hotel-Dieu  in  November,  1907, 
most  of  the  symptoms  were  still  present.  The  blepharoptosis  and  the 
ophthalmoplegia  showed  no  change,  the  thirst  was  severe,  and  the  urine 
amounted  to  6  or  7  litres  'per  diem ;  the  headache  came  back  at  intervals, 
the  palato-pharyngeal  paralysis  -had  by  no  means  disappeared,  liquids 
frequently  regurgitated  through  the  nose,  and  food  could  be  swallowed 
only  with  many  precautions,  passing  with  difficulty  through  the  pharynx, 
and  causing  a  most  painful  feeling  of  constriction.  The  tongue  was  atro- 
phied and  markedly  deviated  to  the  right  side,  the  left  angle  of  the  mouth 
was  drawn  outwards,  and  the  upper  part  of  the  trapezius  was  wasted ;  in 
short,  the  hope  of  recovery  from  the  polioencephalitis  was  most  slender, 
and  there  was  every  reason  to  fear  an  active  return  of  trouble. 

As  I  was  convinced  of  the  syphilitic  nature  of  the  lesion,  I  gave,  at 
short  intervals,  forty-seven  injections  of  biniodide  of  mercury  (^  to  \  of  a 
grain).  Genviine  improvement  was  soon  evident.  Early  in  December,  the 
eyes,  which  had  been,  so  to  speak,  fixed  in  the  orbit  for  ten  months,  began 
to  move  slightly.  The  eyelids  began  to  lift.  The  headache  disappeared. 
Deglutition  became  more  easy.  The  thirst  was  less  acute,  and  the  quantity 
of  urine  fell  to  4  litres  per  diem. 

In  January,  1908,  when  I  showed  the  patient  during  a  lecture  on  the 
n.  85 


1334  TEXT-BOOK  OF  MEDIOINE 

case,  the  improvement  was  astonishing.  The  paralysis  of  the  velum  palati 
and  pharynx  had  cleared  np.  The  voice  was  no  longer  nasal,  deglutition 
was  normal,  and  the  patient  could  whistle  (because  the  lips  were  no  longer 
paralyzed,  and  there  was  no  deviation  of  the  tongue);  the  blepharoptosis 
had  disappeared,  and  the  ophthalmoplegia  was  much  less  marked. 

On  November  11,  1908,  we  saw  him  again,  and  the  polioencephalitis 
was  practically  ciu-ed.  Strange  to  say,  the  muscular  atrophies  had  quite 
disappeared ;  the  power  of  contraction  was  equal  on  both  sides. 

The  above  case  is  not  unique.  Achard  has  published  the  case  of  a 
woman  suffering  from  visceral  syphilis  and  partial,  bilateral,  and  sym- 
metrical external  ophthalmoplegia.  The  paralysis  had  involved  on  each 
side  the  levator  palpebrse  and  also  the  internal  rectus,  the  superior  and 
inferior  recti,  and  the  two  obliques  being  affected  to  a  lesser  degree. 
Achard  diagnosed  syphilitic  polioencephalitis  of  the  pons,  and  gave  intra- 
venous injections  of  mercury  cyanide  in  doses  of  a  sixth  of  a  grain. 

The  result  was  "Prompt  improvement,  diminution  of  the  ptosis,  and 
increase  in  the  movements  of  the  eyeballs.  This  rapid  result  removed  all 
doubt  as  to  the  specific  nature  of  the  case.  After  a  fortnight's  interval 
eleven  fresh  injections  were  given,  as  well  as  thirty  grains  of  iodide  daily. 
The  ptosis  quite  disappeared,  the  eyeballs  regained  their  power  of  move- 
ment, and,  when  the  patient  left  the  hospital,  some  slight  weakness  in 
adduction  alone  remained  "  (Achard), 

Syphilitic  polioencephalitis  is,  therefore,  a  definite  entity,  revealing 
itself  by  ophthalmoplegia  and  by  bulbar  symptoms.  The  bulbar  symptoms 
and  the  ophthalmoplegia  may  occur  alone  or  in  association,  but  as  soon  as 
there  is  good  reason  to  suspect  that  the  polioencephalitis  is  syphilitic, 
specific  treatment  must  be  exhibited,  and  if  if  is  really  syphilitic  ia  nature, 
we  may  hope  for  success,  provided  the  treatment  be  timely,  sufficient  and 
protracted. 

As  yet  we  cannot  speak  definitely  regarding  606  ;  details  are  given  in 
the  Appendix,  but,  for  the  time  being,  we  have  in  mercurial  treatment  a 
powerful  method. 

In  my  case,  I  believe  death  would  have  ensued  but  for  the  mercurial 
treatment.  The  pathogenesis  of  certain  cases  of  polioencephalitis,  perhaps, 
requires  revision,  acquired  and  hereditary  syphilis  being  at  times  difficult 
to  recognize.  Perhaps,  too,  labio-glosso-laryngeal  paralysis,  a  progressively 
fatal  malady,  is  at  times  syphilitic  in  origin,  and  amenable,  therefore,  to 
specific  treatment. 


POLIENCEPHALJTIS  1335 


IV.  ACUTE  AND  SUBACttTE  POLIOENCEPHALITIS. 

The  description  of  glosso-labio-laryngeal  paralysis  and  of  nuclear  oph- 
thalmoplegia refers  to  the  chronic  form  of  polioencephalitis.  In  some 
cases,  however,  the  polioencephahtis  runs  an  acute  course,  and  generally 
proves  fatal  in  a  few  days,  while  in  other  cases  it  is  subacute,  and  more  often 
curable. 

The  acute  form  of  polioencephalitis  generally  appears  without  a  definite 
cause.  The  subacute  form  is  dependent  on  toxi-infectious  agents  (diph- 
theria, typhoid  fever,  scarlatina,  influenza,  measles,  and  pneumonia),  or 
on  toxic  substances  (alcohol,  nicotine,  lead,  oxide  of  carbon,  or  poisonous 
food).  In  these  cases  the  lesion  of  the  nuclei  is  associated  with  the  lesion 
of  the  nerves  (neuritis),  but  the  relative  importance  of  these  two  factors  is 
still  obscure. 

Under  Glosso-labio-laryngeal  Paralysis  I  have  already  described  the 
acute  fulminant  forms  of  inferior  bulbar  polioencephalitis.  Further  refer- 
ence is  therefore  unnecessary.  The  acute  form  of  superior  polioencephalitis 
remains  to  be  described. 

This  form  comes  rather  under  the  category  of  the  haemorrhagic  lesions — 
haemorrhage  into  the  walls  of  Sylvius's  aqueduct  and  into  the  third  ventricle. 
Wernicke,  who  in  1883  saw  three  cases,  has  called  this  lesion  hsemor- 
rhagic  superior  polioencephalitis.  Since  that  date  many  other  cases  have 
been  published  (Thomsen,  Kahler,  Kojewnikofi).  The  symptoms  of  this 
affection  reveal  themselves  by  acute  ophthalmoplegia,  which  is  far  more 
serious  than  in  the  chronic  form.  The  paralysis  rapidly  involves  the 
external  muscles  of  the  eye,  with  or  without  participation  of  the  intrinsic 
muscles.  It  is  often  accompanied  by  bulbar  paralysis,  which  may  prove 
quickly  fatal.  Often,  also,  grave  cerebral  phenomena  supervene,  such  as 
vertigo,  intense  headache,  and  vomiting,  with  invincible  somnolence.  This 
condition  has  nothing  in  common  with  coma,  but  resembles  the  strange 
disease  known  as  sleeping  sickness.  The  patient  is  apathetic,  indifferent 
to  every  stimulus,  and  chained  to  his  bed  by  extreme  weakness,  although 
the  limbs  are  not  paralyzed.  The  patient  sinks  into  collapse,  and  dies  in 
less  than  three  weeks. 

What  are  the  lesions  in  this  acute  form  ?  Is  it  a  process  differing  in 
its  mode  of  evolution,  but  analogous  in  its  systematic  nuclear  distribution 
to  the  process  of  the  chronic  form  ?  Wernicke,  Thomsen,  Kojewnikoff,  and 
Charcot's  school  have  adopted  this  view.  Acute  ophthalmoplegia  is  said  to 
be  the  reproduction  of  acute  bulbar  paralysis  and  of  acute  anterior  spinal 
paralysis,  but  it  has  not  been  proved  that  this  opinion  is  exact.  The  results 
of  post-mortem  examinations  published  by  Thomsen,  by  Kojewnikoff,  and 

85—2 


1336  TEXT-BOOK  OF  MEDICINE. 

by  Wernicke  himself,  show  that  the  lesion  was  not  seated  in  the  nuclei  of 
the  pons  and  crura,  or  only  affected  them  in  a  secondary  manner.  The 
lesion,  in  the  shape  of  microscopic  haemorrhages,  affected  the  subependymal 
grey  matter  in  the  walls  of  the  third  ventricle,  of  Sylvius's  aqueduct,  and  of 
the  fourth  ventricle,  cutting  off  the  nuclei.  Acute  ophthalmoplegia  in  the 
grave  form,  described  by  Wernicke  as  haemorrhagic  polioencephalitis^ 
would  not  then  be  of  nuclear  origin,  but  would  belong  to  the  obscure 
group  of  supranuclear  ophthalmoplegias.  It  sometimes  appears  to  be 
associated  with  alcoholism. 

V.  WE  BEE'S  SYNDEOME— BONNIER'S  SYNDEOME. 

Certain  lesions  of  the  pons  and  crura  are  due  to  external  causes  (ex- 
ostoses of  the  base  of  the  skull,  aneurysm  of  the  basilar  artery)  or  to  in- 
ternal causes  (tubercles,  syphilitic  gummata,  hsemorrhage,  and  softening). 
The  tubercles  may  reach  the  size  of  a  pea  or  of  a  hazel-nut.  The  haemor- 
rhages arise  under  similar  conditions  to  those  causing  cerebral  haemor- 
rhage. The  sclerosis  is  generally  associated  with  insular  sclerosis  or  with  a 
descending  sclerosis. 

Description. — According  as  the  lesion  is  sudden  (haemorrhage,  em- 
bolism) or  slow  (tumours)  in  its  evolution,  the  symptoms  are  sudden  or 
progressive.  Certain  of  these  sym.ptoms,  such  as  headache,  apoplexy,  and 
convulsions,  are  common  to  many  cerebral  lesions,  but  there  are  others 
which  are  more  especially  peculiar  to  the  lesions  of  the  pons  and  crura. 
The  latter  show  the  following  characteristics  :  (1)  crossed  paralysis  (2)  fre- 
quent sensory  troubles. 

In  crossed  paralysis  the  limbs  on  one  side  and  the  face  on  the  other  side 
are  affected.  To  give  an  example,  the  arm  and  the  leg  are  paralyzed  on  the 
left  side,  whilst  the  paralysis  on  the  right  side  attacks  the  face  (facial  hemi- 
plegia) and  the  external  rectus  (converging  strabismus),  or  the  sensory 
portion  of  the  trigeminal  nerve  (facial  hemianaesthesia). 

Weber's  Syndrome. — A  most  remarkable  form  of  crossed  paralysis  is 
that  which  bears  the  name  of  Weber's  syndrome.  This  syndrome,  due  to 
a  lesion  of  the  inferior  and  interior  part  of  the  cerebral  peduncle,  is  con- 
stituted by  paralysis  of  the  common  oculo-motor  nerve  on  one  side  (side  of 
the  lesion),  and  by  paralj'sis  of  the  limbs  and  of  the  facial  and  the  hypo- 
glossal nerves  on  the  opposite  side  (crossed  paralysis  on  the  side  opposed  to 
the  lesion).  Clinically,  peduncular  haemorrhage  behaves  like  cerebral 
haemorrhage.  The  paralysis  of  the  common  oculo-motor  nerve  is  either 
partial  or  total.  When  it  is  partial,  the  internal  musculature  of  the  eye  is 
normal.  The  different  partial  paralyses  of  the  eye  are  due  to  the  fanlike 
dLsposition  of  the  root  fibres  of  the  nerve  in  the  interior  of  the  peduncles. 


rOLIENCEPHALITIS  ISST 

The  j);ual3'sis  is  only  total  wlicii  tlu;  h^sion  is  very  extensive,  or  wlien  it 
affects  the  trunk  of  the  common  oculo-niotor  nerve  near  its  emergence  from 
the  podunclc,  after  it  has  already  received  tlie  nerve  fihres  for  the  internal 
musculature  of  the  eye. 

In  these  cases  of  alternate  ])aralysis,  the  paralysis  of  the  limbs  is  on  the 
opposite  side  to  the  lesion,  whilst  the  paralysis  of  the  face  is  direct — that  is, 
on  tlie  same  side  as  the  lesion.  This  fact  admits  of  an  easy  interj)retation  : 
any  lesion  above  the  neck  of  the  bulb  gives  rise  to  crossed  hemiplegia,  be- 
cause the  motor  fibres  for  the  limbs  cross  in  the  region  of  the  bullj,  whilst 


Red  nucleus 
Locus  niger 
N  eentraUs  superior 
N  of  the  pons 

Fifth  nerve  (motor) 
Fifth  nerve  (sensory) 
Superior  olivary  body 

Facial  nerves 

Trapezoid  nucleus 
Auditory  nerves 


_Ui)lith:ilmic  nerves 

^Extomal  geniculate  body 

•Snterlor  corpora  quadrigemina 
Oculo-motor  nerves 

Corpus  parabigeminiim 

Foiu-th  nerves 

Posterior  corpora  quadrigemi)ia 

Reticulate  nucleus 

Fifth  nerves 

Locus  coeruleus 
Sixth  nerves 

.— r  Fifth  nerves 


Inferior  olivary  body 
N.  centralis  inferior 

Respiratory  nucleus 

Glosso-pharyngeal  nerves 

Nucleus  ambiguus 


Fifth  nerves 
Anterior  lateral  nucleus 
Spinal  accessory  nerves 


Small-celled  nucleus  of  auditory  nerve 
Tubcrculum  acusticum 
Internal  nucleus  of  auditory  nerve 
Deiters'  nucleus 


Nucleus  of  restiform  body 
Nucleus  of  funiculus  teres 


?■  Hypoglossal  nerves 

Vagus  nerve 

*  <•  Sh  Cuneiform  nucleus 
Nucleus  gracilis 

Posterior  lateral  nucleus 


j^iG.  60. — Nuclei  nsr  the  Medulla  and  the  Pons. 


a  lesion  of  the  nerves  arising  from  the  pons  or  from  the  bulb  gives  rise  to  direct 
paralysis.  In  crossed  paralysis  the  lesiou  must  affect  at  the  same  time 
the  motor  tracts  of  the  limbs  (they  are  situated  in  the  anterior  portion  of 
the  pons)  and  the  nuclei  of  the  sixth,  seventh,  and  eighth  nerves  ;  and  if 
the  tumour  in  the  pons  encroach  slightly  backwards  into  the  bulb,  it 
meets  with  the  nuclei  described  under  Griosso-labio-laryngeal  Paralysis,  and 
causes  the  symptoms  due  to  a  lesion  of  these  nerves.  A  patch  of  sclerosis 
uniting  the  bulbar  and  peduncular  centres  might  cause  a  variety  of  alter- 
nate paralysis  with  Weber's  syndrome  (paralysis  of  the  right  oculo-motor 


1338  TEXT-BOOK  OF  MEDICINE 

nerve  and  left  hemiplegia),  to  which  would  be  added  right  neuro-paralytic 
keratitis,  with  ansesthesia  of  the  right  trigeminal  nerve. 

Sensory  troubles  are  fairly  common  in  lesions  of  the  pons.  A  special 
hemianaesthesia,  due  to  the  lesion  of  the  posterior  bundle  of  the  pons, 
which  transmits  sensory  impressions,  may  be  observed.  The  hemianaesthesia 
of  the  hmbs  is  crossed  like  the  hemiplegia ;  the  hemiansesthesia  of 
the  face,  of  the  tongue,  and  of  hearing  is  direct.  The  preservation  of 
sight  and  of  smeU  enables  us  to  differentiate  pontine  hemiansesthesia  from 
hemiansesthesia  of  cerebral  origin.  In  a  case  of  alternate  hemiailcesthesia 
of  embolic  origin  in  a  patient  suffering  from,  heart  disease,  Raymond  was 
able  to  localize  the  lesion  exactly.  The  focus  was  seated  in  the  pons  at  the 
point  where  Reil's  band  approaches  the  sensory  fibres  of  the  trigeminal  nerve. 

Bonnier's  Syndrome. — Bonnier  has  recently  described  a  new  bulbar 
syndrome,  dependent  on  lesions  of  Deiters'  nucleus,  with  accompanying 
symptoms,  due  to  intermediate  radiations.  This  nucleus,  which  is  fairly 
large  and  deeply  situated  in  the  bulb,  is  one  of  the  most  important  centres 
of  the  vestibular  root  of  the  eighth  nerve.  Besides  its  situation  among  the 
fibres  and  the  nuclei,  placed  in  series  from  the  pons  to  the  cord,  it  is  in  direct 
anatomical  and  functional  relation  with  the  nuclear  systems  of  the  auditory 
centres,  the  trigeminal  nerve,  the  oculo-motor,  glosso-pharyngeal,  pneumo- 
gastric,  and  general  vasomotor  centres,  and  the  neighbouring  respiratory 
centres.  It  is  likewise  in  immediate  relation  with  the  cerebellum  and  with 
the  ascending  parietal  convolution.  The  cardinal  symptom  is  vertigo, 
with  partial  or  total  loss  of  the  power  to  maintain  the  vertical  position. 
The  accompanying  symptoms  are  :  (1)  Oculo-motor  troubles,  of  varying 
severity  and  duration — ^myosis,  mydriasis,  nystagmus,  troubles  of  accom- 
modation, diplopia,  binocular  and  uniocular  triplopia,  etc.  ;  (2)  pain  in  the 
region  of  the  superior  trigeminal  branch — orbital,  temporal,  tympanic,  or 
vertical  neuralgia ;  (3)  auditory  troubles — deafness  and  paroxysmal  buzzings 
in  the  ear ;  (4)  nausea,  thirst,  and  anorexia,  all  of  which  are  paroxysmal ; 
(5)  pneumogastric  troubles,  dyspnoea,  tachycardia,  or  bradycardia ;  or,  on 
the  contrary,  a  feeling  that  the  respiration  is  quickened ;  (6)  secretory, 
circulatory,  and  thermic  troubles. 

Certain  troubles  remain  unilateral,  but  the  oculo-motor  phenomena  may 
be  crossed.  Bonnier's  sylidrome  may  be  the  first  index  of  a  bulbar  affec- 
tion.   It  may  coexist  with  albuminuria,  glycosuria,  sick  headache,  and  tabes. 

I  had  in  my  wards  a  woman  who  was  suffering  from  glycosuria,  tem- 
porary diplopia,  and  from  the  above  syndrome.  I  expressed  the  opinion 
that  the  patient  was  suffering  from  a  lesion  of  Deiters'  nucleus. 

She  died  suddenly,  and  at  the  post-mortem  examination  we  actually 
did  find  foci  of  softening  in  Deiters'  nucleus  and  obliterating  endarteritis. 


CHAPTER  III 
DISEASES  OF  THE  CEREBELLUM 

ABSCESS,  TUMOURS,  AND  SYPHILIS  OF  THE 
CEREBELLUM. 

In  this  chapter  I  shall  especially  consider  abscesses  of  the  cerebellum, 
quoting  from  my  communication  to  the  Academic  de  Medecine.*  The 
other  lesions  of  the  cerebellum  (tumours,  haemorrhage,  and  syphilis)  will 
be  considered  when  the  diagnosis  is  discussed.  The  following  case  sums 
up  the  question  : 

On  May  7  a  man  was  admitted  for  violent  headache  and  attacks  of  vertigo. 
Wlxilst  he  was  walking  up  to  the  ward,  he  was  seized  with  vertigo,  and  fell  doT^n  as  if 
in  an  epileptic  fit.  His  body  was  thrown  violently  towards  the  left,  and  in  his  fall  the 
left  side  of  the  head  received  the  shock.  Xext  day  a  large  bruise  appeared  round 
the  left  eye,  and  spread  to  the  eyelids,  the  supra-orbital  region,  and  the  right  eye. 
The  ecchymosed  parts  were  bluish  and  swollen,  and  the  left  eyeball  was  hidden  b^- 
the  swollen  eyeUd.  The  patient  was  much  depressed — not  on  account  of  his  fall,  but 
on  account  of  his  previous  condition.  Although  his  answers  were  slow,  he  could, 
nevertheless,  give  some  precise  details  concerning  his  illness.  He  came  to  the  hospital 
because  for  the  past  twelve  days  or  so  he  had  suffered  from  violent  pains  in  the  occipital 
region,  the  neck,  the  forehead,  and  the  vertex.  His  sufferings  lasted  day  and  night. 
Furthermore,  on  making  a  movement,  or  even  without  appreciable  cause,  severe  stabbing 
pains  supervened.  By  pressure  and  percussion  we  discovered  that  the  chief  seat  of  the 
pain  was  in  the  occipital  region.  The  pain  was  not  superficial,  as  in  neiiralgia,  and  had 
not  the  characteristics  of  syphilitic  osteoperiostitis.  It  was  a  deep-seated  headache, 
with  radiations  and  paroxysms. 

Soon  after  the  headache  vertigo  appeared.  The  sensation  of  giddiness  occurred 
several  times  a  day.  Sometimes  objects  seemed  to  tarn  in  various  directions ;  at  other 
times  the  patient  seemed  to  be  drawn  by  oscillatory  movements  to  the  right  and  left. 
These  attacks  of  vertigo  were  increased  by  standing  or  walking.  They  grew  less  when 
he  sat  down,  and  disappeared  when  he  lay  in  bed.  The  vertigo  was  accompanied  by  a 
loss  of  equilibrium,  which  made  his  gait  like  that  of  a  drunken  man.  He  walked  with 
his  legs  apart,  stopping  at  times  to  gain  a  point  of  support. 

A  stroke  occurred  on  May  3,  the  patient  being  thrown  to  the  right.  A  fresh  stroke, 
with  a  fall  to  the  left,  occurred  on  his  admission  to  the  Hotel-Dieu.  For  the  past  three 
days  he  had  suffered  from  spontaneous  vomiting.  The  most  trifling  causes,  such  as  a 
change  of  position,  rising  or  sitting  down,  brought  on  the  vomiting.  Nothing  was 
noticed  so  far  as  the  Umbs  were  concerned-     The  movements  were  free,  though  slow. 

*  Dieulafoy,  "  Les  Abces  du  Cervelet,"  communication  a  I'Academie  de  Medecine. 
seance  du  19  Juin,  1900. 

1.3.39 


1340  TEXT-BOOK  OF  MEDICINE 

The  case  might  have  been  taken  for  one  of  muscular  asthenia.  No  paralysis,  no  con- 
tractures, no  tremors,  no  epileptiform  fits,  and  no  anaesthesia.  The  face  and  the  organs 
of  the  senses  were,  for  the  time  being,  not  aiiected.  The  senses  of  hearing  and  smell 
were  normal.  Neither  facial  nor  ocular  paralysis  was  noticed.  There  was  no  nystag- 
mus. The  right  pupil  reacted  well  to  hght  and  to  accommodation.  There  was 
neither  myosis  nor  mydriasis.  Speech  was  normal,  though  slow.  It  was  neither 
stuttering  nor  scanning.  Respiration  and  deglutition  were  not  affected.  The  inteUi- 
gence  was  intact.  It  was,  however,  necessary  to  repeat  a  question  in  order  to  get  an 
answer.  The  patient  was  drowsy,  and  lay  in  the  dorsal  decubitus.  The  urinary  func- 
tions were  normal,  the  urine  containing  neither  albumin  nor  sugar.  The  pulse-rate, 
which  was  slow  at  the  time  of  his  admission,  in  a  few  days  increased  from  56  to  lOS. 
The  temperature  did  not  rise  above  101°  F. 

To  sum  up,  the  patient,  who  had  been  iU  for  about  twelve  days,  was  first  seized 
with  violent  occipital  headache,  followed  by  severe  vertigo,  loss  of  equiUbrium,  and 
repeated  fits  of  vomiting.  I,  therefore,  had  no  hesitation  in  diagnosing  a  lesion  of 
the  cerebellum.  Meniere's  disease,  meningitis,  tumours  of  the  brain  and  of  the  mesen- 
cephalon were  in  turn  eHminated.  There  was  no  question  of  cerebro -spinal  meningitis, 
Kernig's  sign  being  absent  and  lumbar  puncture  negative.  It  was,  therefore,  logical  to 
admit  a  lesion  of  the  cerebellum,  but  we  had  stiU  to  discover  its  nature.  In  such  a  case 
abscess  of  the  cerebellum  must  be  first  considered.  It  frequently  foUows  acute  or 
chronic  otitis.  The  patient  was  asked  several  times  whether  he  had  ever  had  pains  in 
the  ears  or  purulent  discharge.  The  answer  was  negative,  rurthermore,  our  examina- 
tion showed  that  his  hearing  was  normal.  Pressure  on  the  mastoid  region  caused  no 
pain.     The  patient  had  no  fever.     We  had,  therefore,  to  find  some  other  cause. 

It  was  not  a  case  of  cerebellar  hjemorrhage,  because  the  symptoms  had  been  neither 
sudden  nor  simultaneous.  They  had  been  successive  and  progressive,  taking  twelve 
days  to  reach  their  maximum.  It  might  have  been  tuberculosis  (large  tubercle  of  the 
nerve  centres),  which  had  so  far  been  latent,  although  the  patient  was  not  tubercular. 
The  probabilities  were  against  ghoma  or  sarcoma,  because  in  these  tumours  the  appear- 
ance of  the  symptoms  is  much  more  sjiaced  out.  Was  it  a  syphihtic  lesion  of  the  cere- 
bellum, gumma,  or  obhterating  arteritis  ?  The  patient  denied  syphUis,  and  showed 
no  stigmata.  As  everything  is  possible  in  syphilis,  however,  I  ordered  a  daily  injection 
of  biniodide  of  mercury. 

During  May  8,  9,  and  10  the  situation  grew  worse.  The  torpor  became  more  marked, 
and  the  patient  lay  on  his  back  absolutely  motionless.  At  night  he  was  restless  and 
dehrious,  and — an  important  fact — the  left  labial  commissure  was  paretic.  As  the 
treatment  made  no  difference,  I  asked  Marion  to  see  the  case. 

On  May  111  requested  Brissaud  to  give  me  his  opinion.  He  at  once  admitted  the 
diagnosis  of  a  lesion  in  the  cerebellum.  In  addition  to  the  cerebellar  syndrome  already 
described,  we  noticed  ocular  symptoms  which  did  not  exist  at  the  time  of  the  patient's 
admission — nystagmus  and  paresis  of  the  left  external  oculo -motor  nerve.  The  paresis 
of  the  left  labial  commissure  had  also  become  more  marked.  Ophthalmoscopic  examina- 
tion showed,  on  the  right  side,  haemorrhage  into  the  retina,  and  on  the  left  optic  neioritis. 
The  knee-jerks  were  abohshed.  The  patient,  who  was  sunk  in  coma  vigil,  rephed  only 
with  great  difficulty.  Everything  pointed  to  a  fatal  termination,  and  Brissaud  and 
myseK  were  of  opinion  that  the  only  chance  of  salvation  lay  in  surgical  intervention. 

The  operation  was  therefore  fixed  for  the  next  morning,  Saturday,  and  Marion  asked 
us  a  question  of  the  utmost  importance  :  "  On  which  side  of  the  cerebellum  was  the 
lesion  seated  ?"  This  question  required  an  answer,  but  on  what  were  we  to  base  the 
diagnosis  of  the  locahzation  ?  As  headaches,  vertigo,  staggering  gait,  vomiting,  and 
nystagmus  are  symptoms  common  to  the  cerebellar  lesions  of  both  lobes  and  of  the 
vermis,  they  were  of  no  help  in  locahzing  the  lesion  either  on  the  right  or  on  the  left 
side.     The  state  of  the  eyes  (neuritis  and  retinal  haemorrhages)  was  of  no  value,  because 


DISEASES  OF  THE  CEREBELLUM  1P.41 

both  eyes  wore  afifoctod.  The  stroke  and  falling  of  the  patient  to  the  loft  were  valueless 
as  a  few  days  pioviousiy  a  similar  stroke  had  thrown  the  patient  to  the  right.  Two  signs 
helped  us  in  the  tupograpliic-.i!  diagnosis  of  locaUzation — the  paresis  of  the  left  external 
oculomotor  norvo  and  of  the  loft  facial  nerve.  Apart  from  tlio  paresis  of  the  left  labial 
commissure,  which  was  three  days  old,  Brissaud  was  struck  by  the  flaccidity  of  the  left 
oheek.     The  lesion  was,  therefore,  in  the  loft  lobe  of  the  corebollura. 

Under  ether  .Marion  trephined  in  three  places — over  the  left  fos.sa  of  the  cerebellum — 
two  below  and  one  above,  at  the  angles  of  au  isosceles  triangle.  At  this  moment  the 
respiration  ceased.  The  heart  continued  to  beat,  but  the  beats  soon  grew  weak,  and 
then  stopped.  For  ten  minutes  every  means  was  used  to  restore  respiration.  Rhyth- 
mical traction  on  the  tongue  had  no  re.sult.  Marion,  in  the  hope  of  lessening  the  intra- 
cranial pressure,  opened  up  the  inner  table,  incised  the  dura  mater,  and  exposed  the 
cerebellum.  The  pulse  came  back.  The  patient  was,  therefore,  not  quite  dead,  although 
he  had  not  breathed  for  twenty  minutes. 

On  opening  the  skull  no  lesion  was  seen,  the  meninges  being  normal  and  the  cere- 
bellum appearing  to  be  healthy.  Marion  explored  in  every  direction,  and  during  this 
exploration  his  finger  touched  against  the  posterior  surface  of  the  bulb.  Immediately, 
to  the  surprise  of  those  present,  the  patient  made  a  long  and  noisy  inspiration.  Wlien 
the  finger  was  withdrawn,  the  respiration  at  once  stopped.  The  finger  being  again 
pushed  against  the  posterior  surface  of  the  bulb,  the  inspirations  reappeared  and  kept 
on,  but  they  ceased  as  soon  as  the  compression  of  the  bulb  ceased.  Similar  experiments 
were  made  several  times  following,  with  the  same  result,  and  in  the  end  the  respiration 
was  definitely  re-established. 

The  patient  was  dressed  and  taken  back  to  bed.  During  the  day  his  condition  was 
about  the  same  as  before  the  operation.  He  replied  with  difficulty,  the  respiration  was 
normal,  and  the  pulse  was  120.  Next  day  his  wife  told  us  that  her  husband,  a  month 
before  his  ilhiess,  had  complained  of  pains  in  the  left  ear,  followed  by  discharge.  The 
patient  had,  therefore,  had  otitis  after  all,  although  he  had  denied  it,  thus  withholding 
valuable  information.  The  otitis  had  been  neither  severe  nor  obstinate,  because  the 
patient  had  lost  all  recollection  of  it.  It  was  evident  that  the  lesion  on  the  left  side  of 
the  cere1>ellum,  as  shown  by  the  cerebellar  syndrome,  was  an  abscess  following  on  otitis. 
Although  the  condition  of  the  patient  had  grown  worse,  several  punctures  of  the  cere- 
bellum were  made  in  the  hope  of  striking  the  pus.  We  were  not  successful,  and  the 
patient  died  during  the  day. 

This  final  result  left  me  uneasy.  I  asked  myself  whether  there  had  been  a  flaw  in 
the  diagnosis.  Was  the  cerebellar  lesion  really  on  the  left  side,  and  had  we  told  the 
surgeon  correctly  in  pointing  out  to  him  the  left  lobe  of  the  cerebellum  as  the  sphere 
for  action  ?     The  post-mortem  examination  removed  this  doubt. 

The  abscess  was  of  the  size  of  a  large  hazel-nut,  and  was  seated  in  the  anterior  region  of 
the  left  lobe  (which  is  the  most  usual  place).  It  had  developed  in  the  white  matter,  not  in 
the  centre,  but  between  the  dentate  nucleus  and  the  cortical  grey  matter,  a  little  upwards 
and  outwards.     The  punctures  had  passed  quite  close  to  the  abscess  without  reaching  it. 

This  abscess,  which  was  of  recent  formation  and  non-encysted,  contained  2  grammes 
of  greenish  creamy  pus.  The  pneumococcus  was  the  only  pathogenic  agent,  and  even 
then  the  pneumococcus  was  not  at  all  abundant.  It  had  lost  its  virulence,  for  cultures 
remained  sterile,  and  did  not  'cause  death  when  inoculated  into  a  mouse. 

The  abscess  was  the  only  lesion  present,  the  remainder  of  the  cerebellum,  the  cere- 
brum, and  the  mesencephalon  being  healthy.  There  was  not  a  trace  of  meningitis. 
The  sinuses  were  healthy ;  the  petrous  bone  was  normal.  The  abscess  could  not,  there- 
fore, be  explained  by  the  contiguity  of  the  lesions.  It  was,  indeed,  a  "  remote  abscess," 
comparable  with  the  remote  abscesses  of  appendicitis,  and  had  no  apparent  connection 
with  the  original  focus.  The  otitis  had  been  cured,  sections  of  the  middle  and  of  the 
internal  ear  revealing  no  lesions. 


1342  TEXT-BOOK  OF  MEDICINE 

Pathogenesis. — The  first  point  to  note  is  :  mild  otitis  may  in  a  few  weeks 
produce  a  fatal  abscess  in  the  cerebellum,  just  as  mild  appendicitis  may 
in  a  few  weeks  cause  suppuration  in  the  liver*  and  in  the  pleura. f  In  this 
case  the  otitis  had  only  lasted  a  few  days,  and  was  so  slight  that  the  patient 
had  no  recollection  of  it,  and  yet  it  had  started  the  remote  abscess  in  the 
cerebellum. 

Otitis  is  rightly  considered  to  be  the  most  common  cause  of  cerebellar 
abscesses.  The  cause  of  the  otitis  (angina,  coryza,  measles,  influenza, 
pneumonia,  etc.),  and  the  kind  of  organism  (pneumococcus,  streptococcus, 
staphylococcus,  etc.),  as  well  as  the  duration  and  course,  are  of  minor  im- 
portance. When  the  tympanum  is  infected,  abscess  of  the  cerebellum  or 
of  the  cerebrum  may  foUow.  In  some  cases,  as  in  my  patient,  the  otitis  is 
recent,  and  the  abscess  forms  a  few  weeks  later.  In  other  cases  the  cere- 
bellar infection  supervenes  in  people  who  have  for  many  years  been  suffering 
from  chronic  otitis.  In  Chatelier's  patient,  with  a  cerebellar  abscess  at  the 
age  of  twenty-six,  the  otitis  commenced  in  infancy.  In  a  case  quoted  by 
Netter  and  Delpeuch  the  cerebellar  abscess  appeared  at  the  age  of  sixteen, 
while  otitis  had  existed  since  the  age  of  three  years. 

These  quotations  are  sufiicient  to  prove  that  any  case  of  otitis  can  cause 
a  cerebellar  abscess,  and  that  the  otitis  may  date  back  a  few  weeks,  or  even 
thirty  to  forty  years.  The  pain  in  the  ear  may  be  acute  or  moderate  ;  the 
running  may  be  abundant,  slight,  or  intermittent,  and  the  hearing  may  be 
more  or  less  affected.  But  when  the  tympanum  is  infected,  and  remains 
infected,  cerebellar  and  cerebral  abscesses  are  to  be  feared.  It  is  a  question  of 
exaltation  of  the  virulence  in  a  closed  cavity,  the  pathogenesis  being  the 
same  as  in  appendicitis,  as  I  showed  in  my  first  communication  on  appendi- 
citis to  the-  Academic. 

The  course  of  events  is  as  follows  :  The  middle  ear  is  infected  through 
the  Eustachian  tube.  If  the  tube  is  obliterated,  a  closed  cavity  is  formed, 
and,  by  a  general  law  of  pathology,  exaltation  of  the  virulence  generally 
foUows.  Perforation  of  the  membrana  tympani,  or  removal  of  the  obstruc- 
tion in  the  tube,  may  suppress  the  closed  cavity,  and  complications  are 
warded  off  for  a  time.  Thfe  antrum  and  the  mastoid  cells,  however,  lend 
themselves  admirably  to  the  formation  of  secondary  closed  cavities  at  a 
more  or  less  distant  interval ;  and  then  the  migration  of  organisms,  with  or 
without  lesions  in  the  petrous  bone,  may  lead  to  a  series  of  complications — 
phlebitis  and  thrombosis  of  the  sinuses  (especially  of  the  lateral  sinus), 
diffuse  or  localized  meningitis,  pachymeningitis,  cerebro-spinal  meningitis, 
and  abscess   of    the   cerebellum   and   cerebrum.      In  these  cases,   as  in 

*  Dieulafoy,  Clinique  Medicale  de  V Hotd-Dieu,  tome  ii.,  p.  167. 

t  Dieulafoy.     Communication  a  I'Academie  de  Medecine,  10  Avril,  1900. 


DISEASES  OF  THE  CEREBELLUM 


1343 


appendicitis,  the  lesions  may  be  brought  about  by  contiguity,  r)r  may  be 
remote. 

The  otic  infection,  elaborated  in  the  closed  cavity,  may  spread  in  various 
directions.  Spread  of  infection  downwards  and  outwards  through  the 
external  table  of  the  mastoid  process  and  through  the  inferior  wall  of  the 
mastoid  cells  may  lead  to  an  abscess  of  the  neck  (De  Quervain).  Spread 
of  infection  through  the  roof  of  the  t>Tnpanum  and  backwards  along  the 
groove  of  the  transverse  sinus  may  end  in  multiple  intracranial  lesions. 


Fig.  G1. — Section  theottgh  the  Ear. 

T,  Membrana  tympani ;  CT,  cavity  of  tympanum  ;  E,  Eustachian  tube  ;  A,  adenoid 
tissue  around  the  tube ;  NA,  cochlear  nerve  ;  NT  and  NL,  vestibular  nerves  ;  F  and 
OE,  fibres  communicating  with  the  nucleus  of  the  facial  nerve  (F)  and  the  sixth 
nerve  (OE) ;  P,  pons  ;  C,  cerebellum  ;  V,  expansion  of  the  vestibular  nerve  in  the 
cerebellum  ;  L,  labyrinth ;  AjM,  mastoid  antrum  ;  S,  lateral  sinus. 

The  organisms  passing  through  the  roof  of  the  tympanum  cause  abscesses  of 
the  brain,  whilst  the  organisms  passing  through  the  posterior  surface  of 
the  petrous  bone  and  of  the  mastoid  process  cause  abscesses  of  the  cere- 
bellum. 

These  routes  of  migration  are,  however,  not  always  followed  when  the 
suppuration  takes  place  by  continuity,  and,  according  to  the  judicious  remark 
of  Picque  and  Mauclaire,  the  germs  may  take  any  direction,  no  matter  what 
is  the  initial  point  of  departure. 

In  most  cases  the  cerebellar  abscess  does  not  exist  as  an  isolated  lesion, 


1344 


TEXT-BOOK  OF  MEDICINE 


but  is  associated  with  other  intracranial  lesions  which  precede  or  follow  it. 
Amongst  these  lesions  I  shall  especially  mention  caries  and  necrosis  of  the 
bones,  pachymeningitis,  and  phlebitis  of  the  sinuses,  especially  of  the  lateral 
sinus,  which  is  attacked  in  half  of  the  number  of  cases  (Picque  and  Mauclaire). 
Abscess  of  the  cerebellum  (jften  provokes  neighbouring  lesions.  The 
more  marked  these  lesions  are,  the  less  chance  of  success  has  surgical  inter- 
vention. The  following  statistical  table  of  Paul  Koch,  in  sixty-four  cases  of 
abscess  of  the  cerebellum,  verified  by  post-mortem  examination,  shows  that 
forty-four  times  the  cerebellar  abscess  had  caused  lesions  in  the  vicinity. 


Purulent  meningitis,  consequent  on  perforation  of  the  abscess  into 

the  arachnoid  membranes 
Purulent  meningitis  by  infiltration    . . 
Sero-fibrinous  meningitis,  continuous  with  the  abscess 
Meningeal  hypersemia 

Opening  of  the  abscess  into  the  fourth  ventricle 
Free  opening  of  the  abscess . . 
Diffuse  encephahtis 
Ai'ea  of  softening  around  the  abscess . . 
Abscess,  having  perforated  the  dura  mater 
Tissues  apparently  healthy  around  the  abscess  , 


7 
3 
5 
3 
3 
4 
2 
7 
9 
21 


times. 


The  interesting  point  in  the  case  quoted  is  that  the  cerebellar  abscess 
was  single,  not  large,  clearly  localized  in  the  white  matter  of  the  left  cere- 
bellum, and  unaccompanied  by  any  other  lesion.  Cerebrum,  mesen- 
cephalon, meninges,  sinuses,  bones,  and  nerves  were  all  healthy.  We  may, 
therefore,  be  quite  certain  that  amongst  the  numerous  symptoms  present 
in  this  case  there  was  no  symptom  due  to  a  neighbouring  lesion.  The  cere- 
bellar syndrome  existed  in  a  state  of  purity,  and  the  case  was,  therefore,  most 
favourable  for  the  clinical  study  of  this  syndrome.  As  a  matter  of  fact, 
when  a  lesion  of  the  cerebellum  tends  to  become  external  (this  is  very 
common  in  the  case  of  glioma,  gliosarcoma,  tuberculoma,  or  parasitic 
tumour),  the  proper  symptoms  of  the  lesion  of  the  cerebellum  are  often 
masked  by  other  symptoms  (crossed  paralysis,  spasms,  etc.),  due  to  the 
lesions  or  to  the  irritation  of  the  neighbouring  organs,  and  the  result  is 
that  the  cerebellar  syndrome  is  rendered  obscure.  This  remark  also 
holds  good  if  the  cerebellar  abscess  is  associated  with  other  neighbouring 
lesions  (abscess  of  the  brain,  pachymeningitis,  abscess  of  the  dura  mater, 
phlebitis,  and  thrombosis  of  the  lateral  siims).  In  such  a  case  the  cerebellar 
syndrome  is  also  defaced. 

In  my  patient,  on  the  contrary,  the  cerebellar  syndrome,  I  repeat, 
remained  in  a  condition  of  purity.  A  small  abscess  in  the  white  matter 
of  one  lobe  of  the  cerebellum  was  sufficient  to  cause  headache,  loss  of 
equilibrium,  vomiting,  vertigo,  stroke,  nystagmus,  bilateral  optic  neuritis, 
homologous  paresis  of  the  left  external  oculo-xaotor  nerve  and  of  the  left 


DISEASES  OF  'rilK  ( •|';i{KI'.ErJATM  iU^ 

faoial  tiorvo,  somiioloiico,  and  coma  vif^il.  These  symptoms  may  all  exist, 
no  iiuittei-  whetlior  the  ah.scoss  is  in  the  rij^ht  lobe,  the  left  lobe,  or  the 
vermis.  It  is  only  paresis  of  the  sixth  and  seventh  nerves  whieli  indicates 
the  side  of  the  lesion. 

Diagnosis.  It  mi^ht  bo  supposed  that  the  diagnosis  of  cerebellar  abscess 
is  an  easy  matter.  As  a  matter  of  fact,  the  difUculties  are  often  great. 
Let  us  suppose  that  a  man  has  beeii  suffering  from  recent  or  old  otitis.  At 
a  given  moment  the  complete  cerebellar  syndrome  appears,  and  we  find 
headache,  vertigo,  loss  of  equilibrium,  vomiting,  and  nystagmus.  An 
abscess  of  the  cerebellum  consequent  on  otitis  will  be  immediately  thought 
of,  and  the  idea  of  surgical  intervention  will  present  itself.  And  yet  the 
man  is  not  suffering  from  an  abscess  of  the  cerebellum  :  the  syndrome 
arises  from  the  ear,  and  not  from  the  cerebellum. 

Certain  lesions  of  the  ear  cause  symptoms  (auditory  troubles,  buzzings, 
vertigo,  and  ictus)  grouped  under  the  name  of  Meniere's  vertigo.  Other 
symptoms  (headache,  vomiting,  and  nystagmus)  may  also  be  present,  and 
the  auricular  lesion  gives  rise  to  the  cerebellar  syndrome.  A  case  of  this 
kind  is  published  in  Raymond's  "  Le9ons  Cliniques"  : 

A  man  who  had  gone  to  bed  feeling  well,  and  who  had  committed  no  excesses  during 
the  previous  day,  awoke  during  the  night  with  intense  malaise,  vomiting,  vertigo, 
buzzing  in  the  ears,  and  cold  sweats.  He  got  up,  biit  he  was  seized  with  such  severe 
vertigo  that  he  fell  do\vn,  and  could  hardly  get  back  to  bod.  He  suffered  from  headache, 
which  lasted  for  two  days.  A  week  later  the  vertigo  became  less  severe.  The  patient, 
reeling  Uke  a  dnmken  man,  came  to  the  out-patient  department  of  the  Salpetriere, 
where  his  di-unken  gait,  nystagmus,  trembling  of  the  eyelids,  and  mydriasis  were 
noticed.  Examination  of  the  oars  revealed  a  "  sclerotic  constriction  of  the  tympanum, 
incomplete  obstruction  of  the  Eustachian  tube,  and  extreme  mobility  of  the  stapes, 
causing  relative  deafness  and  compression  of  the  labyrinth."  Raymond  discusses  the 
pathogenic  diagnosis,  rejecting  the  hypothesis  of  a  lesion  in  the  cerebellum,  and  men- 
tions the  labyrinthine  lesion  as  the  cause  of  all  the  symptoms. 

I  have  seen  a  patient  suffering  in  a  similar  manner.  It  is,  moreover, 
an  admitted  fact  that  the  cerebellar  and  labyrinthine  syndromes  are 
identical.  This  is  very  natural,  because  a  part  of  the  cerebellum  may  be 
considered  as  a  centre  of  the  labyrinthine  nerve.  These  ideas  are  of  recent 
date,  and  are  largely  due  to  the  remarkable  work  of  Bonnier,  who  has  eluci- 
dated this  question  in  numerous  publications.  In  both  syndromes  it  is, 
therefore,  the  labyrinthine  nerve  which  is  affected,  either  in  its  terminal 
expansions  (vestibular  branch  of  the  eighth  pair)  or  at  its  cerebellar  origin. 

In  spite  of  the  analogy  between  the  cerebellar  and  the  labyrinthine 
syndrome,  it  is  possible  to  distinguish  between  them,  and  hence  to  avoid 
an  operation  for  a  non-existent  cerebellar  abscess.  The  following  are  the 
distinctive  signs  :  headache  of  labyrinthine  origin  has  neither  the  intensity, 
the  persistence,  nor  the  localization  of  the  headache  of  cerebellar  origin. 


1346  TEXT-BOOK  OF  MEDICINE 

Furtliermorej  in  the  case  of  abscess  of  the  cerebellum  fever  is  frequent. 
When  the  symptoms  have  shown  themselves,  they  do  not  become  less 
marked.  The  somnolence  becomes  more  severe  every  day.  This  feature 
is  absent  in  the  labyrinthine  syndrome.  It  is  also  difficult  to  distinguish 
abscess  of  the  cerebellum  from  an  abscess  of  the  brain  (temporo-sphenoidal 
and  occipital  lobes).  These  abscesses  of  the  brain  consequent  on  otitis  are 
as  common  as  abscesses  of  the  cerebellum.  How  are  we  to  arrive  at  the  diag- 
nosis, an  essential  factor  in  the  surgical  intervention  ?  A  patient  with 
otitis  complains  of  headache,  vomiting,  vertigo,  and  paralytic  troubles, 
with  or  without  contractures  and  convulsive  movements.  We  notice,  in 
short,  symptoms  of  cerebral  origin,  and  we  have  every  reason  to  believe 
that  a  cerebral  abscess  is  forming.  The  question  is  :  How  are  we  to  know  the 
seat  of  the  abscess  ?  Is  it  in  the  cerebellum,  or  in  the  temporo-sphenoidal 
or  the  occipital  lobe  ?  In  the  case  of  cerebral  abscess  we  may  find  some  of 
the  symptoms  of  cerebellar  abscess,  but  they  are  less  marked  :  the  vertigo 
is  less  pronounced,  the  gait  is  less  reeling,  the  headache  has  its  maximum 
of  intensity  in  the  temporal,  and  not  in  the  occipital,  region.  The  motor 
troubles  are  on  the  side  opposite  to  the  cerebral  lesion,  and  consequently 
on  the  opposite  side  to  the  otitis.  The  motor  troubles  do  not  reach  the  stage 
of  complete  paralysis.  It  is  a  case  of  hemiplegic  paresis,  with  or  without 
spasms  and  with  or  without  contractures.  Finally,  two  signs  are  of  great 
value  —  word-blindness  and  hemianopia.  Word-blindness  and  crossed 
hemianopia  are  considered  to  be  valuable  signs  of  cerebral  abscess  by  Lannois 
and  Jaboulay. 

The  diagnosis  must  still  be  made  between  abscesses  and  tumours  of  the 
cerebellum.  Gliomata,  gliosarcomata,  tuberculomata,  and  parasitic  tumours 
may  also  cause  the  cerebellar  syndrome.  Tumours  of  the  cerebellum, 
however,  run  a  much  slower  course  than  abscess.  The  symptoms  are  further 
separated  as  regards  time.  Furthermore,  the  tumours  have  a  tendency  to 
grow  externally,  compressing  and  irritating  the  organs  and  the  nerves  in 
the  neighbourhood.  We,  therefore,  fijid  borrowed  symptoms  which  have 
nothing  to  do  with  a  lesion  limited  to  the  cerebellum.  Finally,  the  existence 
of  otitis  is  in  favour  of  abscess. 

Although  syphilis  of  the  cerebellum  is  stUl  an  obscure  matter,  we  must 
not  forget  that  syphilitic  arteritis  occurs  in  the  vessels  of  the  cerebellum, 
and  gives  rise  to  softening,  with  the  cerebellar  syndrome.  Zuber  has 
reported  the  following  case  : 

A  man  who  had  syphihs  was  taken  ill  sixteen  and  twenty  years  later  with 
apoplectiform  strokes,  accompanied  by  headache  and  amnesia.  Later  the  cerebellar 
symptoms  supervened — vertigo  and  reeling  gait.  The  patient,  whether  lying  down  or 
standing,  suffered  from  continual  vertigo.  He  walked  hke  a  dninken  man,  spreading 
his  legs  apart  to  increase  his  base  of  support.     He  suffered  from  sHght  facial  paralysis 


DISEASES  OF  THE  CEREBELLUM  1.'^47 

on  the  left  aide.  Aitt^r  a  temporary  improvemoat  under  antisypliilitio  treatment,  thn 
situation  bocamo  woruo,  homiplogia  of  the  right  side  being  followed  by  contractures 
and  partial  panilysis.  Tho  pationt  died  in  coma.  At  the  post-mortem  examination 
an  old  focus  of  yellow  softening  was  found,  which  had  destroyed  tho  inferior  part  of  the 
right  hemisphere  of  tho  corobollura.  This  focus  corresponded  to  tho  area  sui)phed  by 
the  inferior  artery  of  the  cerebellum,  which  showed  obUtcrating  arteritis.  The  left 
cerebellar  hemisphere  showed  a  focus  of  softening  and  obliterating  arteritis  of  the 
inferior  cerebellar  artery.  In  this  case  the  cerebellar  syndrome  was  deffvced,  because 
cortical  and  central  softening  were  present  in  the  cerebrum.  Syphihtic  lesions  of  the 
cerebellum  are  amenable  to  specific  treatment.  They  must,  therefore,  be  distinguished 
from  the  other  lesions  of  the  cerebellum. 

The  treatment  of  the  tumours  and  of  the  abscesses  of  the  cerebellum  is 
purely  surgical.  It  is  necessary  to  operate  before  the  secondary  lesions 
have  had  time  to  arise.  Prophylactic  treatment  consists  in  curing  the  otitis. 
Any  individual  who  suffers  from  otitis  should  know  the  danger  to  which 
he  is  exposed. 


CHAPTER  IV 
DISEASES  OF  THE  BRAIN 

I.    CEREBRAL   CONGESTION. 

etiology. — Cerebral  congestion  may  be  active  or  passive.  Active  conges- 
tion may  accompany  the  rigor  of  intermittent  fevers  and  acute  rheumatism. 
It  is  caused  by  insolation,  by  the  sudden  suppression  of  a  habitual  flux 
(haemorrhoids,  menstruation),  by  prolonged  cold,  by  alcoholic  beverages, 
by  the  presence  of  tumours  and  other  brain  lesions.  Passive  congestion 
arises  from  any  cause  which  interferes  directly  or  remotely  with  the  venous 
circulation  of  the  brain — compression  of  the  cerebral  sinuses  and  of  the 
veins  of  the  neck,  tumours  of  the  neck  and  of  the  mediastinum,  prolonged 
efforts,  and  valvular  lesions  of  the  heart. 

Description. — Jaccoud  describes  three  forms  of  cerebral  congestion. 
The  slight  form  is  characterized  by  pains  in  the  head,  with  pulsation  of  the 
carotid  and  temporal  arteries,  and  injection  of  the  face  and  of  the  eyes. 
In  the  grave  form  there  are  also  added  psychical  troubles,  with  insomnia, 
restlessness,  and  delirium.  Elderly  persons  are  subject  to  a  variety  of  cere- 
bral congestion  which  betrays  itself  by  delirium  followed  by  coma  (Durand- 
Fardel).  In  children  convulsions  replace  the  delirium.  The  apoplectic 
form  of  cerebral  congestion  lasts  for  one  or  two  days,  and  may  then  disappear, 
without  leaving  any  traces.  It  is  sometimes  followed  by  a  temporary  hemi- 
plegia, or  is  only  the  prelude  of  the  delirious  form.  Apoplectiform  conges- 
tion, sometimes  associated  with  epileptiform  convulsions,  is  not  rare  in 
certain  diseases  of  the  nerve  centres,  such  as  insular  sclerosis,  general 
paralysis,  and  descending  scleroses  of  the  mesencephalon. 

The  diagnosis  of  cerebral  congestion  must  be  made  with  regard  to  its 
particular  form.  The  mild  form  must  not  be  confounded  with  gastric 
vertigo  ;  and  apoplectiform  congestion  must  be  differentiated  from  vertigo 
ab  aure  Icesa,  from  cerebral  haemorrhage,  and  from  epilepsy.  Furthermore, 
cerebral  congestion,  formerly  looked  upon  as  frequent,  has  become  much  less 
common,  since  we  know  better  the  differences  between  it  and  the  diseases 
with  which  it  was  confounded. 

The  prognosis  may  be  grave.    Apoplectiform  congestion  from  insolation 

1348 


DISEASKS  OK  'nil-:   I'.RAIX  1849 

or  from  <'nj(l  is  oiton  accompanied  i)y  puliiuMiarv  oongestion.  Tlio 
delirious  form  may  cause  rapid  death  (Audral).  The  treatment  consiHts 
in  general  or  local  bleeding,  revulsives,  purgatives,  and  cold  applications 
to  the  head. 

II.  CEREBRAL  ANAEMIA. 

Cerebral  anaemia  may  be  limited  to  the  brain  or  may  be  associated  with 
ge'neral  ana?mia,  the  brain,  more  than  the  other  organs,  experiencing  the 
effects  thereof.  Cerebral  anaemia  is  due  to  a  change  in  the  quantity  or  in 
the  quality  of  the  blood.  The  quantitative  changes  have  as  their  cause 
haemorrhages,  rapid  or  excessive  evacuation  of  abdominal  fluid,  and  changes 
in  the  cerebral  circiUation  under  the  direct  or  reflex  influence  of  the  vaso- 
motor nerves.  The  qualitative  changes  are  due  to  long  and  grave  diseases, 
to  inanition,  to  cachexia,  etc. 

The  symptoms  of  cerebral  anaemia  vary  according  to  the  cause.  When 
the  quantity  of  blood  withdrawn  from  the  system  is  considerable,  or  when 
the  loss  has  been  rapid,  the  patient  has  attacks  of  vertigo  and  noises  in  the 
ears.  He  becomes  cold  and  loses  consciousness,  his  pallor  is  extreme,  the 
pulse  grows  small  and  irregular,  the  respiratory  movements  become  slower, 
and  we  sometimes  meet  with  general  convulsions  and  fatal  syncope.  When 
the  cerebral  anaemia  comes  on  slowly,  the  principal  symptoms  are  vertigo, 
palpitation,  insomnia,  and  general  depression,  joined  to  an  exaggerated 
excitability  of  the  senses.  Total  anaemia  of  an  area  due  to  obliteration  of 
a  vessel  (thrombosis  or  embolism)  will  be  described  under  Cerebral  Softening. 

When  the  anaemia  is  sudden  (loss  of  blood),  the  head  should  be  lowered, 
the  patient  l5"ing  down.  The  treatment  of  the  other  forms  is  that  of  the 
general  anaemia. 

III.  CEREBRAL  HEMORRHAGE. 

The  description  of  cerebral  haemorrhage  deserves  special  notice — first, 
on  account  of  its  importance,  and,  secondly,  because  several  of  its  primary 
symptoms  (apoplexy,  hemiplegia),  and  also  of  its  secondary  symptoms, 
(contractures,  tremors)  are  common  to  other  cerebral  diseases,  and  require 
a  thorough  knowledge  of  the  anatomy  of  the  brain  and  of  the  circulation 
in  its  various  territories. 

Pathological  Anatomy. — The  blood  extravasated  into  the  brain  tissue 
collects  in  foci,  and  does  not  retract.  On  coagulating,  it  assumes  the  look 
of  gooseberry  jelly.  These  characters  vary  according  as  the  haemorrhagic 
focus  is  recent  or  old.  If  the  haemorrhage  is  recent  and  abundant,  the  walls 
of  the  focus  are  irregular  and  formed  of  shreds  of  the  cerebral  matter  ; 
bloodvessels  and  miliary  aneurysms  are  sometimes  found.  When  the 
haemorrhage  is  several  months  old,  the  clot  and  the  walls  of  the  focus 
II.  86 


1350  TEXT-BOOK  OF  MEDICINE 

become  changed.  The  blood  is  deprived  of  its  serous  portion;  the  solid 
elements  (corpuscles  and  fibrin)  are  transformed,  and  the  granule -fatty- 
degeneration  facilitates  their  absorption,  but  the  heematoidin  remains 
indefinitely,  and  the  cicatrices,  even  after  ten  to  fifteen  years,  still  pre- 
serve an  ochre  -  like  colour.  In  the  long  run  the  walls  of  the  focus 
are  transformed  into  sclerotic  tissue.  If  these  waUs  do  not  unite,  a  cyst 
results  :  in  the  contrary  case,  a  cicatrix  is  formed. 

The  hsemorrhagic  foci  vary  much  in  size.  They  are  sometimes  sym- 
metrical. They  may  burst  into  the  ventricles  and  through  the  meninges. 
By  the  side  of  a  focus  as  large  as  an  egg  we  sometimes  meet  with  capiUarv 
foci  (Cruveilhier's  capillary  apoplexy)  smaller  than  a  pin's  head.  The  brain 
tissue  is  studded  with  red  points,  presenting  at  the  centre  a  capillary  vessel, 
the  lymphatic  sheath  of  which  is  distended  by  blood  and  torn  at  some  point 
which  cannot  always  be  discovered.  These  capillary  haemorrhages  are  often 
the  first  stage  of  a  focal  hsemorrhage. 

Topography  of  the  Haemorrhage. — The  hsBmorrhages  do  not  occur  in  an  indis- 
criminate manner,  but  they  select  the  grey  more  often  than  the  white  matter,  and  the 
convolutions  are  rarely  attacked,  as  compared  with  the  central  gangha.  In  order  to 
form  an  exact  idea  of  the  topogi'aphy  of  the  focus,  of  the  possible  inundation  of  the 
lateral  ventricles,  of  the  invasion  of  the  internal  capsule,  of  the  lesions  of  the  pyramidal 
tract,  of  the  secondary  sclerotic  degenerations  that  may  be  the  result  of  the  hsemorrhage, 
and  of  the  muscular  atrophy  which  complicates  this  degeneration,  it  is  first  necessary 
to  understand  the  anatomical  conformation  of  this  central  region. 

If  we  separate  the  two  hps  of  the  fissure  of  Sylvius,  we  find  a  group  of  four  or  five 
short,  convolutions  covered  by  the  branches  of  the  Sylvian  artery.  This  is  the  island  of 
Reil.  If  the  brain  is  hardened,  and  if  the  convolutions  of  the  island  of  Reil  are  care- 
fully scraped  away,  we  meet  with  a  lamina  of  white  matter,  2  millimetres  in  thickness, 
caUed  the  external  capsule,  and  surrounding  a  tract  of  grey  matter  called  the  claustrum. 
If  we  remove  the  external  capsule,  we  find  a  large  mass  of  grey  matter,  known  as  the 
lenticular  nucleus,  and  divided  into  several  segments.  If  we  next  remove  the  nucleus, 
we  meet  with  a  thick  tract  of  white  matter — the  internal  capsule — which  is  of  supreme 
importance.  The  internal  capsule  being  detached,  we  find  the  grey  caudate  nucleus, 
and  iiaaUy  a  mass  of  grey  matter — the  optic  thalamus — which  projects  into  the  lateral 
ventricle.  It  is  to  be  noted  that,  according  to  this  disposition,  the  three  masses  of  grey 
matter,  the  optic  thalamus,  and  the  nuclei  of  the  striate  body  are  fixed  to  the  internal 
capsule,  Hke  cotyledons  (FoviUe). 

Internal  Capsule. — The  internal  capsule  (Burdach)  plays  such  an  important  part  in 
this  region  that  I  do  not  hesitate  to  give  fuU  details.  In  order  to  study  the  internal 
capsule  properly,  a  horizontal  section  of  the  brain  must  be  made,  either  from  without 
inwards,  a  httle  above  the  fissure  of  Sylvius  (Flechsig),  or  from  within  outwards,  by 
directing  the  knife  a  httle  downwards  and  backwards  (Brissaud).  The  internal  capsule 
shows — (1)  an  anterior  segment  (lenticulo-striate)  directed  inwards  and  backwards,  and 
bounded  internally  by  the  caudate  nucleus,  and  extemaUy  by  the  lenticular  nucleus  ; 
(2)  a  genu,  or  bend,  situated  between  the  optic  thalamus  and  the  striated  body ;  (3)  a, 
posterior  segment  (lenticulo-optic),  directed  outwards  and  backwards,  and  bounded 
extemaUy  by  the  lenticular  nucleus,  and  internally  by  the  optic  thalamus.  The  fibres 
of  the  internal  capsule,  after  having  passed  the  region  between  the  central  nuclei,  enter 
the  centrum  ovale,  form  the  corona  radiata,  and  disperse  in  all  dii'ections  towards  the 


rUite    VII. 


Motor  and  Sensory  Tracts  in  the  Brain  and  Spjnal  Cord. 

I,  Cerebral  hemispheres;  2,  internal  capsule;  3,  cerebral  peduncles;  4,  sec- 
tion of  the  peduncles;  5,  pons;  6,  bulb;  7,  section  of  the  cord  (dorsal);  8,  conus 
medullaris;  P,  frontal  lobes  (psychical);  A,  Broca's  convolution;  F,  foot  of 
ascending  frontal  convolution;  M,  motor  areas;  S,  sensory  areas;  O,  optic 
thalamus;  V,  caudate  nucleus;  L,  lenticular  nucleus;  D,  direct  pyramidal 
tract;  C,   crossed  pyramidal   tract;  B,  Burdach's  column;  G,  Coil's  column. 

I.  Psychical  bundle  (white)  passing  up  from  the  peduncles  to  the  frontal  lobes; 

II.  Aphasia  bundle  (yellow)  descending  from  Broca's  convolution  to  the  nuclei 
in  the  pons  and  bulb;  III.  Geniculate  bundle  (green)  descending  from  the 
foot  of  the  ascending  frontal  convolution,  and  crossing  in  the  pons  to  end 
below  in  the  facial  and  hypoglossal  nuclei;  IV.  Pyramidal  motor  bundle  (red) 
descending  from  the  central  convolution,  and  decussating  the  bulb,  after 
going  oft  the  direct  pyramidal  tract;  V.  Sensory  bundle  (blue)  arising  in  the 

f>osterior  columns  of  the  cord,  passing  up  to  the  bulb,  where  it  decussates, 
orming  the   posterior  part  of   the  peduncles,  and  ending  in    the  occipital 
convolutions. 


To  face  p.   i35o 


DISbLVSES  UK  THE  BRAIN  1351 

IMsriphomI  parts  of  tlio  Imiiii.  Thti  inttirrml  capsule  oontaiiis  the  coiitrifufi.il  and  rcntri- 
petal  norvo  tibrcs  of  various  origins.  Homo,  coming  from  tho  peripheral  portions  of 
the  brain,  end  in  tlie  lenticular  nucleus,  the  caudate  nucleus,  and  in  the  optio  thalamus  ; 
others  do  not  end  in  the  central  ganglia,  but  form  commissures  between  the  cerebrum 
on  the  one  hand  and  the  mesencephalon  and  the  spinal  cord  on  the  other,  constituting 
the  pyramiihil  tract,  the  geniculate  tract,  and  the  sensory  tract. 

The  pyramidal  tract,  thus  named  on  accoimt  of  the  importance  which  it  has  in  the 
anterior  pyramids  of  the  bulb,  might  also  be  called  the  voluntary  tract  (Ferrier),  because 
it  transmits  voluntary  impulses  from  the  motor  arc-as  of  the  brain  to  the  various  segments 
of  the  spinal  cord.  The  nerve  fibres,  arising  in  the  largo  cells  of  the  motor  convolutions 
(ascending  frontal  and  parietal  convolutions  and  paracentral  lobule),  descend  through 
the  centrum  ovale,  and  occupy  the  posterior  segment  of  the  internal  capsule.  The 
tract,  then,  passes  through  the  middle  portion  of  the  peduncles,  forms  the  anterior 
pyramid  of  the  bulb,  giving  off  fibres  to  the  motor  centres  of  the  bulb,  and  decussates 
in  the  neck  of  the  bulb  with  the  other  pyramidal  tract,  in  order  to  pass  over  to  the 
opposite  side  of  the  spinal  cord.  The  decussation  of  the  fibres  is  more  or  less  complete, 
but  the  most  important  part  of  the  pyramidal  bundle  (that  which  has  undergone 
decussation)  occupies  in  the  opposite  side  of  the  spinal  cord  the  portion  farthest  away 
from  the  lateral  cord  in  the  neighbourhood  of  the  posterior  roots.  This  tract,  which  is 
large  in  the  cervical  region,  diminishes  in  size  as  it  approaches  the  lumbar  region.  The 
nerve  fibres  of  which  it  is  composed  enter  into  direct  relation  in  the  various  levels  of 
the  spinal  cord  with  the  motor  cells  in  the  anterior  comua.  The  latter,  in  their  turn, 
enter  into  relation  ^^^th  the  muscles  by  the  prolongations  which  they  send  into  the 
peripheral  nerves.  The  other  portion  of  the  pyramidal  tract  (Turck's  direct  pyramidal 
tract)  occupies  the  internal  portion  of  the  anterior  columns  of  the  spinal  cord,  and  does 
not  descend  below  the  lumbar  region. 

The  geniculate  tract  of  the  internal  capsule  (Brissaud)  is  of  small  size.  It  also 
starts  from  the  motor  area  of  the  brain,  and  is  situated,  in  the  genu  of  the  internal 
capsule.  It  is  composed  of  motor  fibres,  which  go  to  the  nuclei  of  the  bulb,  and  it 
governs  the  voluntary  movements  of  the  head  and  face. 

The  sensory  bundle,  coming  from  the  posterior  tracts  of  the  spinal  cord,  crosses  at 
the  neck  of  the  bulb,  passes  through  the  anterior  pyramid,  the  pons,  the  posterior  bundle 
of  the  cer.ebral  peduncle,  and  reaches  the  internal  capsule.  It  occupies  the  posterior 
tliird  of  the  posterior  segment  of  the  internal  capsule,  and  passes  into  the  grey  cortex 
of  the  cerebral  convolutions. 

Bloodvessels. — The  regions  of  the  brain  just  described  are  supplied  by  branches  of 
the  middle  cerebral  or  Sylvian  artery. 

This  vessel  enters  the  fissure  of  Sylvius,  and  gives  out  branches  which  diverge  between 
the  convolutions  of  the  insula.  These  branches  are  cortical  and  central.  The  former, 
destined  for  the  peripheral  parts  of  the  brain,  will  be  described  in  the  nest  section,  on 
Softening  of  the  Brain.  The  latter  arise  from  the  Sylvian  artery  before  the  cortical 
branches  enter  the  foramina  of  the  anterior  perforated  space,  and  take  the  name  of 
striate  arteries.  These  striate  arteries  are  internal  and  external.  The  internal  ones, 
which  are  less  important,  give  out  branches  to  the  two  first  segments  of  the  lenticular 
nucleus  and  to  the  corresponding  part  of  the  internal  capsiile ;  the  external  striate 
arteries,  which  are  much  more  important,  spread  out  on  the  surface  of  the  lenticular 
nucleus,  and  divide  into  two  groups — an  anterior  group,  or  lenticulo -striate  arteries,  and 
a  posterior  group,  or  lenticulo-optic  arteries.  The  lenticulo-striate  artery  (anterior 
group)  plunges  into  the  third  segment  of  the  lenticular  nucleus,  traverses  the  internal 
capsule,  and  terminates  in  the  caudate  nucleus.  It  is  so  often  the  origin  of  the  haemor- 
rhage that  it  has  been  called  the  artery  of  cerebral  haemorrhage  (Charcot).  The  len- 
ticulo-optic artery  (posterior  group)  traverses  the  part  farthest  from  the  internal  capsule, 
and  enters  the  optio  thalamus.     It  supplies  the  sensory  portion  of  the  internal  capsule. 

8(3—2 


1352 


TEXT-BOOK  OF  MEDICINE 


The  importance  of  these  vessels  will  be  understood,  because  the  central  gangUa  of 
the  brain  are  supphed  by  them — not  in  an  absolute  manner,  however,  because  the 
anterior  cerebral  artery  sometimes  sends  a  branch  to  the  caudate  nucleus,  and  the 
posterior  cerebral  artery  gives  off  a  branch  to  the  internal  part  of  the  optic  thalamus. 

These  anatomical  facts  will  help  us  to  grasp  the  topography  of  haemorrhages  in  the 
central  regions  of  the  brain. 

1.  The  haemorrhage  occurs  most  frequently  in  the  area  of  the  lenticulo-striate  artery, 
where  this  vessel  ascends  over  the  external  surface  of  the  lenticular  nucleus,  so  that  the 
initial  focus  arises,  not  in  the  thickness  of  the  grey  matter,  but  on  its  surface  between 
the  nucleus  and  the  external  capsule.  The  resulting  hemiplegia  is  curable,  because  the 
lesions  of  the  external  capsule,  hke  the  lesions  of  the  grey  nuclei,  are  not  followed  by 
sclerosis.  If,  however,  the  hsemorrhagic  focus  is  large,  it  pushes  the  external  capsule, 
with  the  convolutions,  outwards,  and  displaces  inwards  the  lenticular  nucleus,  the 
internal  capsule,  and  the  other  central  gangha,  and  it  may,  by  compressing  these  parts, 
diminish  or  destroy  their  fimctional  activity. 

2.  The  haemorrhage  takes  place  into  the  corpus  striatum  (the  lenticulo-striate 
artery)  or  into  the  optic  thalamus  (region  of  the  lenliculo-optic  artery).     In  such  a 


Fig.  62.— Distribution  of  the  Sylvian"  Aeteby. 
1,  Sylvian  artery ;  2,  orbital  artery ;  3,  inferior  frontal  artery ;  4,  ascending  frontal 
artery ;  5,  ascending  parietal  artery ;  6,  inferior  parietal  artery ;  7,  artery  oi  the 
angular  gyrus  ;  8,  9,  10,  temjioral  arteries  ;  11,  perforating  arteries. 


case,  the  focus,  if  of  small  size,  remains  confined  to  the  grey  matter,  and  only  causes  a 
shght  hemiplegia ;  if  it  is  of  large  size,  it  invades  the  neighbouring  parts,  or  at  least  it 
compresses  them  en  masse,  and  causes  grave  phenomena. 

3.  The  haemorrhage  takes  place  in  the  caudate  nucleus  (lenticulo-striate  artery,  and 
sometimes  the  anterior  cerebral  artery).  This  condition  is  serious,  because  the  focus 
fairly  frequently  opens  into  the  lateral  ventricle. 

4.  The  haemorrhage  takes  place  in  the  internal  portion  of  the  optic  thalamus  (the 
internal  posterior  optic  artery,  from  the  posterior  cerebral).  The  haemorrhage  is  very 
grave,  because  it  is  often  followed  by  inundation  of  the  ventricle. 

Secondary  Sclerotic  Degeneration. — Haemorrhage,  softening,  encephaUtis,  and  in 
some  cases  tumours,  may  cause  descending  sclerosis  through  the  brain,  the  mesen- 
cephalon, and  the  spinal  cord.  Descending  sclerosis  does  not  occur  if  the  cerebral 
lesion  is  hmited  to  the  grey  matter  of  the  corpus  striatum  and  to  the  optic  thalamus, 
or  to  the  grey  matter  of  the  motor  convolutions;  but  if  the  lesion  attacks  the  pyramidal 
tract  in  any  part  of  its  course,  the  tract  below  the  lesion  may  become  the  seat  of  de- 
scending sclerosis. 

The  sclerotic  tract  can  be  made  out  with  the  naked  eye,  and  under  the  microscope 
it  corresponds  exactly  to  the  pyramidal  tract.     Its  consistency  is  firm,  and  its  colour 


DISEASES  OF  THE  BRAIN 


13r, 


is  soraotimea  greyish.  It  occupies  the  anterior  two-tliirds  of  tlio  posterior  segment  of 
tlio  interna!  ca[)suio,  the  median  part  of  the  inferior  stage  of  the  cerebral  |>odun(lt), 
and  the  anterior  pyramid  of  the  Inilb.  It  decussates  at  the  neck  of  the  bulb,  and 
descends  into  the  spinal  cord,  diminishing  progressively  m  size.  In  transverse  sections 
of  the  spinal  cord  it  is  soon  to  occupy  the  posterior  part  of  the  lateral  column. 

Under  the  microscope  the  nerve  fibres  are  in  part  atrophied,  or  have  disappeared. 
The  connective  tissue  is  abundant  and  fibrillary.  The  destructive  cerebral  lesion 
causes  a  change  comparable  with  Waller's  degeneration.  The  nerve  fibre  becomes 
degenerated,  and  the  connective  prohferation  is  a  secondary  production. 

In  some  cases  the  secondary  degeneration  does  not  stop  in  the  fibres  of  the  spinal 
cord,  but  is  carried  by  these  fibres  as  far  as  the  anterior  comua  of  the  spinal  cord,  with 
which  they  are  in  connection.  The  anterior  comu  diminishes  in  size  ;  the  nerve  cells  are 
granular,  and  lose  their  nuclei  and  their  prolongations.     Muscular  atrophy  is  the  result. 

-ffitiology — Pathogenesis.— Many  people  who  suffer  from  cerebral 
hsemorrhage  have  the  so-called  apoplectic  constitution  (short  neck  and 
congested  face).     The  aetiology  of  cerebral  haemorrhage  is  complex,  but 


Fig.  63. — Traxsverse  Section-  op  the  Erai^-. 
1,  Internal  carotid  artery ;  2,  anterior  cerebral  artery ;  3,  Sylvian  artery ;  4,  internal 
striate  arteries  ;  5,  external  striate  arteries  ;  6,  lenticulo-striate  artery,  with  miliary 
aneurysm  ;  7,  cerebral  haemorrhage ;  8,  caudate  nucleus ;  9,  optic  thalamus ; 
10,  internal  capsule  ;  II,  claustrum  ;  12,  external  capsule  ;  13,  insula  ;  14,  lenticular 
nucleus. 


side  by  side  with  secondary  or  rare  causes,  such  as  blood-changes,  purpura, 
icterus  graAis,  leucocythsemia,  etc.,  there  exists  one  cause  which  dominates 
the  pathogenesis  of  cerebral  haemorrhage — I  mean  the  change  in  the  blood- 
vessels. The  diseased  artery  becomes  ruptured ;  this  is  the  initial  fact, 
and  the  haemorrhage  is  only  the  consequence.  What,  however,  is  this  change 
in  the  vessel  ?  Is  it  a  fatty  degeneration  of  the  walls,  an  endarteritis  with 
atheroma,  or  a  periarteritis  ? 

Certain  writers  (Paget)  supposed  that  the  hgemorrhage  depends  on  fatty 
degeneration  of  the  arterioles,  but  this  so-called  degeneration  is  only  an  accu- 
mulation of  fatty  granulations  in  the  lymphatic  sheath  of  the  vessel,  an  accu- 
mulation consequent  on  the  necrobiosis  of  the  cerebral  matter  by  softening, 
haemorrhage,  etc.  (Billroth).     The  whole  interest  in  the  question  is  centred  in 


1354  TEXT-BOOK  OF  MEDICINE 

tlie  vascular  lesions  of  endarteritis  and  periarteritis.  But  what  share  belongs 
to  each,  of  these  lesions  in  the  causation  of  haemorrhage  ?  Are  endarteritis 
and  atheroma  sufficient  to  cause  rupture  of  the  vessel  (BouiUaud,  Roki- 
tansky),  or  are  thev  only  concomitants  of  the  periarteritis,  which  is  said  to 
be  the  real  cause  of  the  miliary  aneurysms,  which  rupture  and  give  rise  to 
the  heemorrhage  ? 

We  know  that  the  vascular  system  of  the  brain  may  be  attacked  by 
diffuse  periarteritis  or  endoperiarteritis  of  slow  course,  and  leading  to  a 
change  in  the  vessel  walls.  The  arterioles  are  invaded  by  sclerotic  tissue. 
The  lesion  commences  in  the  tunica  externa  and  in  the  tunica  intima 
(endoarteritis),  whilst  the  contractile  elements  of  the  tunica  media  become 
atrophied  and  disappear  without  fatty  substitution.  These  partial  losses 
of  substance  diminish  the  resistance  of  the  vessels,  and  are  the  cause  of 
miliary  aneurysms. 

These  small  aneurysms,  which,  on  an  average,  have  a  diameter  of 
^  millimetre,  and  which  are  in  most  cases  visible  to  the  naked  eye,  finally 
rupture  and  cause  haemorrhage.  These  miliary  aneurysms  had  been  noticed 
by  Cruveilhier,  Meynert,  Heschel,  and  Charcot,  but  Bouchard  was  the  first 
to  show  the  relations  between  the  miliary  aneurysm  and  cerebral  haemor- 
rhage. We  know  how  the  miliary  aneurysms  are  formed,  and  how  they 
become  ruptured,  and  we  have  been  able  to  follow  the  lesion  from  the 
initial  periarteritis  to  the  terminal  haemorrhage.  These  changes  do  not 
resemble  the  atheromatous  lesions  of  endarteritis,  which  are  limited  to  the 
deep  layers  of  the  tunica  intima,  and,  whilst  cerebral  atheroma  is  especially 
connected  with  thrombosis  and  softening,  sclerotic  periarteritis  provokes 
the  haemorrhage.  Does  this  mean  that  atheroma  is  to  be  banished  from 
the  pathogenesis  of  cerebral  haemorrhage  ?  The  answer  is  negative,  because 
we  find  both  the  lesions  of  endarteritis  and  those  of  periarteritis.  The 
lacunae  of  cerebral  disintegration,  which  are  frequent  in  old  people,  may 
be  the  cause  of  the  haemorrhage.     We  must  not  forget  injury. 

The  vascular  changes  that  lead  to  miliary  aneurj^sms  are  often  asso- 
ciated with  certain  morbid  conditions,  such  as  Bright's  disease  (arterio- 
sclerosis), alcoholism,  gout,  and  diabetes.  Let  me  add  that  cerebral 
congestion  from  any  cause  tends  to  produce  haemorrhage  in  a  predis- 
posed individual  (high  tension,  cardiac  hypertrophy,  sudden  action  of 
cold). 

The  pathogenic  role  of  syphilis  is  evident.  Syphilitic  arteritis,  which 
shows  a  preference  for  the  cerebral  arteries,  causes  either  the  obliteration 
of  the  vessel  and  consequent  thrombosis  and  softening,  or  aneurysm, 
rupture  of  the  bloodvessel,  and  haemorrhage,  I  shall  refer  to  this  question 
under  Cerebral  Syphilis. 

Although  cerebral  haemorrhage  may  be  the  appanage  of  advanced  age,  it 


DISEASES  OF  THE  BRAIN  1355 

shows  itself  also  during  various  periods  of  life.  It  is  essentially  hereditary,* 
as  I  have  shown  in  a  previous  monograph — more  hereditary,  even,  than 
]>htliiflis  and  ciuicer.  In  the  same  family  it  causes  ajioydexy  and  hemi- 
ploiria.  The  gravity  of  the  case,  recovery,  and  rapid  death  or  survival,  are 
subordinate  only  to  the  localization  of  the  cerebral  lesion.  It  strikes  several 
members  of  the  same  family,  and  it  sometimes  happens  that,  in  the  same 
])rogeny,  a  younger  generation  is  attacked  before  an  older  one. 

Description. — Cerebral  haemorrhage  shows  itself — (1)  by  primary  symp- 
toms, which  supervene  at  the  time  of  the  haemorrhage,  or  shortly  afterwards  ; 
(2)  by  secondary,  symptoms,  which  only  appear  some  weeks  or  months 
later.  In  some  cases  cerebral  haemorrhage  is  preceded  by  prodromata 
(headache,  hot  flushes,  and  temporary  congestion  of  the  head),  which  may 
last  for  weeks  or  months.  As  a  rule,  prodromata  are  absent,  and 
apoplexy  or  hemiplegia  comes  on  suddenly  while  the  individual  is  in  good 
health. 

1.  Primary  Symptoms. — Apoplexy  is  not  a  frequent  symptom  in  cere- 
bral hremorrhage  ;  we  might  almost  say  that  it  is  rare.  Apoplexy  means 
total  loss  of  movement  and  of  sensation,  according  to  the  ancient  definition 
of  Galen — a  definition,  unfortunately,  changed  by  Rochoux,  and  turned  by 
him  from  its  true  sense.  Rochoux  was  so  convinced  that  apoplexy  is 
always  the  result  of  cerebral  haemorrhage  that  he  made  a  synonym  of  it, 
and  from  that  time  the  word  apoplexy,  carelessly  used,  serves  to  designate 
the  lesion  (that  is  to  say,  the  haemorrhage)  or  tlie  symptom  (that  is  to 
say,  the  loss  of  movement  and  of  sensation).  The  custom  having  once  been 
acquired,  "  capillary  apoplexy "  (Cruveilhier)  was  written  for  capillary 
haemorrhage,  "  apoplexy  of  the  lung  "  for  haemorrhage  into  the  lung — faulty 
terms  which  must  be  abandoned.  The  word  "  apoplexy  "  usually  awakens 
the  idea  of  suddenness.  Let  me  explain.  Fulminant  apoplexy  is  very  rare 
(bulbar  haemorrhage)  ;  most  frequently  the  apoplexy  comes  on  slowly, 
taking  ten  minutes,  half  an  hour,  or  even  longer,  to  develop  (Trousseau). 

The  patient  is  in  a  condition  of  complete  unconsciousness.  His  face  is 
congested  and  his  features  are  drawn  towards  the  healthy  side,  whilst  the 
lips  and  the  cheek  of  the  paralyzed  side  are  flaccid  and  puffed  out  at  each 
expiration.  The  head  is  most  frequently  turned  to  the  non-paralyzed  side, 
and  the  eyes  are  turned  towards  the  same  side  (Vulpian  and  Prevost).  This 
conjugate  deviation  of  the  head  and  eyes  generally  ceases  when  the  apoplexy 
disappears. 

During  the  apoplectic  period,  or  after  the  unconsciousness,  convulsions 
and  contractures  may  appear.  They  have  been  called  "  early "  to  dis- 
tinguish them  from  the  late  contractures,  and  must  be  considered,  says 

*  Dieulafoy.  Communication  k  I'Academie  de  M6decine  (see  Qazette  Hebdumadaire^ 
1876). 


1356  TEXT-BOOK  OF  MEDICINE 

Straus,  "  rather  as  tonic  convulsions  tlian  as  real  contractures."  These 
convulsions  and  contractures,  which  may  be  limited  to  the  paralyzed  side 
or  may  invade  both  sides  and  the  face,  are  phenomena  of  excitation,  and 
generally  indicate  that  the  hsemorrhage  affects  the  ventricles,  the  meninges, 
or  the  mesencephalon.  They  are  hardly  ever  seen  in  apoplexy  from  cerebral 
softening.  In  the  apoplectic  patient  most  of  the  reflex  movements  are 
abolished  ;  micturition  and  defsecation  are  affected  (incontinence  or  reten- 
tion). The  respiration  is  noisy,  irregular,  slowed,  and  then  accelerated. 
The  temperature  falls  in  the  initial  period,  and  rises  later  as  high  as  106°  F. 
The  patient  may  recover,  but  the  gradual  acceleration  of  the  respiration 
and  of  the  pulse,  the  constant  rise  of  the  temperature,  and  the  appearance 
of  general  convulsions,  are  fatal  signs. 

Lumbar  puncture  yields  limpid  yellowish  or  bloody  fluid  (Sicard).  It 
is  probable  that  the  red  tint  only  exists  when  there  is  diffusion  of  the  blood 
by  ventricular  inundation,  consequent  on  cerebral  hsemorrhage,  or  else 
hsemorrhage  into  the  posterior  part  of  the  spinal  pia  mater,  consequent  on 
cerebral  hsemorrhage. 

The  pathogenesis  of  apoplexy  in  cerebral  hsemorrhage  has  been  variously 
interpreted.  The  irruption  of  the  blood  into  the  interior  of  the  ventricles 
or  on  the  surface  of  the  brain  realizes  the  most  favourable  conditions  for 
the  production  of  apoplexy,  often  accompanied  in  such  a  case  by  convulsions 
and  contractures.  How  are  we  to  explain  apoplexy  produced  by  hsemor- 
rhage limited  to  the  opto -striate  bodies  ?  Congestion  of  the  encephalon, 
pressure  produced  by  the  focus  and  cerebral  ansemia,  have  in  turn  been 
suggested  (Niemayer).  I  prefer  the  more  rational  interpretation  of  reflex 
apoplexy  to  these  hypotheses  (Jaccoud). 

Hemiplegia. — Hemiplegia  means  paralysis  of  one  side  of  the  body.  It 
is  on  the  opposite  side  to  the  cerebral  lesion :  hsemorrhage  on  the  left  side, 
hemiplegia  on  the  right  side,  and  vice  versa.  The  hemiplegia  may  be  total 
or  partial.  When  it  is  total,  it  involves  the  leg,  the  arm,  and  one  side  of 
the  face  ;  when  it  is  partial,  it  spares  one  or  other  of  these  parts.  Hemi- 
plegia foUows  sometimes  on  an  attack  of  apoplexy,  but  it  more  often  appears 
from  the  outset,  without  apoplexy  and  without  any  loss  of  consciousness. 
A  patient  wakes  up  with  hemiplegia,  having  been  stricken  with  cerebral 
hsemorrhage  during  sleep.  Another  patient  witnesses  his  hemiplegia  ;  he 
experiences  a  sensation  of  tingling  in  his  hand,  he  drags  his  leg,  his  mouth 
is  .twisted,  he  sputters,  and  the  hemiplegia  takes  a  quarter  of  an  hour,  half 
an  hour,  or  even  a  few  hours,  to  become  complete,  without  any  intellectual 
failing. 

In  the  face  the  paralysis,  unlike  the  peripheral  paralysis  of  the  facial 
nerve,  does  not  attack,  or  attacks  but  slightly,  the  orbicularis  palpebrarum. 
Facial  hemiplegia  betrays  itself  by  deviation  of  the  mouth,  the  healthy 


DISEASES  OF  THE  BRAIN  1.^57 

muscles  drawing;  tlie  anj^l<'  of  ilir  mouth  upwards  and  outwards  towards 
the  healthy  side.  When  the  tongue  is  put  out,  its  tip  is  directed  towards 
the  ])anihzed  side  of  the  face  (action  of  the  genio-glossus  muscle). 

In  tlie  limbs  tlie  liemiple^na  is  more  marked  in  tiie  arm  than  in  the  leg. 
All  forms  are  seen,  from  absolute  loss  of  movement  to  simple  paresis.  The 
temperature  is  generally  higher  on  the  paralyzed  side ;  the  muscular  con- 
tractility is  preserved. 

The  symmetrical  muscles,  the  movements  of  which  are  associated  with 
those  of  the  opposite  side,  escape  paralysis  ;  they  are  the  muscles  of  the 
thorax  and  abdomen  and  the  motor  muscles  of  the  eyes. 

In  some  cases  the  hemiplegia  is  crossed  (Gubler),  the  limbs  being  para- 
lyzed on  the  left  side,  and  the  face  on  the  right.  These  paralyses,  resulting 
from  a  lesion  in  the  pons  or  in  the  bulb,  have  been  described  in  one  of 
the  preceding  sections. 

The  duration  of  hemiplegia  is  variable.  After  some  days  or  weeks 
movement  reappears  in  the  leg,  and  then  in  the  arm.  Persons  have  been 
known  to  have  two  or  three  attacks  and  recover.  Some  remain  hemiplegic, 
the  paralyzed  limbs  being  flaccid ;  but  flaccid  hemiplegia  is  extremely  rare. 
Finally,  others — and  they  are  numerous — have  a  progressive  contracture, 
which  is  permanent  and  localized  in  the  paralyzed  limbs. 

Hemiancesthesia. — Hemiansesthesia  means  the  loss  of  sensation  in  one- 
half  of  the  body.  When  it  is  general,  it  affects  the  skin,  the  mucosae,  and 
the  sense  organs  (sensitivo-sensorial).  It  is  rare  in  haemorrhage,  and  more 
frequent  in  softening.  It  appears  when  the  posterior  third  of  the  posterior 
segment  of  the  internal  capsule  is  affected,  this  region  being  traversed  by 
the  sensory  fibres.  These  fibres  are  said  to  be  the  general  sensory  conductors, 
and  a  lesion  in  their  cerebral  course  is  said  to  cause  sensitivo-sensorial  hemi- 
ansesthesia,  whereas  a  lesion  in  the  mesencephalon  is  said  to  cause  incom- 
plete hemiansesthesia  (sight  and  smell  being  normal).  There  are,  however, 
cases  in  which  a  lesion  of  the  lenticular  nucleus  may  attack  only  a  part  of 
the  sensory  fibres  in  the  internal  capsule.  In  this  case  general  sensibility 
is  abolished,  the  special  senses  being  unaffected,  because  their  nerve  fibres 
occupy  the  innermost  part  of  the  sensory  tract  (Ballet).  The  territory 
which  forms  the  sensory  tract  is  supplied  by  the  lenticulo-optic  artery,  so 
that  haemorrhage,  embolism,  softening,  and  tumours  cause  hemiansesthesia. 
Vascular  and  Trophic  Troubles. — Vascular  and  trophic  troubles  belong 
to  the  initial  period  of  cerebral  haemorrhage.  In  apoplexy  the  patient  is 
exposed  to  such  grave  troubles  as  bastard  pneumonia,  pulmonary  conges- 
tion, with  emphysema  and  haemorrhage,  lesions  recalling  the  broncho-pul- 
monary changes  that  follow  experimental  section  of  the  pneumogastric 
nerves  (Charcot).  We  must  also  mention  polyuria,  albimiinuria  (011i\aer), 
ecchymoses  of  the  pleura,  of  the  endocardium,  of  the  pericardium,  of  the 


1358  TEXT-BOOK  OF  MEDICINE 

stomacli,  and  of  tlie  kidneys.  Tlie  various  joint  troubles  generally  belong 
to  tlie  secondary  period,  but  the  gluteal  bedsore  appears  in  the  initial  period. 
This  bedsore  develops  in  the  centre  of  the  gluteal  region  on  the  paralyzed 
side,  whereas  the  bedsore  of  acute  myelitis  develops  in  the  middle  of  the 
sacral  region.  The  bedsore  begins  with  diffuse  redness,  which  appears  a 
day  or  two  after  the  attack;  a  pustule  then  forms,  breaks,  and  ends  in 
ulceration.     The  gluteal  bedsore  is  of  very  grave  significance  (Charcot). 

2.  Secondary  Symptoms. — These  symptoms  supervene  some  weeks  or 
months  after  the  haemorrhage. 

Secondary  Contracture. — In  some  patients  with  hemiplegia  we  notice, 
two  or  three  months  after  the  haemorrhage,  in  the  paralyzed  limbs  more  or 
less  pronounced  contracture,  which  is  at  times  permanent  and  incurable. 
This  contracture  is  due  to  descending  sclerosis  in  the  pyramidal  tract.  The 
sclerosis  is  consecutive  to  a  destructive  lesion  of  the  cerebral  expansion  of 
the  pyramidal  tract. 

Pathological  anatomy  has  proved,  in  fact,  that,  when  cerebral  haemor- 
rhage or  softening  remains  confined  to  the  optic  thalamus  or  the  claustrum, 
descending  sclerosis  does  not  occur,  and  the  patient  may  recover  from 
the  hemiplegia  ;  but  when  the  lesion  involves  the  pyramidal  tract,  either  in 
the  corona  radiata  or  in  the  internal  capsule,  secondary  sclerosis  is  seen  in 
the  inferior  part  of  the  cerebral  peduncle,  the  pons,  the  bulb,  and  the 
opposite  lateral  colunm  of  the  spinal  cord.  This  sclerosis  is  accompanied 
by  contracture. 

Descending  sclerosis  and  contracture  are  not  provoked  by  cortical 
lesions  when  the  lesion  only  involves  the  grey  matter  of  the  convolutions. 
When  the  subjacent  white  matter  is  attacked — and  it  is  always  attacked  in 
embolism  of  the  branches  of  the  Sylvian  artery  which  supply  the  motor 
territories  of  the  cortex — we  meet  with  descending  sclerosis  and  contracture. 
I  may  add  that  outside  the  motor  regions  the  cortical  white  matter  of  the 
other  regions  may  be  affected  without  giving  rise  to  secondary  sclerosis. 

The  irritative  lesion  of  the  fibres  of  the  lateral  columns, by  communicating 
an  abnormal  excitability  to  the  anterior  grey  matter  of  the  spinal  cord 
(motor  cornua),  leads  to  an  exaggerated  tonus,  which  by  its  severity  or 
permanence  constitutes  contracture,  with  exaggeration  of  the  reflexes. 

Secondary  contracture  in  patients  sufiering  from  hemiplegia  is  announced 
by  a  feeling  of  stiffness  and  by  an  exaggeration  of  the  tendon  reflexes. 
When,  two  or  three  weeks  after  the  attack,  a  patient  suffering  from  hemi- 
plegia presents  exaggerated  tendon  reflexes  on  the  paralyzed  side,  contracture 
may  be  foretold.  The  contracture  is  generally  painful,  and  is  localized  at 
first  in  one  of  the  upper  limbs,  more  frequently  in  the  flexor  than  in  the 
extensor  muscles.  The  fingers,  the  wrist,  and  the  forearm  are  forcibly  flexed, 
and  the  arm  is  adducted  against  the  trunk.     The  contracture  only  attacks. 


DISEASES  OF  THE  BRAIN  1359 

the  upper  limb  wlien  the  sclerosis  of  the  lateral  columns  does  not  extend 
bevond  the  su])eri(>r  regions  of  the  8])inal  cord,  but  it  affects  the  lower  limb 
if  the  sclerosis  attacks  the  lumbar  region.  It  is  less  pronounced  in  the 
lower  limb,  and  the  extensor  type  predominates.  The  leg  is  forcibly  ex- 
tended, but  the  toes  are  flexed,  and  chloroform  cannot  overcome  the  con- 
tracture of  hemiplegia,  as  it  overcomes  the  contracture  of  hysterical  patients. 
Babinski's  sign  and  Striimpell's  phenomenon  are  noticed  at  this  period. 
The  muscles  of  the  face  which  are  affected  in  hemiplegia  sometimes  show 
contracture.  The  deviation  of  the  features,  then,  changes  sides,  and 
simulates  crossed  paralysis. 

Contracture  in  patients  with  hemiplegia  varies.  It  is  sometimes  so 
slight  that  it  may  at  first  be  taken  for  flaccid  hemiplegia.  In  other  cases 
it  is  so  marked  that  it  constitutes  an  incurable  deformity.  In  some  patients 
with  hemiplegia  the  contracture  finally  disappears,  but  as  a  rule  the  cure 
is  incomplete.  The  patient  can,  it  is  true,  move  the  limbs  which  have  been 
paralyzed  and  contracted ;  but  if  he  wishes  to  apply  his  attention,  and  to 
make  use  of  his  hand  for  a  specific  purpose,  the  muscular  rigidity  imme- 
diately reappears.  In  other  patients  a  contracture  of  old  standing  dis- 
appears in  a  fairly  rapid  manner,  but  this  disappearance  coincides  with  the 
muscidar  atrophy  of  the  primarily  contracted  muscles. 

The  atrophy  commences  in  the  thenar  eminence  or  in  the  shoulder,  and 
becomes  general.  The  tendon  reflexes  become  sluggish  or  disappear. 
This  muscular  atrophy  is  due  to  the  change  in  the  anterior  cornua  of  the 
spinal  cord,  a  change  carried  to  them  by  the  degenerated  nerve  fibres  of 
the  pyramidal  tract  with  which  they  are  connected.  When  the  limb  is 
attacked  by  atrophy,  the  infirmity  is  incurable.  People  attacked  by  hemi- 
plegia with  contracture  present  the  phenomenon  known  as  syncinesia 
(Vulpian).  When  a  patient  is  told  to  close  the  healthy  hand,  a  similar  but 
imperfect  movement  is  seen  in  the  affected  hand. 

Tremor — Hemichorea — Athetosis. — People  who  have  long  been  suffer- 
ing from  hemiplegia,  and  who  have  been  stricken  with  secondary  con- 
tracture, are  sometimes  attacked  by  a  tremor  which  only  supervenes  at 
the  time  of  a  voluntary  movement.  As  soon  as  the  patient  tries  to  raise 
the  contracted  arm  to  the  head,  the  entire  arm  and  the  hand  are  seized 
with  a  tremor,  made  up  of  regular,  vertical,  and  rapid  oscillations.  This 
tremor  disappears  when  the  arm  is  at  rest,  but  recommences  as  soon  as  the 
muscles  are  contracted.  When  the  foot  is  suddenly  raised  in  paralysis, 
with  contracture  of  the  lower  limb,  the  same  phenomenon  is  produced. 
This  tremor  must  not  be  confounded  with  other  motor  troubles,  such  as 
epileptiform  conviJsions,  which  are  sometimes  seen  in  patients  suffering 
from  hemiplegia.  The  convulsions  are,  without  doubt,  dependent  on  the 
descending  sclerosis  and  on  the  secondary  irritation  of  the  bulb. 


1360  TEXT-BOOK  OF  MEDICINE 

Other  sufferers  from  hemiplegia  show  choreiform  movements  in  the 
paralyzed  limbs.  This  symptomatic  hemichorea  has  all  the  characteristics 
of  true  chorea,  showing  similar  disorder  in  the  voluntary  and  involuntary 
movements,  whether  the  limbs  are  at  rest  or  whether  there  is  voluntary 
movement. 

Hemichorea  generally  shows  itself  in  hemiplegia,  accompanied  by  hemi- 
ansesthesia.  It  appears  progressively  after  several  weeks  or  months,  at 
a  time  when  the  hemiplegia  shows  a  tendency  to  improve,  and  although 
there  is  a  certain  degree  of  contracture  in  the  affected  limbs.  This  hemi- 
chorea, which  is  called  "  post-paraljrfcic  "  because  it  supervenes  after  the  hemi- 
plegia, may  last  indefinitely.  In  some  cases  the  hemiplegia  does  not  declare 
itself  after,  but  before,  the  hemiplegia  ;  it  is  called  "  preparalytic  "  (Grasset), 
a  term  which  is  preferable  to  "  prehaemorrhagic."  This  preparalytic 
hemichorea  may  develop  at  the  moment  of  an  attack  of  apoplexy,  even 
before  the  stage  of  confirmed  hemiplegia,  and  apart  from  any  symptom  of 
hemiangesthesia  and  of  contracture.  It  is  temporary,  and  lasts  only  a  few 
days,  even  when  the  patient  survives  the  apoplexy ;  the  choreiform  move- 
ments are  then  replaced  by  hemiplegia. 

Hemichorea,  like  contracture  and  tremor,  may  be  provoked  by  haemor- 
rhage, softening,  tumour,  or  congenital  atrophy  of  the  brain.  It  is  there- 
fore not  the  nature,  but  the  seat,  of  the  lesion  which  must  be  sought  for  in 
order  to  discover  the  cause  of  the  symptom.  Hemichorea  is  most  frequently 
associated  with  hemiansesthesia.  The  respective  sites  of  the  lesions  must 
be  very  close,  but  it  is  not  a  single  one,  because  the  two  symptoms  may  be 
isolated.  Raymond  places  the  lesions  in  the  posterior  portion  of  the 
internal  capsule.  The  bundles  which  are  said  to  be  more  especially  asso- 
ciated with  hemichorea  are  those  covering  the  posterior  extremity  of  the 
optic  thalamus.  They  are  situated  outside  and  in  front  of  the  bundles, 
wherein  a  lesion  produces  hemiansesthesia.  According  to  the  correct 
remark  of  Grasset,  these  two  regions  have  practically  an  independent 
circulation.  The  lenticulo-optic  artery,  arising  from  the  Sylvian,  supplies 
the  region  wherein  a  lesion  produces  hemianaesthesia,  and  the  posterior 
optic  artery,  arising  from  the  posterior  cerebral,  supplies  the  territory 
wherein  a  lesion  produces  hemichorea. 

According  to  some  authors,  hemichorea  is  said  to  supervene  when  the 
provoking  lesion  is  seated  at  some  point  in  the  pyramidal  tract,  and  the 
loss  of  equilibrium  in  the  muscular  system  is  said  to  be  due  to  the  con- 
tracture (Brissaud)  or  to  the  paralysis.  According  to  other  writers,  the 
provoking  lesion  is  said  to  be  situated  in  the  pyramidal  tract,  but  in  the 
neighbourhood  of  the  optic  thalamus,  the  optic  thalami  containing  reflex 
centres  which  are  important  for  the  nerve  supply  of  the  co-ordinate  muscles 
of  the  body. 


D18ICASKS  OF  THE  liKAIN  1301 

Athetosis  (llaMiiuoiid)  is  a  motor  trouble,  characterized  by  incessant 
movements  of  tlie  fin«^ers  and  of  the  toes.  These  movements  are  hUjw,  and 
are  not  always  Umited  to  the  hngers  and  tlie  toes  ;  they  sometimes  invade  the 
hand  and  the  foot.  It  has  been  suggested  that  athetosis  is  a  special  affection 
of  the  nervous  system,  but  as  certain  patients  have  also  shown  choreiform 
movements,  it  is  probable  that  athetosis  which  supervenes  in  patients  who  have 
long  been  suffering  from  hemii)legia  is  oidy  a  variety  of  post-hemiplegic  chorea. 

Secondary  Trophic  Troubles. — Arthropathy  in  patients  suffering  from 
hemiplegia  may  supervene  a  fortnight,  a  month,  or  much  longer  after  the 
attack.  The  arm  is  chiefly  affected.  The  trouble  is  accompanied  by  ex- 
udative synovitis,  with  swelling  and  pain.  Muscular  atrophy  is  not  rare, 
but  it  has  neither  the  regidarity  nor  the  course  of  progressive  muscular 
atrophy.  On  the  contrary,  the  atrophy  affects  irregularly  a  muscle  or  a 
group  of  muscles  ;  it  ends  by  causing  incurable  infirmity.  The  atrophy 
is  sometimes  masked  by  adiposis  of  the  subcutaneous  connective  tissue. 
This  adiposis,  which  is  rare  in  primary  muscular  atrophy,  is  common  in 
secondary  atrophy.     We  must  not  forget  hemioedema. 

Course — Duration — ^Prognosis. — The  symptoms  of  cerebral  haemor- 
rhage sometimes  commence  with  apoplexy,  but  more  often  with  hemi- 
plegia. Aphasia,  which  is  fairly  frequent  in  softening,  is  here  excessively 
rare,  and  the  differences  in  the  seat  and  in  the  extension  of  the  hsemor- 
rhagic  focus  give  rise  to  various  clinical  types. 

1.  If  the  haemorrhage  originates  in  one  of  the  nuclei  or  on  its  surface, 
and  if  it  remains  limited  there,  without  bursting  into  the  ventricles  and 
damaging  the  internal  capsule,  the  hemiplegia  is  very  frequently  curable 
without  subsequent  contracture. 

2.  If  the  haemorrhage  occurs  in  the  lateral  ventricles  or  on  the  surface  of 
the  brain,  it  is  almost  always  fatal,  and,  in  general,  accompanied  by  apoplexy, 
epileptiform  convulsions,  early  contractures,  coma,  and  rise  in  temperature, 
which  continue  till  death. 

3.  If  the  hsemorrhage  involves  the  pyramidal  tract  in  the  internal  capsule, 
or  if  this  tract  is  compressed  by  a  neighbouring  focus,  irritation  is  the  residt, 
with  descending  sclerosis,  traceable  through  the  corresponding  peduncle, 
the  pons,  the  bulb,  and  the  spinal  cord.  This  sclerosis  becomes  the  starting- 
point  of  late  contractures,  tremors,  and  even  of  muscular  atrophy,  if  the 
irritative  and  destructive  process  spreads  to  the  anterior  cornua  of  the 
spinal  cord.     This  form  of  hemiplegia  is  incurable. 

4.  Another  incurable,  though  much  rarer,  form  is  hemiplegia  which 
persists  indefinitely  in  the  flaccid  condition  (Bouchard),  without  secondary 
contracture  of  the  paralyzed  limbs.  It  is  probable  that  this  flaccid  hemi- 
plegia is  due  to  a  lesion  of  the  motor  tracts  which  has  not  been  followed  by 
descending  sclerosis. 


1362  TEXT-BOOK  OF  MEDICINE 

5.  If  the  hsemorrhage,  by  the  extension  of  the  initial  focus  or  by  com- 
pression, directly  or  indirectly  destroys  the  sensory  tract  in  the  posterior 
segment  of  the  internal  capsule,  hemiansesthesia  accompanies  the  hemi- 
plegia. In  such  a  case  we  may  also  notice  another  symptom — viz.,  hemi- 
chorea  and  athetosis.  Hemiansesthesia  and  hemichorea  are  exceptional, 
because  the  hsemorrhage  rarely  attacks  this  part  of  the  capsule. 

6.  When  the  haemorrhage  remains  confined  to  one  of  the  striate  or  optic 
nuclei,  clinical  medicine  has  not  yet  shown  which  is  the  nucleus  involved, 
and  what  is  the  value  of  this  localization  from  the  point  of  view  of  the 
course  and  of  the  prognosis  of  the  disease. 

7.  Haemorrhages  into  the  cortical  matter  of  the  brain  are  very  rare,  and 
their  symptoms  will  be  better  studied  under  Cerebral  Softening  and  Cerebral 
Localization. 

Diagnosis. — Meningeal  hsemorrhage,  acute  hydrocephalus,  cerebral  con- 
gestion, intracranial  neoplasms  (tumours  of  various  kinds,  gummata,  etc.), 
injuries  to  the  skull,  and  epUepsy,  are  often  accompanied  by  apoplexy. 
I  may  say  as  much  for  ursemia  and  plumbism,  diabetes  (diabetic  coma), 
and  certain  intoxications  (opium,  belladonna,  henbane).  Besides  the  con- 
jugate deviation  of  the  head  and  of  the  eyes,  which  is  a  diagnostic  sign  of 
great  value,  a  rise  in  temperature  will  eliminate  toxic  coma.  Next,  in  these 
various  cases  the  apoplectic  condition  is  more  rarely  accompanied  by 
symptoms  of  hemiplegia,  which  are  met  with  in  cerebral  hsemorrhage. 
The  apoplexy  due  to  cerebral  embolism  is  almost  identical  with  the  apoplexy 
due  to  hsemorrhage. 

Chromo-diagnosis,  based  on  the  colour  of  the  cerebro-spinal  fluid, 
allows  us  to  make  the  diagnosis  of  hsemorrhage  when  the  colour  of  this 
liquid  is  blood-stained,  or  even  yellowish  (Sicard). 

Hemiplegia  due  to  cerebral  hsemorrhage  differs  from  hemiplegia  due  to 
other  lesions  of  the  brain  in  the  course  of  events.  In  cerebral  tumours  the 
hemiplegia  is  incomplete,  slow  rather  than  sudden,  and  almost  always 
announced  by  precursory  phenomena,  such  as  headache,  vomiting,  epilepti- 
form convulsions,  ocular  troubles,  and  paralyses  which,  according  to  the 
seat  of  the  tumour,  attack  one  or  other  of  the  cranial  nerves. 

When  the  hemiplegia  is  due  to  thrombosis  of  the  cerebral  arteries,  the 
patient  shows  the  usual  causes  of  arteritis  and  atheroma  (old  age,  gout, 
syphUis,  alcoholism).  In  some  cases  the  peripheral  arteries  are  converted 
into  hard  tortuous  cords.  The  hemiplegia  is  variable,*  slow,  and  pro- 
gressive ;   it  is  less  often  sudden  and  complete  from  the  outset. 

Hysteria  may  cause  apoplexy  and  hemiplegia,  with  or  without  contrac- 
ture, but  hysterical  hemiplegia  rarely  attacks  the  face.    It  is  rarely  accom- 

*  In  variable  hemiplegia  the  alternate  progressive  and  retrograde  march  points  to 
a  lesion  which  at  the  first  blow  does  not  destroy  the  functions  of  the_invaded  area. 


DISEASES  OF  TIIK   HKAIN  1363 

panied  by  roiitructuri'!  of  the  facial  muscles  oii  tlu;  side  oiJ|)Osite  to  the 
hemi])legia.  It  is  almost  always  accompanied  by  hemiuna^sthesia.  Fmther- 
more,  the  motor  troubles  in  hysteria  are  in  general  associated  with  other 
manifestations  of  this  neurosis,  such  as  ovarian  hyperajsthesia,  globus 
hystericus,  abdominal  tympanism,  anorexia,  ocular  troubles,  hysterogenous 
zones,  etc. 

The  diagnosis  is  sometimes  difficult  because  hystero- organic  associations 
are  not  rare  (Babinski).  Fever,  incontinence  of  faeces,  and  acute  bedsores  are 
in  favour  of  organic  hemiplegia.  The  diagnosis  of  organic  hemiplegia  is  also 
based  on  the  following  signs :  Signe  du  feaucier,  exaggerated  flexion  of  the 
forearm,  combined  flexion  of  the  thigh  and  of  the  trunk  (Babinski).  The 
signe  du  'peaucier  is  as  follows  :  when  a  patient  w4th  organic  hemiplegia  is 
asked  to  yawn,  blow,  or  whistle,  the  platysma  contracts  better  on  the 
healthy  side  than  on  the  diseased  side.  When  the  forearm  is  placed  in 
the  position  of  supination  and  flexed  on  the  arm,  the  flexion  on  the  para- 
lyzed side  is  greater  than  on  the  healthy  side.  Finally,  if  the  patient  lies 
flat  on  a  resisting  horizontal  plane,  and  is  asked  to  assume  a  sitting  position, 
it  will  be  noticed  that  the  thigh  of  the  paralyzed  side  flexes  on  the  pelvis. 
This  movement  of  flexion  is  much  less  marked  on  the  healthy  side.  These 
facts  point  to  relaxation  of  the  muscles  in  the  case  of  organic  hemiplegia. 
We  must  also  inquire  into  the  cutaneous  plantar  reflex  (Babinski's  sign). 
If  the  plantar  surface  of  the  foot  is  pricked,  we  see  flexion  of  the  toes  on  the 
healthy  side  and  extension  of  the  toes,  especially  of  the  big  toe,  on  the 
affected  side.  This  extension  never  exists  in  hysterical  hemiplegia,  where 
flexion  is  the  rule.  Babinski's  sign  has,  then,  a  diagnostic  value,  which 
has  been  confii-med  by  several  observers  (Letienne,  Cestan,  and  Le  Sourd). 
Such  are  the  chief  factors  in  the  diagnosis  between  hysterical  and  organic 
hemiplegia. 

Hemiplegia  of  syphilitic  origin  (gummata,  sclero-gummatous  meningitis, 
obliterating  arteritis,  rupture  of  an  aneurysm)  is  often  preceded  by  pro- 
dromata  (headache,  paresis  of  the  third  and  seventh  nerves,  etc.).  It  may 
nevertheless  resemble  in  all  points  hemiplegia  due  to  cerebral  hsemorrhage. 
Although  it  is  more  frequent  in  the  tertiary  stage,  it  sometimes  appears, 
with  or  without  apoplexy,  in  the  secondary  stage.  The  history  of  the  patient 
must  be  carefully  inquired  into,  and  we  must  look  on  the  skin  or  elsewhere 
for  the  marks  of  syphilis,  in  order  to  institute  treatment  -^dthout  delay 
(m(?e  Cerebral  Syphilis). 

Treatment. — Apoplexy  is  treated  by  bleeding,  leeches  behind  the  ears, 
enemata,  purgatives,  and  counter -irritation  of  the  lower  extremities.  Hemi- 
plegia may  be  alleviated  by  means  of  the  continuous  current.  The  early 
movement  of  the  joints  is  of  great  use.  By  moving  the  joints  of  the  shoulder, 
of  the  Angers,  of  the  wrist,  or  of  the  elbow,  etc.,  and  massaging  the  muscles. 


1364  TEXT-BOOK  OF  MEDICINE 

we  can  obtain  remarkable  results  (Gilles  de  la  Tourette).  The  patient  should 
be  advised  to  go  to  the  seaside  or  to  a  saline  watering-place.  Balaruc  seems 
to  enjoy  a  well-merited  reputation  (Grasset).  The  cure  at  La  Malou  is 
also  of  service.  We  must  always  remember  the  possible  existence  of  syphilis, 
in  order  to  have  recourse  to  mercurial  preparations  and  to  large  doses  of 
iodide  of  potassium. 

IV.  CEREBKAL  SOFTENING— EMBOLISM— ATHEROMA. 

The  expression  "  cerebral  softening  "  does  not  answer  to  a  morbid  entity.  Soften- 
ing of  the  brain  does  not  constitute  a  disease,  but  is  the  result  of  various  pathological 
conditions,  such  as  encephaUtis,  atheroma,  arteritis,  thrombosis,  and  embolism  of  the 
cerebral  vessels.  Encephahtis  will  be  described  separately.  I  shall  here  describe 
cerebral  softening  due  to  vascular  lesions  (atheroma,  arteritis,  and  embolism). 

Rostan  (1820)  was  the  first  to  fix  the  chnical  history  of  softening,  and,  clever  observer 
that  he  was,  he  took  care  to  assign  various  causes  for  it,  having  remarked  that  in  some 
cases  cerebral  softening  is  the  product  of  an  inflammation,  and  that  in  other  circum- 
stances it  is  secondary  to  vascular  changes  due  to  senihty  or  other  causes.  The  writers, 
however,  who  continued  the  study  of  softening  after  Rostan  (LaUemand,  Bouillaud, 
Durand-Fardel)  were  so  imbued  with  the  teaching  of  Broussais,  and  the  idea  of  inflam- 
mation was  then  so  dominant,  that  cerebral  softening  was  made  synonymous  with 
encephahtis,  acute  softening  being  looked  upon  as  an  acute  encephalitis,  and  chronic 
softening  as  a  chronic  encephahtis.  In  1847  Virchow  produced  his  first  monograph  on 
embohsm  and  thrombosis,  and  though  others  had  previously  indicated  or  foreseen  the 
troubles  consequent  on  the  vascular  lesions  of  the  brain,  it  is  just  to  recognize  that 
Virchow  originated  the  anatomical  and  experimental  researches  (Prevost  and  Costard) 
which  have  shed  Hght  on  the  pathogenic  history  of  cerebral  softening. 

Pathological  Anatomy. — When  the  circulation  is  arrested  in  an  area 
of  the  brain  by  obliteration  of  the  arteries,  veins  or  capillaries,  by  an  obliterat- 
ing body  arising  in  situ  (thrombus  and  thrombosis),  or  by  a  migratory  body 
(embolus  and  embolism),  and  the  collateral  circulation  does  not  come  to  the 
help  of  the  ansemic  area,  this  area  degenerates  (necrobiosis)  and  softens. 
Such  is,  in  a  few  words,  the  principle  of  softening  from  vascular  lesions,  but 
these  lesions  do  not  aU  produce  cerebral  softening  for  the  same  reason. 

Thus  obliteration  of  the  capillary  vessels,  simple  or  specific  capillary 
emboli,  pigmentary  emboli,  which  are  said  to  be  one  of  the  results  of  melan- 
aemia  (Frerichs),  calcareous  emboli  (Virchow),  and  putrid  emboli  (Panum), 
may  cause  small  foci  of  softening,  but  their  history  is  too  obscure  for  exact 
details. 

Thrombosis  of  the  venous  sinuses  is  a  rare  cause  of  softening,  and  in  this 
case  the  softening  is  superficial,  and  generally  associated  with  other  brain 
lesions — oedema,  hydrocephalus,  and  changes  in  the  meninges. 

Tlirombosis  and  embolism  of  the  arteries  are  the  most  frequent 
sources  of  cerebral  softening,  and  if  the  collateral  circulation  is  oftec 
powerless  to  re-establish  the  course  of  the  blood  in  an  affected  vessel,  it 
is  because  this  collateral  circulation  is  little  developed  in  the  brain.     Thfi 


DISEASES  OK  THE   I'.RAIN  1365 

central  and  cortical  arteries  of  the  brain  are  terminal  arteries  (Cohnheini) — 
that  i8  to  say,  arteries  which  from  their  orifrin  to  their  termination  receive 
hardly  any  anastomotic  vessels.  Accordingly,  obliteration  of  these  vessels 
is  readily  followed  by  necrobiosis  of  the  region  supplied  by  them,  and  the 
residt  is  a  focus  of  softening. 

In  the  post-mortem  examination  of  an  individual  who  has  died  during 
the  first  period  of  acute  softening  of  the  brain,  or  in  that  of  an  animal  in 
which  artificial  embolism  has  been  produced  (Prevost  and  Cotard),  the  em- 
bolized  region  forms  a  focus  which  is  more  deeply  coloured  at  the  circum- 
ference than  in  the  centre,  and  which  is  often  stippled  red  ;  this  is  red 
softening.  Embolism  of  the  small  vessels  usually  causes  an  infarct  in  the 
embolized  region.  The  word  infarct  means  infiltration  of  the  parenchyma 
by  the  extravasated  blood  (Hirtz  and  Straus).  The  process  is  as  follows  : 
When  the  obliteration  attiicks  an  arteriole,  the  embolized  region  is  rendered 
ischaemic  in  the  centre  and  hypersemic  at  the  circumference.  The  ischgemia 
of  the  centre  is  explained  by  the  arrest  of  the  circulation  in  the  vessel,  and 
the  peripheral  hyperaemia  arises,  no  doubt,  from  the  collateral  congestion 
of  the  arterioles  in  the  neighbourhood  of  the  obstruction.  This  collateral 
congestion  raises  the  tension  in  the  capillaries,  causing  oedema,  diapedesis 
of  the  blood-corpuscles,  and  even  hasmorrhage  into  the  lymphatic  sheath  of 
the  vessels.  The  nerve  tissue  now  becomes  affected  ;  its  elements,  deprived 
of  nutrition,  become  dissociated  ;  the  myeline  breaks  up,  and  we  have 
red  softening.  Later  the  broken  up  myeline  undergoes  fatty  degeneration, 
the  fatty  granules  infiltrate  the  leucocytes  and  the  sheath  of  the  vessels, 
the  colouring  matter  of  the  blood  is  altered,  and  the  softening  assumes  a 
yellowish  tint  (yellow  softening).  Finally,  in  the  last  stage  the  cerebral 
pulp  assumes  the  characteristics  of  a  milky  liquid,  and  we  have  white  soften- 
ing. These  successive  phases,  which  have  been  produced  experimentally, 
do  not  always  occur  in  man,  and  in  certain  large  foci  the  initial  congestion 
is  absent,  and  white  softening  takes  place  from  the  outset. 

The  foci  vary  in  size  from  a  pin's  head  (Parrot)  to  an  orange.  They  are 
often  irregular,  and  attack  especially  the  cerebral  convolutions— milike 
haemorrhage,  which  is  most  common  in  the  central  portions.  When  the 
goftening  is  very  extensive,  the  cerebral  convolutions  which  form  the  wall 
of  the  focus  are  depressed,  and  even  before  opening  the  brain  we  may,  by 
the  external  conformation,  judge  where  the  focus  of  softening  is  seated. 
In  old  cases  of  softening  chronic  encephalitis  occurs,  and  the  sclerosed 
neuroglia  afiects  the  walls  of  the  focus.  If  the  walls  do  not  become  adherent, 
a  cyst  results  ;  in  the  contrary  case,  a  cicatrix  is  formed.  These  cicatrices 
have  a  yellowish  colour  (Durand-Fardel) ;  they  are  indurated,  and  formed 
of  connective  tissue,  of  fatty  matter,  and  of  haematoidin.  At  these  points 
the  convolutions  are  deformed  and  atrophied. 

II.  87 


1366  TEXT-BOOK  OF  MEDICINE 

As  secondary  degenerations  occur  under  the  same  conditions  as  in 
hsemorrliage,  I  refer  the  reader  to  the  preceding  section  for  details  con- 
cerning descending  sclerosis. 

Besides  the  cerebral  lesions  vrhich  I  have  just  described,  we  find,  post 
mortem,  vascular  lesions,  which  are  the  cause  of  the  softemng — arterial 
embolism,  atheroma,  and  obliterating  arteritis. 

Pathogenesis. — Let  us  now  consider  the  pathogenesis  of  (1)  softening 
by  embolism  and  (2)  softening  by  thrombosis. 

1.  Softening  by  Embolism. — We  have  to  consider  the  origin,  course, 
and  termination  of  the  embolism. 

Clironic  diseases  of  the  left  side  of  the  heart,  especially  mitral  stenosis 
(Duroziez),  acute  endocarditis,  especially  the  emboligenous  and  infective 
forms,  fibrinous  coagula  in  the  auricle  in  the  aged  (Yulpian),  and  lesions 
of  the  aorta,  are  the  most  common  sources  of  cerebral  embolism.  The 
embolus  rarely  enters  the  innominate  trunk,  which  opens  obliquely  into  the 
aorta.  It  nearly  always  follows  the  left  carotid,  which  is  the  more  direct 
prolongation  of  the  aortic  trunk.  The  embolus  passes  into  the  internal 
carotid,  and  almost  always  enters  the  middle  cerebral  artery.  It  then 
obliterates,  according  to  its  size,  the  trunk  of  the  vessel  before  or  after  the 
origin  of  the  perforating  arteries.  It  may  also  block  a  secondary  arteriole, 
producing  symptoms  and  paralyses,  which  vary  according  to  the  region 
involved.  As  the  history  of  these  symptoms  and  paralyses  is  inseparable 
from  a  knowledge  of  the  cerebral  circulation,  and  especially  of  the  dis- 
tribution of  the  Syh-ian  artery,  I  shall  briefly  mention  these  anatomical 
points. 

The  middle  cerebral  artery  in  the  fissiire  of  Sylvius  gives  oS  branches  Tvhich  diverge 
between  the  convolutions  of  the  insula.  These  branches  are  of  two  kinds — central  and 
cortical.  The  central  or  perforating  branches,  described  under  Cerebral  Haemorrhage, 
are  destined  for  the  corpus  striatum,  the  optic  thalamus,  the  internal  capsule,  and  the 
corona  radiata,  and  one  of  them  acquires  a  great  importance  from  the  lenticulo -optic 
branch,  which  it  furnishes  to  that  portion  of  the  internal  capsule  in  which  a  lesion  causes 
hemiansesthesia. 

The  cortical  branches,  which  arise  fi'om  the  middle  cerebral  artery  after  the  central 
branches,  are :  the  artery  of  the  iaferior  frontal  convolution  (a  lesion  in  this  region 
produces  aphasia) ;  the  arteries  of  the  motor  centres— that  is  to  say,  the  artery  of  the 
ascending  frontal  convolution — which  sends  a  branch  to  the  middle  frontal  convolution  ; 
and  the  artery  of  the  ascending  parietal  convolution.  Then  come  the  parieto-sphenoidal 
and  the  sphenoidal  arteries. 

Accordingly,  an  embolus  which  obliterates  the  SyMan  artery  before  the 
origin  of  the  perforating  arteries  causes  softening,  which  extends  both  to  the. 
central  portions  of  the  brain  and  also  to  the  cortical  regions  just  enumerated. 
We  fimd,  therefore,  hemiplegia,  hemiansesthesia,  and  aphasia.  If  the  em- 
bolus blocks  the  artery  beyond  the  origin  of  the  perforating  vessels,  we 
find  hemiplegia  and  aphasia  without  hemianeesthesia,  because  the  lenticulo- 


DISEASES  OF  THE  BRAIN  1367 

optic  artery  remains  patent.  Isolated  softening  of  the  third  left  convolu- 
tion has  often  caused  aphasia  without  paralysis,  so  tliat  aphasia  and  para- 
lysis of  the  arm,  of  the  leg,  and  of  the  face  may  be,  according  to  circum- 
stances, isolated  or  associated.  Tlio  localization  of  the  softening  depend.s, 
therefon\  oii  the  situation  of  the  embolus,  which  abolishes  the  circulation 
in  a  given  region,  as  we  shall  see.  under  Cerebral  Localization. 

'2.  Softening  by  Thrombosis. — Atheroma  of  the  arteries  of  the  brain 
plays  a  part  in  the  aetiology  and  in  the  progress  of  atheroma  in  general. 
Old  age,  alcoholism,  gout,  diabetes,  and  the  infectious  diseases  are  the 
most  potent  causes  of  obliterating  arteritis  and  of  atheroma.  Chronic 
arteritis  and  atheroma  narrow  the  lumen  of  the  vessel.  Fibrin  is  deposited 
on  the  granulations,  due  to  the  endarteritis  and  on  the  patches  of  atheroma. 
An  obliterating  clot  is  formed,  and  when  the  thrombosis  is  complete,  the 
area  supplied  by  the  obliterated  vessel  undergoes  necrobiosis,  unless  the 
collateral  circulation  is  established. 

Syphilitic  Arteritis. — Amongst  the  vascular  lesions  capable  of  causing 
cerebral  softening,  syphilitic  arteritis  is  of  the  highest  importance  ;  it  shows 
a  marked  predilection  for  the  cerebral  arteries.  Syphilitic  arteritis  and  its 
results  will  be  discussed  under  Cerebral  Syphilis. 

Symptoms. — According  to  circumstances,  the  commencement  of  cere- 
bral softening  is  sudden  or  gradual. 

1.  Softening  of  Sudden  Onset. — The  sudden  appearance  of  symptoms 
(apoplexy,  hemiplegia,  aphasia)  is  especially  caused  by  embolism,  because 
the  embolus  art  once  blocks  the  vessel  which  was  permeable,  whereas  the 
slow  and  gradual  appearance  of  symptoms  is  rather  reserved  for  thrombosis, 
which  gradually  obliterates  the  lumen  of  the  vessel.  This  rule  is  not  abso- 
lute, and  although  thrombosis  is  slow  to  cause  complete  obliteration  of  the 
artery,  yet  there  are  cases,  especially  in  syphilitic  lesions  (arteritis,  sclero- 
gummatous  lesions,  tumour)  where  the  symptoms  appear  almost  as 
brusquely  as  in  vascular  obliteration  by  embolism. 

Softening  of  sudden  onset  and  cerebral  haemorrhage  have  many  symp- 
toms in  common.  Softening,  however,  especially  when  it  is  dependent  on 
syphilitic  lesions,  is  more  often  preceded  by  prodromata  (headache).  In 
both  cases  apoplexy  may  open  the  scene,  with  its  visceral  congestion? 
(pulmonary  congestion)  and  its  trophic  troubles  (gluteal  bedsores). 

Apoplexy  is  often  absent,  and  the  softening  commences  with  hemiplegia. 
The  hemiplegia  has  all  the  characteristics  described  under  Cerebral  Haemor- 
rhage. It  is  peculiar  in  that  it  attacks  the  right  side,  and  in  this  case 
it  is  frequently  associated  with  aphasia.  This  association  of  right  hemi- 
plegia and  of  aphasia  is  due  to  the  predilection  of  the  lesions  for  the  left 
Sylvian  artery — a  predilection  especially  marked  in  embolism. 

As  apoplexy  and  hemiplegia  have  been  described  in  detail  under  Cerebral 

87—2 


1368  TEXT-BOOK  OF  MEDICINE 

Hsemorrhage,  further  reference  is  unnecessary.  Amongst  the  troubles 
produced  by  cerebral  softening,  one  of  the  most  important  is  aphasia 
(loss  of  speech),  which  may  exist  alone  or  may  be  associated  with  right 
hemiplegia  and  with  hemianaesthesia.  For  the  description  of  aphasia  I 
refer  the  reader  to  the  next  section. 

We  may  also  observe  homonymous  lateral  hemianopia  (loss  of  half  of 
the  visual  field)  in  softening  of  the  cuneus  of  the  occipital  lobe  or  of  the 
gyrus  supramarginalis. 

2.  Softening  of  Gradual  Onset. — When  softening  of  the  brain  is  not 
due  to  embolism,  the  early  s}Tnptoms  are  slow  and  progressive  :  the  patient 
complains  of  headache,  vertigO;,,  twitchings  of  the  fingers,  and  numbness 
in  the  foot ;  the  hand  becomes  awkward,  the  speech  is  embarrassed,  and 
the  mouth  is  crooked.  This  course  of  events  occurs  in  syphilitic  obliterating 
arteritis.  Sometimes,  and  especially  in  the  case  of  atheroma,  the  troubles 
may  be  dissociated,  and  so  slight  that  the  patient,  especially  if  he  is  an 
old  man,  is  scarcely  conscious  of  them.  They  grow  better  or  worse  under 
the  influence  of  various  causes  (digestive  troubles),  and  the  hemiplegia, 
wliich  is  rarely  complete,  is  called  variable. 

In  some  cases  an  acute  phase  follows  this  slow  onset,  and  the  sym.ptoms, 
which  are  at  first  mild,  speedily  reach  their  maximum.  More  frequently 
a  chronic  phase  succeeds  the  slow  phase  of  the  onset ;  this  is  the  typical 
form  of  chronic  softening. 

Sometimes  intellectual  troubles  precede  or  overshadow  the  paralytic 
troubles.  The  patient  loses  his  memory,  especially  the  'recollection  of 
recent  events.  His  ideas  are  incoherent,  his  speech  is  embarrassed  ;  he 
laughs  and  cries  without  reason,  and  is  subject  to  a  kind  of  wandering, 
prone  to  end  in  delirium.  These  complications  are  slow  and  progressive, 
lasting  for  months  and  years.  They  are  sometimes  interrupted  by  apoplecti- 
form or  epileptiform  attacks,  by  phases  of  excitation  (restlessness,  delirium, 
or  mania),  and  by  periods  of  depression  (somnolence  and  coma).  In  addi- 
tion to  these  motor  and  psychical  troubles,  which  succeed  one  another 
or  appear  together,  we  find  in  rare  instances  obstinate  vomiting,  and  con- 
tractures, which  may  assume  a  capital  importance. 

Secondary  Symptoms. — Softening,  like  cerebral  hemorrhage,  may  be 
followed  by  secondary  symptoms — progressive  and  permanent  contracture, 
tremor,  post-hemiplegic  hemichorea,  and  muscular  atrophy,  proving  that 
the  descending  sclerosis  of  the  p\Tamidal  tract  depends  on  the  situation 
of  the  invaded  region,  and  not  upon  the  nature  of  the  lesion. 

In  describing  cerebral  softening,  I  have  confined  my  attention  to  the 
most  common  varieties,  wliich  correspond  anatomically  with  a  fairly  ex- 
tensive lesion ;  but  there  are  cases  in  which  the  lesion  is  limited  to  a  restricted 
area  of  the  brain,  with  or  without  implication  of  the  meninges.     It  occupies 


DISEASES  OE  TFFE  BRAIN  incn 

only  one  convolution  of  tln^  bniin,  or  a  part  of  the  convolution,  attacking 
the  grey  matter  or  the  subjacent  white  matter.  Isolated  symptoms  are 
then  noticed,  and  depend  on  the  localization  of  the  lesion.  These  symp- 
toms are  paralysis  of  the  arm,  paralysis  of  the  l(!g,  with  or  without  contrac- 
ture and  epileptiform  movements.  These  various  symptoms  will  be  dis- 
cussihI  in  detail  under  Cerebral  Localization  and  Cerebral  Syphilis. 

Diagnosis  Prognosis. — Cerebral  softening  of  sudden  onset  has  many 
symptoms  in  common  with  cerebral  hajmorrhage  (apoplexy,  hemiplegia). 
Certain  signs  are,  however,  in  favour  of  softening.  If  the  patient  has  right 
hemiplegia  and  also  aphasia,  softening  may  be  diagnosed,  for  aphasia  is 
very  seldom  due  to  haemorrhage.  If  the  patient  has  mitral  or  aortic  disease, 
embolism  is  the  probable  cause  of  the  softening.  If  he  has  atheromatous 
arteries,  softening  by  thrombosis  is  naturally  suspected ;  and  if  the  patient 
is  syphilitic,  it  is  probable  that  the  softening  has  its  origin  in  the  com- 
pression of  an  artery  by  a  syphiloma,  or  more  often  in  obliterating  arteritis. 

Softening  is  sometimes  difficult  to  distinguish  from  the  clinical  syndrome 
caused  by  lacunse  of  the  brain.  A  patient  suffering  from  lacuna  is  one 
who  has  been  attacked  by  a  sudden  but  slight  stroke,  without  loss  of  con- 
sciousness, followed  by  partial  and  incomplete  hemiplegia.  The  gait  is 
somewhat  affected,  and  is  known  under  the  name  of  the  marclie  a  petits 
pas.  We  also  find  troubles  of  pronunciation  and  of  deglutition,  as  well  as 
spasmodic  laughing  and  cr^dng.  Softening  of  slow  onset,  due  to  cerebral 
atheroma,  is  difficult  to  diagnose,  because  its  manifestations  are  often 
incomplete  and  insidious.  It  must  be  remembered  that  the  aged  are  subject 
to  apoplectiform  or  epileptiform  symptoms  and  to  intellectual  troubles 
dependent  on  cerebral  atheroma.  When  a  patient  shows  at  the  same  time 
signs  of  general  atheromasia,  it  is  probable  that  his  cerebral  troubles  are  due 
to  cerebral  softening  of  atheromatous  origin. 

The  gravity  of  the  prognosis  is  readily  understood.  Softening  by  embo- 
lism is  serious  on  account  of  the  extent  of  the  lesion.  Softening  by  throm- 
bosis is  formidable,  because  it  is  often  associated  with  general  arterio-sclerosis. 

Treatment  is  generally  useless,  except  in  syphilitic  cases.  If  syphilis 
is  even  suspected,  active  specific  treatment  must  be  employed  without 
delay.  Mercurial  injections  and  iodide  of  potassium  in  large  doses  are 
especially  indicated. 

V.  APHASIA. 

Description.— In  the  preceding  section  I  pointed  out  that  obliteration 
of  the  left  ISylvian  artery  by  embolism  or  by  thrombosis  may  be  followed 
by  right  hemiplegia  and  by  aphasia. 

What,  then,  is  aphasia  ?  It  is  the  loss  of  speech.  It  is  even  more. 
Aphasia,  when  complete,  includes  not  only  loss  of  speech,  but  also  loss  of 


1370  TEXT-BOOK  OF  MEDICINE 

the  power  of  writing,  of  making  gestures,  and  of  mimicry.  In  a  word,  it 
is  the  loss  of  language,  the  word  "  language  "  being  taken  in  the  widest 
acceptation  of  the  term.  This  question  of  language  has  been  well  put 
by  Gratiolet.  There  is  a  natural  language  by  which  the  internal  condition 
of  the  individual  is  revealed,  in  spite  of  himself ;  and  there  is  an  artificial 
language,  in  which  thought,  clothed  in  a  certain  form,  is  expressed,  this 
form  being,  according  to  circumstances,  speech,  writing,  or  gesture.  In 
aphasia,  then,  the  person  preserves  natural  language  ;  if  he  has  a  feeling  of 
gladness,  of  sadness,  or  of  anger,  this  feeling  betrays  itself  in  his  whole 
person,  in  spite  of  himseK.  But  artificial  language  is  absent,  and,  if  you  ask 
him  to  express  this  same  sentiment  by  means  of  speech,  writing,  or  mimicry, 
he  is  absolutely  incapable  of  telling  you  the  name  of  an  object,  the  use  of 
which  he  knows  perfectly,  and  he  is  conscious  of  this  incapacity,  which 
betrays  itself  by  gestures  of  impatience. 

When  the  aphasia  declares  itself,  the  patient  usually  has  some  intellectual 
troubles  (loss  of  memory,  hebetude).  These  troubles  are  generally  temporary; 
volition  and  understanding  are  preserved,  and  the  patient  can  conceive  and 
associate  ideas,  but  he  has  lost  the  means  of  communicating  them  to  others, 
and  when  he  wishes  to  transform  his  ideas  into  signs,  to  adapt  the  proper 
words  to  them,  or  to  reproduce  them  in  writing,  he  is  incapable  of  so  doing. 

The  person  suffering  from  aphasia  has  at  his  command  only  a  few  mono- 
syllables or  a  single  word,  which  he  articulates  perfectly,  and  invariably 
repeats  apropos  of  everything.  One  man  can  only  say  "  yes  ";  another  only 
the  word  "  tan."  One  of  Trousseau's  patients  could  only  say  the  word 
"  cousisi."  If  the  patient  is  shown  a  knife  or  a  pencil,  although  he  knows 
the  object  and  its  use,  he  cannot  clothe  the  idea  with  the  proper  word. 
Tell  him  the  name  of  the  object,  and  his  gestures  wiU  immediately  manifest 
his  satisfaction  at  finding  this  word  again  ;  but  ask  him  to  repeat  the  word 
"  knife  "  or  "  pencil,"  and  he  is  quite  unable  to  do  so,  or  else  after  an 
effort  he  utters  some  word  or  other.  The  phonatory  apparatus  is  intact, 
but  the  apparatus  which  puts  the  conceived  idea  into  words  is  broken.  In 
the  long  run  the  patient  regains  this  function,  but  when  the  lesion  is  deeply 
seated  the  patient  suffering  from  aphasia  does  not  completely  recover ;  he 
is  lame  in  his  brain  (Trousseau).  It  will,  therefore,  be  understood  that  the 
capacity  of  patients  suffering  from  aphasia  to  make  a  will  should  be  raised. 

In  some  cases,  as  we  have  said,  the  trouble  of  language,  joined  to  a 
defect  of  transmission,  is  revealed  by  agraphia.  The  patient  can  no  longer 
write.  Paralysis  of  the  right  arm,  which  is  often  associated  with  aphasia, 
may  prevent  our  noticing  this  symptom,  but  even  if  the  paralysis  is  slight 
or  absent,  the  patient  attacked  by  agraphia  can  no  more  write  (eithet  with 
the  right  hand  or  the  left)  than  the  patient  suffering  from  aphasia  can 
speak.     Agraphia  may  exist  alone  or  may  coincide  with  aphasia. 


DISEASES  OF  THE  BRAIN  IHTl 

In  addition  to  the  variety  of  nphasia  which  I  have  just  descrihcd,  and 
which  represents  the  most  common  case,  we  find  other  varieties.  In  certain 
subjects  the  intellectual  faculties  are  affected  on  account  of  the  extent 
of  the  cerebral  lesion  ;  in  others  the  aphasia  is  incomplete,  and  the  patient 
substitutes  in  the  midst  of  a  word  or  of  a  phrase  letters  or  syllables  which 
make  tiie  word  or  phrase  imintelligible.  This  is  called  paraphasia.  The 
patient  also  makes  tliis  substitution  when  he  writes.  Sometimes  the  various 
modes  of  expression  are  alone  attacked.  Lassegue  speaks  of  a  musician 
suffering  from  aphasia  who  could  neither  read  nor  write,  but  who  jotted 
down  a  musical  phrase  which  he  had  heard  sung.  The  power  of  mimicry' 
is  not  always  lost  in  aphasia.  It  is  at  times  exaggerated.  The  form  of 
aphasia  just  described  has  received  the  name  of  motor  aphasia,  in  order  to 
distinguish  it  from  sensory  aphasia,  which  we  shall  now  consider. 

Certain  individuals  are  not,  properly  speaking,  suffering  from  aphasia 
because  thev  can  speak  and  write,  but  they  are  affected,  according  to 
Kussmaul's  expression,  with  word-blindness  or  word-deafness.  In  word- 
deafness  the  sense  of  hearing  has  preserved  its  delicacy,  since  the  ticking  of  a 
watch  is  readily  perceived ;  the  intelligence  is  intact,  and  the  subject  replies 
clearly  and  aloud  to  the  questions  addressed  to  him  in  writing.  If  he  is  spoken 
to,  he  understands  nothing,  hearing  only  a  succession  of  noises,  which  do 
not  convey  to  him  the  form  of  words,  and  have  no  signification  to  his  mind. 

In  word-blindness  the  patient  is  able  to  speak  and  to  write,  but  he  is 
unable  to  read.  The  letters  only  represent  to  his  mind  a  succession  of 
lines,  just  as  in  the  case  of  word-deafness  the  words  only  represent  a  suc- 
cession of  noises.  In  such  cases  the  association  is  broken  between  the  con- 
ventional sign  (the  spoken  or  written  word)  and  the  idea.  In  motor  aphasia 
the  patient  is  incapable  of  transforming  his  ideas  into  external  signs,  but  he 
perceives  these  external  signs  (speech,  writing)  perfectly.  In  word-blind- 
ness and  word-deafness  the  apparatus  of  reception  which  is  to  receive  these 
signs  in  the  brain  and  give  them  their  value  is  destroyed.  In  the  first  case 
there  is  trouble  in  the  transmitting  apparatus  ;  in  the  second  case  there  is 
trouble  in  the  receiving  apparatus. 

Pathogenesis. — All  spoken  language  is  made  up  of  a  series  of  conventional 
sounds  which  form  speech,  just  as  written  language  is  formed  by  a  series  of 
conventional  signs  which  form  writing.  These  conventional  sounds  and 
signs  are  learnt  and  retained  by  the  memory,  which  plays  the  greatest  part 
in  the  first  act  of  language.  The  sense  of  hearing  perceives  the  sounds ; 
the  arrangement  of  these  sounds  produces  the  word,  and  the  impression 
of  the  words,  with  the  idea  attached  thereto,  is  stored  up  in  the  first  left 
temporal  convolution.  This  is  called  auditory  memory— that  is  to  say, 
the  memory  of  the  conventional  sounds,  perceived  by  the  sense  of  hearing, 
and  forming  the  spoken  language. 


1372  TEXT-BOOK  OF  MEDICINE 

Let  us  suppose  the  destruction  of  the  first  temporal  convolution  by 
softening.  What  will  be  the  condition  of  the  patient  ?  The  patient  will 
be  able  to  speak,  write,  read,  and  understand  what  he  reads,  bat  he  can 
no  longer  understand  anything  of  what  is  said  to  him.  The  words  repre- 
sent only  sounds  to  him.  In  losing  the  temporal  convolution  he  has  lost 
the  memory  of  the  value  and  of  the  order  of  those  sounds  which  form 
spoken  language  ;  he  is  affected  with  word-deafness.  This  is  a  case  of 
sensory  aphasia. 

The  same  remark  applies  to  written  language.  Writing,  as  we  have 
said,  is  but  the  conventional  union  of  a  certain  namber  of  signs.  The 
eye  perceives  these  signs,  as  the  sense  of  hearing  perceives  the  sounds,  and 
then  the  value  and  the  order  of  these  signs  impress  the  cerebral  centre  in 
the  inferior  parietal  lobule  on  the  left  side,  where  visual  memory  stores 
up  the  impression  of  the  conventional  signs  called  writing. 

Let  us  suppose  the  destruction  of  this  inferior  parietal  lobule,  the  centre 
for  visual  memory.  The  patient  can  speak,  write,  and  understand  what  is 
said  to  him,  but  he  can  no  longer  read  writing.  The  writing,  as  far  as  he 
is  concerned,  only  represents  a  series  of  signs,  without  value.  In  losing  the 
function  of  the  left  inferior  parietal  lobule,  he  has  lost  the  memory  of 
written  signs  ;  he  has  word-blindness. 

The  cerebral  regions,  in  which  the  auditory  and  verbal  recollections  are 
stored,  form  the  apparatus  for  the  reception  of  language.  By  this  cerebral 
process  the  teaching  of  language  commences  in  the  little  child  whose  brain 
is  undergoing  evolution,  or  in  the  individual  learning  a  new  language.  A 
child  or  an  adult  is  supplied  with  the  necessary  apparatus  for  understanding 
the  language  of  others,  but  before  they  can  communicate  with  others,  either 
by  speech  or  writing,  they  must  clothe  their  ideas  with  the  conventional 
signs,  which  constitute  spjech  and  -^vriting.  The  education  of  a  new  cerebral 
region,  Broca's  convolution,  or  the  third  left  frontal  convolution,  now  inter- 
venes. It  has  so  far  been  a  question  of  the  centres  of  sensory  elaboration  ; 
it  now  becomes  a  question  of  the  centre  of  motor  elaboration.  After  a  long 
apprenticeship  the  child  learns  to  educate  this  motor  centre  of  co-ordination, 
in  order  to  speak  or  to  read.  This  region  of  motor  co-ordination  is  developed 
parallel  with  the  regions  of  sensory  elaboration.  Broca's  convolution 
preserves  the  memory  of  the  co-ordination  of  the  movements  necessary  for 
speech  and  writing.  The  order  to  execute  these  movements,  properly 
co-ordinated,  is  transmitted  to  the  cerebral  cells  of  the  neighbouring  regions 
(motor  zone),  and  thence  to  the  nerves  and  muscles ;  and  the  organs  which 
transmit  spoken,  written,  or  mimic  language,  enter  into  action. 

Let  us  suppose  softening  of  Broca's  convolution.  The  patient  can  under- 
stand what  is  said  and  what  he  reads,  but  he  cannot  put  his  thoughts  either 
into  speech  or  writing.     He  has  lost  the  cerebral  region  in  which  thought 


DISEASES  OF  THE  BRAIN  137:^ 

clothes  the  exterior  signs  by  which  man  communicates  with  his  fellows. 
He  is  attacked  by  motor  ajihasia  ami  ajifraphia. 

All  attempt  has  been  made  to  dissociate  aphasia  from  agrap)iiu  by 
making  agraphia  dependent  on  lesions  of  the  left  middle  frontal  convolution 
It  is  hardly  probalile  that  there  is  a  special  centre  for  agraphia.  Aphasia 
and  agraphia  are  a  part  of  the  same  whole.  As  we  advance  in  the  studv  of 
agraphia,  says  Dejerine,  we  see  that  Trousseau  spoke  correctly,  in  his  clinical 
lectures  on  Aphasia,  of  agraphia  occurring  in  patients  suffering  from  aphasia, 
lie  said  regarding  patients  suffering  from  cortical  motor  aphasia,  the  only 
form  known  in  his  day  :  "  Under  ordinary  circumstances,  the  patient  suffer- 
ing from  aphasia  is  no  more  fit  to  express  his  thoughts  in  words  than  in 
writing  ;  and  though  he  can  use  his  hands  with  as  much  precision  as  for- 
merly, he  is  as  powerless  to  write  a  word  w4th  his  pen  as  he  is  powerless  to 
utter  a  spoken  word." 

The  examples  that  I  have  chosen  to  demonstrate  sensory  and  motor 
aphasia  are  tj^ical  cases.  In  many  circumstances,  however,  these  types 
do  not  appear  in  a  pure  condition.     I  quote  examples  : 

Motor  and  sensory  aphasia  may  exist  in  the  same  subject,  or  either 
may  be  present  alone. 

Aphasia  may  exist  with  complete  preservation  of  the  mental  faculties,  or 
may  be  accompanied  by  intellectual  troubles  ;  it  is  a  matter  of  localization. 

Word-blindness  and  word-deafness  are  sometimes  accompanied  by 
pronounced  paraphasia. 

Word-blindness  shows  two  distinct  clinical  forms :  in  the  one,  agraphia 
is  accompanied  by  word-blindness  ;  in  the  other,  the  power  of  writing  is 
preserved. 

Localizations. — As  I  have  already  remarked,  motor  aphasia  is  due  to 
cerebral  lesions  in  the  posterior  third  of  the  third  left  frontal  convolution 
(Dax,  Broca).  It  is  also  caused  by  lesions  of  the  white  fibres  which  arise 
from  this  cortical  centre,  and  which  Pitres,  in  kis  description  of  the  centrum 
ovale,  has  described  under  the  name  of  inferior  pediculo-frontal  bundles. 

The  lesions  which  attack  the  anterior  segment  of  the  internal  capsule 
and  the  internal  bundle  of  the  foot  of  the  peduncle,  must  provoke  aphasia 
because  the  bundles  which  constitute  it  degenerate  when  the  third  convolu- 
tion is  affected  (Charcot  and  Fere). 

The  inferior  frontal  artery,  which  arises  from  the  middle  cerebral 
artery,  may  be  considered  as  the  artery  of  aphasia  or  of  Broca's  convolu- 
tion. Charcot  has  seen  a  case  in  which  obliteration  of  this  arteriole  had 
caused  aphasia  without  hemiplegia. 

Word-deafness  coincides  with  lesions  of  the  first  left  temporal  convolu- 
tion, especially  in  its  postero-superior  extremity,  and  word-blindness  is 
due  to  the  lesions  of  the  left  inferior  parietal  lobule. 


1374 


TEXT-BOOK  OF  MEDICINE 


The  cerebral  lesions  which  produce  aphasia  are  almost  always  situated 
on  the  left  side.  This  law,  though  not  absolute,  is  the  rule.  Why  is 
aphasia  associated  with  lesions  on  the  left  side  ?  The  probable  reason  is 
that  we  are  accustomed  to  speak  with  our  left  brain,  just  as  we  acquire  the 
habit  of  using  our  right  hands.  Aphasia  is  rarely  caused  by  haemorrhage. 
In  most  cases  it  is  due  to  softening,  and  consequently  to  various  causes — 
embolism,  thrombosis,  obliterating  arteritis,  or  tumour. 

I  have  already  remarked  that  aphasia  is  usually  associated  with  right 
hemiplegia,  the  explanation  being  that  the  lesion  involves  the  neighbouring 
motor  convolutions.  The  paralysis  is  generally  slight  in  the  face,  and  the 
more  marked  the  paralysis  of  the  lower  limb,  the  less  marked  the  aphasia. 
Aphasia  is  often  associated  with  hemiansesthesia  of  the  right  side  (G-rasset) — 


Fig.  64 — Cerebral  Hemisphere, 


P„  F„ 


Fg,  frontal  convolutions : 


Fa,  ascending  frontal  convolution ;  Pa,  ascending 
parietal  convolution ;  P^,  Pg,  parietal  convolutions ;  Tj,  T^,  Tg,  temporal  con- 
volutions ;  0, ,  Og,  Og,  occipital  convolutions ;  A,  centre  for  motor  aphasia ; 
Ag,  centre  for  agraphia ;  Cv,  word  bUndness ;  Sv,  word  deafness. 

a  fact  explained  by  the  seat  of  the  lesion,  because  the  lenticulo-optic  portion 
of  the  internal  capsule  is  very  close  to  the  convolutions  of  the  insula. 

New  Doctrine  of  Aphasia. — The  classical  conception  of  the  mechanism 
and  of  the  cerebral  localization  of  aphasia  has  been  modified  by  recent 
researches.  Pierre  Marie,  from  a  careful  examination  of  the  brain  in  some 
fifty  cases,  has  met  with  several  instances  of  aphasia  in  which  Broca's  con- 
volution showed  no  lesion.  On  the  other  hand,  he  has  found  lesions  in  the 
third  left  frontal  convolution  which  had  caused  no  disorder  of  speech. 

Marie,  in  consequence  of  these  fresh  facts  and  observations,  thinks  that 
the  lesions  producing  aphasia  occupy  a  so-called  lenticular  zone,  bounded 
in  front  by  a  transverse  line  through  the  anterior  sulcus  of  the  insula  to  the 
corresponding  point  of  the  lateral  ventricle,  and  behind  by  a  similar  line 
from  the  posterior  sulcus  of  the  insula  to  the  corresponding  point  of  the 
lateral  ventricle.     This   quadrilateral   area   contains   the    lenticular  and 


DISEASES  OF  THE  BRAIN  1375 

oandate  uuclei  aiid  Llic  internal  and  external  capsules.  The  region  whose 
lesions  contrihuti!  to  the  production  of  aphaHia  also  (•outains  the  zone  of 
Wernicke,  formed  by  the  gyrus  HUi)rainarginali.s,  the  angular  gyrus,  and  the 
foot  of  the  two  first  temporal  convolutions.  Particular  disorders  follow, 
according  as  the  lesion  is  in  the  lenticular  zone  or  in  Wcjrnicke's  zone.  If 
the  lesion  only  affects  the  lenticular  zone,  we  have  classical  motor  aphasia — 
that  is,  disorder  of  articulate  speech,  called  "  anarthria  "  by  Marie.  If  the 
lesion  only  affects  the  zone  of  Wernicke,  we  find  Wernicke's  aphasia.  The 
patient  can  speak — in  some  cases  he  speaks  too  nmch — but  the  words, 
though  well  articulated,  are  often  incomprehensible,  or,  at  the  very  least, 
incomplete.  The  power  of  reading  and  writing  is  abolished  or  is  imperfect 
(classical  word-blindness).  The  patient  cannot  understand  spoken  language 
(classical  word-deafness).  These  symptoms,  as  a  whole,  constitute  sensory 
aphasia ;  but  Marie  does  not  admit  the  existence  of  special  centres  for  the 
images  of  words  heard  and  for  the  visual  images  of  language.  He  considers 
these  disorders  as  troubles  of  internal  expression,  as  opposed  to  the  disorders 
of  external  or  articulate  expression,  and  he  thinks  that  Wernicke's  zone  is 
the  centre  for  the  intellectual  elaboration  of  language,  just  as  the  lenticular 
zone  is  the  centre  for  the  articulation  of  words. 

This  new  doctrine  has  been  opposed  or  rejected  by  many  neurologists 
(Dejerine,  Ladame,  von  Monakow,  Mills  and  Spiller,  Lloyd,  etc.).  In  the 
discussion  of  such  a  complicated  question,  we  must,  as  Dejerine  has  pointed 
out,  make  our  deductions  only  from  brains  cut  in  series.  This  method 
shows  subcortical  lesions  interrupting  the  fibres  from  Broca's  convolution, 
and  acting  in  the  same  manner  as  do  changes  in  this  convolution ;  in  this 
way  certain  labelled  cases  are  to  be  explained :  motor  aphasia  without  a 
lesion  of  Broca's  convolution.  On  the  other  hand,  the  aphasia  may 
recover,  and  the  individual  (formerly  aphasic)  may  up  to  the  time  of  his 
death  show  no  sign  of  speech  trouble.  In  this  case,  the  lesion  of  Broca's 
convolution  found  post-mortem  will  perchance  be  wrongly  considered  as 
not  having  caused  aphasia.  Letulle  has  published  a  remarkable  case  of 
this  nature. 

Furthermore,  new  specimens  have  shown  lesions  limited  to  the  classical 
convolution  for  language.  In  certain  surgical  cases,  the  traumatic  destruc- 
tion of  this  ai-ea  has  been  shown  by  aphasia.  These  undoubted  facts  are 
opposed  to  Marie's  theory.  Moreover,  Mahaim,  Mills  and  Spiller,  and 
van  Gehuchten  have  shown  that  lesions  of  the  lenticular  nucleus  do  not 
cause  aphasia. 

The  so-calle'd  new  doctrine  of  aphasia,  therefore,  is  much  weakened  in 
many  respects.  In  addition,  several  questions  regarding  aphasia  are  still 
obscure.  We  shall  see  later  that  cerebral  localization  has  lost  some  of  the 
accuracy  formerly  attributed  to  it.     (See  Section  XIII.). 


1376  TEXT-BOOK  OF  MEDICINE 

Transitory  Aphasia. — Besides  the  aphasia  just  described,  and  pro- 
smoked  by  evident  cerebral  lesions,  we  find  in  patients  suffering  from  rheu- 
matism, gout,  syphilis,  typhoid  fever,  hysteria,  ophthalmic  migraine,  etc., 
a  more  or  less  transitory  aphasia,  which  is  not  accompanied  by  paralysis, 
and  which  disappears  without  leaving  any  trace.  This  transitory  aphasia 
is  not  uncommon  in  patients  suffering  from  diabetes.  It  is  an  isolated 
aphasia,  without  any  trace  of  hemiplegia.  It  does  not  occur  only  in  patients 
with  abundant  glycosuria/,  but  it  is  also  met  with  in  people  who  pass  but 
a  few  grains  of  sugar.  I  have  often  seen  this  variety  of  aphasia.  It  may 
last  only  a  few  days,  but,  though  transitory,  it  may  be  total. 

How  are  we  to  explain  these  cases  of  transitory  aphasia,  and  what 
happens  in  such  a  case  to  the  third  left  convolution  ?  Probably  an  altera- 
tion in  the  circulation  takes  place,  such  as  transient  hypergemia  or  anaemia, 
or  a  dynamic  trouble  of  the  nerve  cells.  A  certain  fact  of  importance  in 
prognosis  is  that  aphasia  may  exist  without  a  material  lesion,  just  as  hemi- 
ansesthesia  in  hysterical  patients  is  not  accompanied  by  any  lesion  of  the 
sensory  tract  in  the  brain,  and  just  as  the  permanent  contractures  of  hysteria 
exist  without  sclerosis  of  the  lateral  cords  of  the  spinal  cord,  and,  finally, 
just  as  ordinary  chorea  and  post-hemiplegic  hemichorea,  though  almost 
alike,  are  in  the  one  case  due  to  transitory  functional  trouble,  and  in  the 
other  to  a  lesion  of  the  brain.  Identical  nervous  symptoms  may,  therefore, 
be  caused  by  deep  and  persistent  lesions  or  by  transitory  changes  of  an 
unknown  nature. 

Treatment. — The  treatment  of  aphasia  depends  on  the  cause.  We 
must  always  think  of  syphilis,  especially  in  a  young  man.  Re-education 
may  give  excellent  results  in  patients  suffering  from  aphasia.  It  wiU  be 
much  facilitated  by  the  perfected  methods  employed  in  the  education  of 
deaf-mutes  (Fere). 

VI.  ENCEPHALITIS— ABSCESS  OF  THE  BRAIN. 

Encephalitis  is  inflammation  of  the  brain.  It  is  a  disease  which  was 
formerly  considered  frequent,  at  a  period  when  it  was  confounded  with 
softening  due  to  embolism  or  to  thrombosis.  We  know  that  encephalitis 
is  rare,  in  striking  contrast  to  myelitis,  which  is  relatively  frequent. 

Pathogenesis. — Leaving  traumatism  and  surgical  lesions  out  of  the 
question,  encephalitis  and  abscesses  of  the  brain  are  always  the  result  of 
toxi-infectious  agents.  Nearly  all  the  infectious  diseases — ulcerative  endo- 
carditis, pyaemia,  septicaemia,  suppurative  pneumonia,  acute  tuberculosis, 
bronchiectasis,  appendicitis,  etc. — may  cause  acute  encephalitis  and  abscesses 
of  the  brain.  The  staphylococcus,  the  pneumococcus,  the  coli  bacillus, 
Koch's  bacillus,  and  especially  the  streptococcus,  are  the  most  common 


DISEASES  OF  THE  BRAIN  i:;77 

organisms.     Amongst  the   causes  above   enumerated,   some   demand   our 
attention  for  a  moment. 

The  tubeicle  hacilhis  (-an  cause  cerebral  abscesses.  Fraenkel,  Rendu, 
and  Boulloche  have  reported  cases.  In  such  cases  it  is  a  question  of  patients 
being  attacked  by  miliary  tuberculosis,  and  the  tubercle  bacillus,  with- 
out other  microbes,  may  form  colonies  in  the  brain  tissue,  and  cause 
abscesses. 

Fa^tid  chronic  bronchitis  is  a  fairly  frequent  cause  of  cerebral  abscesses 
(Biermer),  and  I  may  say  the  icme  of  suppuration  and  gangrene  of  the  lung. 
It  seems  that  in  these  various  cases  it  is  necessary  for  the  expectoration  to 
be  foetid.     Putrefaction  appears  to  be  an  essential  condition. 

Lesions  of  the  petrous  bone,  of  the  frontal  sinuses,  and  of  the  orbit,  are 
the  chief  causes  of  suppurative  encephalitis,  suppuration  in  the  ear  being  the 
most  common.  At  the  post-mortem  examination  of  people  who  have  died 
of  affections  of  the  petrous  bone  it  is  not  uncommon  to  find  latent  cerebral 
abscesses.  Chronic  disease  of  the  ear  is  far  more  likely  than  acute  disease 
to  cause  abscesses.  An  individual  who  has,  for  ten  or  twenty  years,  had 
suppurating  otitis  media,  and  who  has  not  troubled  himself  about  this  pain- 
less and  apparently  trifling  lesion,  may  at  a  given  moment  be  taken  ill  with 
acute  meningo-encephalitis  or  with  cerebral  abscess,  as  was  one  of  my  patients 
who  had  had  chronic  otitis  for  many  years,  and  who  died  in  three  days 
from  meningo-encephalitis. 

Suppurative  meningo-encephalitis  and  cerebral  abscess  consequent  on 
otitis  may  be  favoured  by  a  fissure  in  the  bone,  which  leads  to  the  gradual 
formation  of  the  abscess  ;  but  in  many  cases  there  is  no  direct  communica- 
tion between  the  cranial  cavity  and  the  ear,  and  we  meet  with  remote 
abscesses  in  the  opposite  cerebral  hemisphere.  The  mechanism  which  I 
have  employed  to  explain  the  remote  abscesses  of  appendicitis  (closed 
ca\dty)  may  explain  the  pathogenesis  of  the  remote  abscesses  Ln  the  brain, 
"  the  swelling  of  the  auditory  mucosa  opposing  the  exit  of  the  Hquid  " 
(Brissaud).  To  complete  this  question,  I  would  ask  the  reader  to  refer  to 
the  section  on  Abscess  of  the  Cerebellum. 

Pathological  Anatomy. — The  pus  in  acute  encephalitis  may  infiltrate  or 
may  be  collected  into  an  abscess.  On  opening  the  skull  we  sometimes  find 
the  pia  mater  adherent,  and  the  subjacent  convolutions  depressed.  The 
number,  the  seat,  and  the  dimension  of  the  abscesses  vary.  We  may  find 
only  one  large  abscess  or  a  series  of  small  abscesses.  A  temporo-sphenoidal 
abscess  is  generally  secondary  to  lesions  of  the  middle  or  of  the  internal  ear  ; 
an  abscess  of  the  frontal  lobe  foUows  caries  of  the  ethmoid  ;  an  abscess  of 
the  occipital  or  of  the  temporal  lobe  is  especially  met  ^ith  in  caries  of  the 
petrous  bone.  The  encysted  pus  is  sometimes  creamy  and  yellow,  some- 
times greenish  and  sanious,  and  of  a  foetid  odour.     The  abscesses  become 


1378  TEXT-BOOK  OF  MEDICINE 

encysted  by  a  membrane  formed  of  sclerotic  neuroglia,  which  commences  to 
form  about  the  twelfth  day.  The  cerebral  tissue  aroimd  the  abscess  shows 
yellow  softening. 

Description. — It  is  customary  to  describe  three  stages  in  acute  encephalitis. 
The  first  stage,  or  phase  of  excitation,  somewhat  resembles  memngitis  : 
fever,  headache,  vertigo,  uncertainty  in  walking,  visual  troubles,  delirium, 
contractures,  convulsions,  vomiting,  and  constipation.  Headache  is  the 
chief  symptom,  and  lasts  from  four  to  eight  days  ;  it  is  sometimes  limited  to 
one-half  of  the  brain;  If  the  encephalitis  is  due  to  a  lesion  of  the  ear,  the 
catarrh  generally  disappears  as  soon  as  the  brain  is  invaded. 

The  second  stage,  or  phase  of  remission,  is  characterized  by  a  fictitious 
improvement,  the  patient  being  in  a  condition  of  torpor ;  it  may  last  for 
several  weeks,  or  may  give  place  to  the  paralytic,  hemiplegic,  apoplectic,  and 
comatose  stage.  This  last  stage  may,  indeed,  appear  suddenly,  and  cause 
death  in  two  or  three  days,  without  being  preceded  by  the  initial  phases  of 
excitation  and  depression.  Acute  encephalitis  sometimes  passes  into  the 
chronic  condition,  but  the  prognosis  is  none  the  less  fatal.  Fever  is  the 
principal  symptom  on  which  we  must  rely  to  distinguish  encephalitis  from 
softening.  Examination  of  the  ear  must  never  be  neglected,  for  this  exami- 
nation is  often  sufficient  to  give  a  clue  to  the  diagnosis. 

Two  symptoms  are  to  be  noted  in  abscess  of  the  brain — viz.,  aphasia  and 
hemianopsia.  The  aphasia  is  very  rarely  true  motor  aphasia  ;  it  is  rather  a 
case  of  sensory  partial  aphasia.  In  certain  patients  the  examination  of  the 
eye  shows  the  existence  of  hemianopsia.  In  the  case  of  a  patient  reported 
by  Lannois  and  Jaboulay  there  was  sensory  aphasia  and  right  lateral 
homonymous  hemianopsia,  with  preservation  of  Wernicke's  reflex. 

Chronic  Encephalitis. — Sclerosis  of  the  brain  often  coincides  with  sclerotic 
lesions  of  the  spinal  cord  (insular  sclerosis).  Sclerosis  limited  to  the  brain 
(syphilis)  is  very  rare.  In  general  paralysis  of  the  insane  diffuse  interstitial 
encephalitis  is  associated  with  chronic  myelitis  of  a  like  nature. 

VII.— CHEONIC  ENCEPHALITIS  OF  CHILDHOOD— H^MOKRHAGE 
—SOFTENING— PORENCEPHALIA— LOBAE   SCLEROSIS- 
LITTLE'S  DISEASE. 

General  Conditions. — ^The  forms  of  chronic  encephalitis  in  children  from  birth  to 
the  period  of  the  second  dentition  are  often  described  under  different  names,  according 
as  they  are  designated  by  their  anatomical  lesion  (hemorrhage,  softening,  porencephaly, 
lobar  sclerosis),  or  by  their  major  clinical  syndrome  (athetosis,  hemiplegia,  paraplegia, 
spasmodic  diplegia,  or  Little's  disease).  They  deserve  to  be  studied  as  a  whole,  because, 
even  though  they  present,  as  in  the  adult,  varying  symptoms  according  to  the  locahza- 
tion  of  the  lesions,  their  course  is  marked  by  a  common  clinical  basis.  Paralyses  with 
contractures,  and  intellectual  troubles  that  may  be  shght  or  may  end  in  idiocy,  are  the 
elements  of  the  syndrome  common  to  almost  all  forms  of  chronic  infantile  encephahtis. 


DISEASES  OF  THE  BRAIN  1379 

The  fact  that  the  brain  of  the  child  ia  incompiotoly  dovolopod  at  the  time  when  the 
leaion  makes  its  appoaranco  accounts  for  this  special  clinical  proncHS.  Let  mo  add  that 
the  after-effects  of  infantile  st-lorosis  may  appear  in  youth  in  the  form  of  eijilepsy. 
The  writinj^s  of  Bournovillo  and  of  Striimpoll  have  helped  to  elucidate  these  forms  of 
infantile  encephalitis.     Their  natural  liistory  lias  been  accurat«jly  classified  by  Brissaud. 

etiology. — There  are  two  special  aetiological  reasons  for  infantile  en- 
cephalopathies— premature  accouchement,  and  especially  dystocia — which 
explains  how  the  disease  may  arise  even  before  birth  ;  and  infection  (measles, 
scarlatina,  whooping-cough,  etc.). 

Pathological  Anatomy. — Infantile  encephalopathy  may  be  characterized 
by  haemorrhage,  softening,  meningo-encephalitis,  sclerosis,  and  cavities 
(porencephaly),  but  of  all  these  lesions  two  are  peculiar  to  infancy,  and 
demand  our  attention — porencephaly  and  lobar  sclerosis. 

Poreticephaly.  —  This  term  does  not  refer  to  a  particular  lesion  ;  it 
denotes  the  ultimate  result  of  a  series  of  lesions,  characterized  by  the  presence 
of  cavities  {porus),  opening  like  craters  on  the  surface  of  the  hemispheres  ; 
it  is  the  superlative  degree  of  cicatricial  retraction  (Brissaud). 

Following  Bou^ne^^lle  and  Sollier,  we  have  to  consider  two  forms  of  por- 
encephaly, true  and  false.  The  conclusions  of  these  authors  are  :  "  True 
porencephaly  is  the  result  of  arrested  development,  and  is  consequently 
congenital.  In  true  porencephaly  there  is  a  communication  between  the 
depression  and  the  lateral  ventricle.  In  false  porencephaly  this  com- 
munication does  not  exist.  This  want  of  communication  is  not,  however, 
of  an  absolute  value,  because  we  may  readily  suppose  that  the  necrobiotic 
process  may  completely  destroy  the  cerebral  matter  as  far  as  the  lateral 
ventricle,  and  thus  establish  a  wide  communication  with  it.  The  disposition 
of  the  convolutions  has,  on  the  contrary,  a  greater  importance.  In  true  por- 
encephaly the  latter  are  disposed  in  rays  around  the  porus  into  which  they 
plunge.  In  pseudo -porencephaly,  on  the  other  hand,  the  convolutions  are 
cut  irregularly. 

"  The  shape  of  the  depression  is  veTj  different  in  the  two  cases.  In  true 
porencephaly  we  see  a  kind  of  infundibulum,  sometimes  a  simple  sht  or 
an  almost  circular  orifice.  In  pseudo-porencephaly  we  see  a  gaping 
excavation,  the  walls  of  which,  instead  of  being  formed  by  convolutions, 
are  formed  by  the  white  matter  covered  by  the  membrane  of  a  pseudo-cyst, 
which  intimately  adheres  to  it.  In  spite  of  the  relatively  much  larger 
extent  of  the  pseudo-porencephaly,  the  psychic  phenomena  mav  be  less 
marked  than  in  true  porencephaly,  which  is  almost  always  accompanied 
by  complete  idiocy." 

The  porencephalic  lesion,  whether  congenital  or  acquired,  is  always  the 
result  of  an  arterial  lesion.  In  true  porencephaly  we  have  congenital 
absence  of  an  artery,  and  the  region  which  it  ought  to  have  nourished  has 


1380  TEXT-BOOK  OF  MEDICINE 

never  been  properly  developed.  In  acquired  porenceplialy  tlie  arterial 
lesion  results  in  the  forus  through  the  intermediary  of  a  haemorrhagic  focus, 
or  of  softening.     The  chasm  is  filled  with  gliomatous  tissue. 

Primary  Lobar  Sclerosis. — This  lesion  occurs  in  earliest  infancy  or  in 
intra-uterine  life.  It  may  occupy  both  hemispheres  or  be  limited  to  one 
of  them  ;  it  may  even  restrict  itself  to  one  lobe,  such  as  the  occipital  or  frontal 
lobe,  whence  the  name  "  lobar  sclerosis."  In  some  cases  the  sclerosis  limits 
itself  to  a  group  of  convolutions,  such  as  the  convolutions  of  Eolando.  In 
the  case  of  bilateral  sclerosis  the  lesions  are  always  symmetrical  (Richardiere) ; 
they  are  perhaps  brought  about  by  circulatory  troubles  (Marie). 

The  cerebral  matter  is  indurated,  and  the  convolutions  appear  to  be 
retracted.  The  general  topography  remains  recognizable  in  spite  of  the 
marked  atrophy  of  the  diseased  part.  This  atrophy  may  afect  all  the 
constituent  parts  of  the  brain — convolutions,  peduncles,  corpora  striata,  etc. 

The  fundamental  histological  lesions  consist  in  a  diffuse  proliferation  of 
the  neuroglia,  and  in  vascular  and  perivascular  changes.  The  neuroglia  is 
filled  with  branching  cells,  with  dense  and  opaque  nuclei,  and  the  diseased 
parts  are  furrowed  by  large  wavy  bundles  of  connective  tissue,  visible  when 
slightly  magnified.  The  vascular  changes  produce  thickening  of  the  walls  of 
the  capOlaries.  The  perivascular  lymphatic  sheaths  are  enlarged,  and  filled 
with  leucocytes  and  granular  bodies.  The  lesion  m  the  neuroglia  commences 
close  to  the  capillaries.  The  cells  of  the  cortex  are  atrophied,  and  lose  their 
p}T:aniidal  form,  becoming  fusiform,  and  even  disappearing  in  certain  lobes- 
The  lesion  is  slowly  invading,  and  there  are  some  points  at  which  it  is  more 
advanced.  This  pjrogressive  course  explains  the  appearance  of  certain  late 
s}miptoms  (Brissaud). 

Secondary  Lesions. — In  the  infant  the  secondary  lesions  are  always  much 
more  marked  than  in  the  adult.  They  do  not  only  consist  of  a  secondary 
deoreneration,  but  also  of  an  arrested  development  of  the  neuron.  In  the  brain 
the  atrophy  and  the  degeneration  reach  the  capsule,  the  pons,  and  the  bulb. 
The  striate  bodies  are  also  attacked  secondarily.  The  lobe  of  the  cerebellum 
on  the  opposite  side  (Vulpian,  Charcot,  Cottard)  is  generally  much  atrophied 
and  sclerosed. 

The  spinal  cord  on  the  side  opposite  to  the  lesion  does  not  only  show 
lesions  of  descending  sclerosis,  but  also  a  peculiar  atrophy,  which  extends  even 
to  the  bones,  cartilages,  ligaments,  tendons,  and  muscles  of  the  same  side. 
The  same  arrest  of  development  is  observed  in  the  skuU,  face,  and  eyeball  of 
the  paralyzed  side,  whence  the  formation  of  the  keel-like  skuU  and  the 
Olympian  brow.  If  the  lesion  is  bilateral,  the  secondary  degeneration  is 
bilateral,  and  we  have  diplegia  instead  of  hemiplegia. 

Symptoms. — Chronic  encephalitis  of  infancy  may  show  several  clinical 
forms.     They  end  almost  always  in  paralysis,  in  the  form  of  spasmodic 


DISEASKS  OF  THK  BRAIN  1381 

henii|tl('<;ia.  la'iniathctosis,  ('li(nei(;  liciiiiplej^iu,  double  athetosis,  or  spHSiiiodic 
chorea,  and  they  may  be  coin])licated  with  idiocy. 

Whatever  the  pathological  form  of  the  encephalopathy,  says  Brissaud, 
the  general  evolution  of  the  symptoms  is  always  much  the  same — appearance 
of  acute  troubles,  such  as  restlessness,  fever,  vomiting,  and  convulsions  from 
birth,  or  during  earliest  infancy.  A  phase  of  apparent  cure  follows,  lasting 
for  some  days  or  weeks,  and  then  paralysis  supervenes,  sometimes  limited, 
at  other  times  affecting  the  whole  of  one  side  or  the  whole  musculature  of  the 
body.  The  acute  febrile  stage  may  be  absent,  especially  in  the  new-born, 
and  the  paralysis  which  exists  in  the  latent  stage  from  birth  only  reveals  itself 
when  the  child  attempts  to  take  its  first  steps.  All  the  above  types  of 
paralysis  have  a  tendency  to  become  blended  with  one  another.  I  shall 
follow  the  description  given  by  Brissaud. 

Spasmodic  Hemiplegia  of  Infancy. — We  find  three  successive  phases :  A 
phase  of  epileptiform  movements,  localized  to  the  side  which  later  becomes 
paralyzed,  and  showing  a  preference  for  the  limbs.  A  phase  of  hemiplegia, 
which  immediately  follows  the  epHeptiform  movements  ;  the  hemiplegia  being 
generally  flaccid  and  total ;  affecting  the  limbs  and  the  face,  and  generally 
lasting  about  a  fortnight.  At  the  end  of  this  time  the  patient  enters  on  the 
third  stage,  the  hemiplegia  becoming  spasmodic,  incurable,  and  almost  like 
that  of  the  adult.  It  differs  from  it  at  times  by  certain  special  attitudes. 
The  hand  is  flexed  on  the  forearm  in  exaggerated  pronation.  "  The  fingers 
are  flexed  on  the  palm,  or  strongly  extended  in  attitudes  which  absolutely 
recall  those  of  the  hands  of  the  Javanese  dancers."  The  particular  character- 
istic is  a  general  atrophy  of  the  limbs  and  face  on  the  paralyzed  side. 

Hemiathetosis. — It  may  exist  in  a  condition  of  purity,  quite  apart  from 
paralysis  or  contracture.  Most  frequently  it  is  only  a  symptom  superadded 
to  the  hemiplegia,  The  contracture  is  much  less  pronounced  in  spasmodic 
hemiplegia ;  otherwise  the  athetotic  movements  could  not  be  produced. 
The  symptomatology  and  the  character  of  these  athetotic  movements  are  the 
same  in  the  child  as  in  the  adult.  The  localization  of  the  lesions  producing 
them  is  identical.     In  exceptional  cases  hemichorea  has  been  met  with. 

Double  Athetosis. — All  the  muscles  make  slow,  incessant,  and  stiff  move- 
ments. The  face  grimaces  continually.  This  double  athetosis  is  caused  by 
a  symmetrical  lesion  affecting  the  neighbourhood  of  the  pyramidal  tract. 
Chronic  double  chorea,  admitted  as  identical  with  double  athetosis  by  most 
authors  who  have  studied  the  question  (Richardiere,  Audry),  is  produced 
by  an  analogous  lesion  with  a  different  localization. 

Spasmodic  Diplegia. — Bilateral  paralysis,  with  contracture,  appearing  at 

birth  or  in  the  earliest  days  of  life,  has  been  very  carefully  studied  during 

the  past  few  years.     It  is  dependent  on  a  bilateral  lesion  of  Rolando's  area 

or  of  the  paracentral  lobule.     Little,  in  1862,  showed  that  its  causes  were 

n.  8S 


1382  TEXT-BOOK  OF  MEDICINE 

difficult  labour,  premature  accoucliement,  asphyxia  of  the  newborn,  super- 
ficial meningeal  haemorrhage,  and  described  the  various  chnical  forms. 
Little  pointed  out  that  the  contracture  may  be  general,  or  that  it  may  show 
itself  in  the  paraplegic  form. 

Generalized  Contractures. — AU  four  limbs  are  in  a  state  of  contracture. 
The  foot  clonus  is  very  marked,  and  the  reflexes  are  exaggerated.  The  limbs 
are  less  paralyzed  than  they  appear  to  be,  and  this  is  one  of  the  most  interest- 
mg  points  m  this  form  of  the  disease.  The  rigidity  lessens  with  age,  and 
when  the  child  reaches  the  walking  age  we  see  that  he  does  not  take  to  it 
partially  on  account  of  cerebral  dullness,  as  Little  well  remarked.  The  child 
is  backward  in  speech,  intelligence,  and  walking.  The  disease  improves 
with  time,  but  is  never  completely  cured ;  the  legs  always  preserve  some 
degree  of  contracture. 

Paraplegic  Contracture. — This  contracture,  locahzed  in  the  lower  limbs, 
presents  the  picture  of  spasmodic  tabes  dorsahs.  Children  thus  afiected  do  not 
begin  to  walk  till  they  are  about  four  or  five  years  old.  "  Their  walk  is  spas- 
modic, with  double  club-foot,  adduction,  flexion  and  inward  rotation  of  the 
thighs.  The  tendon  reflexes  are  much  exaggerated,  and  in  the  sitting  posture 
the  legs  have  a  tendency  to  raise  themselves  spontaneously  from  the  ground  " 
(Brissaud).  The  little  suSerers  appear  to  be  devoid  of  intelligence,  but  often 
they  are  not  so.  As  Marie  has  pointed  out,  the  spasmodic  condition  of  the 
muscles  of  the  face  paralyzes  the  expression,  and  gives  them  a  stupid  look. 
The  contracture  of  the  leg  is  always  less  curable  than  that  of  the  arms. 
Spasmodic  encephalopathy,  especially  the  congenital  form,  is  often  called 
Little's  disease.  For  the  purposes  of  description  I  have,  following  Brissaud, 
given  clmical  types  which  can  frequently  be  isolated ;  but  these  types  often 
combine,  and  in  their  ensemble  form  a  single  disease. 

Intellectual  Troubles — Miocy.^ — The  intellectual  development  is  arrested 
when  the  lesion  involves  the  frontal  lobe  ;  it  is  specially  delayed  in  the  case  of 
a  bilateral  lesion. 

No  matter  which  side  of  the  brain  is  attacked  by  the  lesions,  persons  who 
are  hemiplegic  from  infancy  never  show  aphasia,  a  fact  already  remarked  by 
Cottard.  x4lS  this  writer  observes,  the  functional  substitution  is  no  doubt 
established  by  means  of  the  zones  which  have  been  spared  in  those  brains 
that  are  as  yet  incompletely  developed. 

Infantile  encephalopathy  is  one  of  the  most  frequent  causes  of  idiocy 
(Bourneville).  Cerebral  scleroses  may,  like  hydrocephalus,  microcephalus, 
chronic  meningitis,  tumours  of  the  brain,  and  pachydermic  cachexia,  cause 
imbecility  and  mental  weakness.  The  congenital  idiot  has  an  asymmetrical 
face,  unequal  frontal  bosses,  projecting  superior  maxillse,  striated  and  un- 
equally set  teeth.  He  generally  presents  the  most  marked  stigmata  of 
degeneration.     In  acc^uired  idiocy  the  skuU  is  regular,  the  expression  less 


DISEASES  OF  THE  BRAIN  1383 

dolt-like,  but  the  disease  is  in  general  more  hopeless.  Feebleness,  want  of 
equilibrium,  and  perversion  of  the  faculties,  may  be  observed  in  all  det^rees 
in  the  idiot,  and  this  condition  of  mental  weakness  may  be  recognized  before 
the  age  of  two  years.  The  cliild  does  not  sleep,  and  cries  continually  ;  the 
sight  is  imperfect,  and  taste  and  smell  are  hardly  developed.  The  sense  of 
hearing  is  tlie  least  rudimentary  of  all  the  senses.  The  cutaneous  sensibility 
is  blunted,  and  the  voluntary  movements  are  retarded  ;  the  speech  is  much 
affected,  and  may  be  reduced  to  unintelligible  mumbling.  The  idiot  often 
does  not  commence  to  pronounce  his  first  words  until  between  the  ages  of 
three  and  eight  years. 

Epilepsy. — Many  individuals  stricken  with  spasmodic  hemiplegia  during 
infancy  become  epileptic  in  adolescence.  "  Many  cases  of  so-called  essential 
epilepsy  are  simply  the  late  manifestation  of  an  infantile  encephalopathy 
which  has  arrived  at  its  definite  anatomical  stage  "  (Brissaud).  Epilepsy 
consequent  on  spasmodic  infantile  hemiplegia  is  said  in  most  cases  to 
recover  about  the  age  of  thirty  (Bourneville  and  Wuillaumier).  Infantile 
encephalopathy  is  always  grave.  Whatever  its  evolution  may  be,  it  always 
makes  a  wealding  of  the  patient. 

Diagnosis.— ^\^len  the  lesion  is  congenital,  the  diagnosis  is  generally 
obvious,  but  when  the  paralytic  and  spasmodic  phenomena  supervene 
during  early  infancy  the  diagnosis  is  often  more  difficult. 

The  acute  onset  may  simulate  meningitis,  but  doubts  are  dispelled  by 
the  later  evolution  of  the  disease.  The  acute  onset  may  also  simulate 
atrophic  spinal  paralysis  of  infancy,  but  in  this  myelopathy  hemiplegia  is 
rare,  and  the  paralysis  is  always  flaccid,  with  abolition  of  the  tendon  reflexes. 

Crepitus  of  the  articular  surfaces  and  cutaneous  eruptions  are  in  general 
sufficient  to  distinguish  it  from  the  syphilitic  pseudo-paralysis  of  Parrot 
and  Troisier. 

Obstetrical  paralysis  is  due  to  the  compression  of  a  motor  nerve  in 
instrumental  delivery ;  it  remains  limited  to  circumscribed  groups  of  muscles. 

Spasmodic  tabes  dorsalis  and  certain  kinds  of  spasmodic  paraplegia — 
Pott's  disease,  for  instance — are  distinguished  by  their  mode  of  appearance, 
by  sensory  troubles,  and  by  the  vesical  and  rectal  disturbances. 

Treatment. — According  to  Pinard,  the  best  measure  in  certain  cases 
is  to  prevent  grave  disturbance  in  the  foetal  circulation  by  performing 
symphysiotomy  in  order  to  hasten  delivery. 

When  the  disease  has  developed,  the  future  of  the  child  depends  on  the 
surgeon,  who  can  by  orthopaedic  measures  improve  the  atrophic  deformities. 
It  will  also  depend  on  the  child's  teacher,  who  may  be  able  to  improve  the 
mental  condition  by  following  Bourneville's  rules. 


88—2 


1384  TEXT-BOOK  OF  MEDICINE 

VIII.  CEREBKAL  TUMOUES. 

Pathological  Anatomy. — In  the  cerebrum  we  meet  with  tumours  of 
every  kind  and  of  divers  origin  ;  they  develop  at  the  expense  of  the  menuiges, 
of  the  vessels,  and  of  the  cerebral  tissue.  Some  tumours  arise  on  the 
exterior,  and  penetrate  into  the  skull  (orbital  tumours) ;  others  arise  in  the 
skull,  and  make  their  way  outwards. 

Cancer  arises  in  the  brain  or  in  the  neighbouring  parts  (bones,  meninges, 
orbital  cavity).  The  encephaloid  variety  is  the  most  frequent ;  the  tumour 
may  assume  the  size  of  a  fist,  perforate  the  cranial  walls,  and  appear 
externally  as  an  erectile,  nodular  tumour.  The  soft  sarcoma  is  much  less 
common  than  cancer  ;  its  course  is  much  slower  and  less  prone  to  invasion  ; 
it  occurs  chiefly  in  young  persons.  It  is  formed  of  pure  embryonic  tissue, 
or  of  the  same  tissue  in  course  of  transformation.  In  the  glioma,  which  is  a 
variety  of  sarcoma,  heemorrhage  sometimes  occurs.  The  tubercle  usually 
attacks  the  cerebellum,  the  mesencephalon,  and  the  surface  of  the  cerebral 
hemispheres.  It  sometimes  forms  large  tumours,  which  are  due  to  an 
agglomeration  of  granulations.  The  centre  of  the  tumour  passes  into  the 
caseous  condition,  and  we  often  find  calcification. 

Syphilis  gives  rise  to  osseous  and  periosteal  gummata,  which  will  be 
described  later. 

Parasites  are  rare  in  the  brain.  We  find  especially  the  echinococcus  and  the 
cysticercus.  Aneurysms  are  found  in  the  arteries  at  the  base,  and  especially 
in  the  basilar  trunk.  One  of  my  patients  had  an  aneurysm  as  large  as  a 
walnut  on  the  left  anterior  cerebral  artery.  Cerebral  tumours,  by  com- 
pressing the  veins  and  the  arteries  of  the  neighbourhood,  cause  secondary 
lesions,  such  as  thrombosis  of  the  sinuses,  oedema,  hydrocephalus,  softening, 
etc.     Numerous  varieties  result  therefrom  in  the  history  of  the  symptoms. 

Description.- — -In  the  fijst  place,  some  cerebral  tumours  remam  latent  for  a 
long  time,  provided  they  develop  slowly  in  the  so-called  tolerant  regions 
(Jaccoud),  such  as  the  white  hemispherical  mass  of  the  posterior  lobes  and  the 
striated  bodies.  This  tolerance  is,  however,  far  from  being  constant,  and 
besides,  a  certain  region  which  is  tolerant  when  slowly  invaded  by  a  tumour 
is  no  longer  so  when  the  hsemorrhagic  lesion  or  the  softening  supervenes 
suddenly. 

It  is  customary  in  treatises  on  pathology  to  devote  a  chapter  to  the 
description  of  cerebral  tumours.  I  must  confess  that  this  description,  when 
confined  to  a  general  survey,  seems  to  me  impossible  ;  the  situation  of  the 
tumour  modifies  the  description  of  the  sj^mptoms  to  such  a  degree,  and,  on 
the  other  hand,  the  physiology  of  certain  cerebral  operations  is  still  so 
obscure,  that  a  methodical  study  of  this  question  cannot  be  attempted  for 
the  time  being.     We  can,  however,  group  the  symptoms  and  divide  them 


DISEASES  OF  TFIE  IJllAIN  1385 

into  two  classes  :  the  one  class  under  the  name  of  diffuse  symptoms,  which 
are  not  exclusivelv  dependent  on  the  seat  of  the  lesion,  and  which  are  the 
result  of  a  direct  or  reflex  excitation  ;  the  other  class  under  the  name  of 
focal  symptoms,  which  are  related  to  the  localization  of  the  lesion,  and 
which  assist  in  its  topographical  diagnosis. 

1.  Diffuse  Symptoms. — The  diffuse  symptoms  are  generally  the  first  to 
appear,  and  thev  may  have  no  constant  relation  with  the  seat  of  the  tumour. 
The  most  important  are  headache,  vertigo,  vomiting,  twitchings  in  the 
limbs,  and  mental  troubles.  Headache  met  with  in  half  of  the  cases  (Ball 
and  Krishaber)  may  be  general  or  partial  ;  it  is  sometimes  paroxysmal.  It 
may  last  for  weeks,  and  may  be  most  severe.  Violent  nocturnal  exacerba- 
tions often  point  to  syphilis.  Vomiting  of  cerebral  origin  takes  place  without 
effort,  mthout  nausea,  and  without  gastric  troubles  ;  the  vomit  may  consist  of 
food  or  simply  of  liquid. 

The  attacks  of  vertigo  and  giddiness  assume  various  forms  :  the  patient 
complains  of  feeling  empty-headed,  of  continuous  giddiness,  or  of  fits  of 
vertigo,  which  recur  several  times  a  day.  Occipital  headache,  vomiting,  and 
attacks  of  vertigo  are  very  common  in  tumours  of  the  cerebellum. 

2.  Focal  Symptoms. — The  various  paralyses  are  focal  sjinptoms  ;  their 
appearance  is  sometimes  slow  and  gradual,  at  other  times  rapid ;  their 
character  is  dependent  on  the  seat  and  extent  of  the  tumour.  They  may  be 
grouped  as  follows  : 

1.  Hemiplegia. — (i.)  Total  hemiplegia  of  the  limbs  and  of  the  face, 
analogous  to  the  hemiplegia  of  cerebral  haemorrhage,  is  a  very  rare  variety. 
The  hemiplegia  of  cerebral  tumours  is  less  complete,  "  less  pure,  less  exactly 
circumscribed,  and  less  systematic  than  common  hemiplegia  "  (Fournier). 

(ii.)  Partial  hemiplegia  of  one  leg,  of  one  arm  (monoplegia),  or  of  an  arm 
and  of  the  face,  is  fairly  frequent.  It  results  in  nearly  every  case  from  a 
lesion  seated  at  a  iSjced  point  of  the  cortical  motor  zone.  These  cases  of 
monoplegia  are  almost  always  associated  with  contractures,  or  attacks  of 
Jacksonian  epilepsy.  This  question  will  be  studied  in  detail  under 
Jacksonian  Epilepsy. 

(iii.)  Crossed  hemiplegia,  which  affects  the  limbs  on  one  side,  and  one  or 
more  cranial  nerves  on  the  other,  is  the  result  of  a  tumour  in  the  mesen- 
cephalon, or  of  several  tumours  variously  situated,  or  of  a  tumour  sufficiently 
large  to  compress  the  cerebral  hemisphere  and  one  of  the  cranial  nerves  at 
the  same  time. 

(iv.)  Hemiplegia,  accompanied  by  hemianaesthesia  or  by  hemichorea, 
indicates  that  the  tumour  is  attacking  the  sensory  bundle  in  the  internal 
capsule.  Permanent  contracture  foUowng  the  paraylsis  proves  that  the 
tumour  has  injured  the  pyramidal  tract  at  some  point  of  its  course,  or  in  the 
anterior  two-thirds  of  the  posterior  segment  of  the  internal  capsule. 


1386  TEXT-BOOK  OF  MEDICINE 

These  varieties  of  hemiplegia  rarely  have  the  sudden  onset  of  the  hemi- 
plegia of  cerebral  haemorrhage  and  of  cerebral  embolism  ;  they  are  usually 
preceded  by  headache,  twitchings  in  the  foot  and  in  the  hand,  giddiness,  and 
weakness.  Amongst  the  tumours  which  give  rise  to  them  we  must  place 
in  the  front  rank  gummata  of  the  meninges  or  of  the  brain.  Hemiplegia  is, 
we  know,  a  frequent  complication  of  the  tertiary  period,  but  it  is  by  no 
means  uncommon  even  within  two  years  of  the  date  of  infection.  Syphilis 
may  cause  hemiplegia,  with  or  without  apoplexy,  with  or  without  aphasia  ; 
the  paralysis  may  be  due  to  gummata,  sclero-gummatous  meningitis,  vascular 
compression,  obliterating  arteritis,  and  consequent  softening. 

2.  Paralysis  of  the  Cranial  Nerves. — The  paralysis  may  strike  one  nerve 
or  several  nerves  at  the  same  time,  or  it  may  be  limited  to  one  of  the  branches 
of  a  cranial  nerve.  Two  hypotheses  are  given  to  explain  paralysis  limited 
to  a  part  of  a  nerve.  In  the  one,  the  lesion  attacks  one  of  the  branches 
arising  from  the  common  trunk — it  is  a  peripheral  paralysis  ;  in  the  other, 
the  lesion  attacks  the  nerve  branch  at  its  origin  before  it  j  oins  the  common 
bundle^ it  is  a  central  paralysis.  Thus,  incomplete  facial  paralysis  may 
be  due  to  a  cortical  tumour  of  the  motor  convolutions  ;  the  paralysis  of  the 
common  oculo-motor  nerve,  which  reveals  itself  by  ptosis,  may  point  to  a 
tumour  in  the  posterior  part  of  the  opposite  parietal  lobe,  the  ptosis  of 
cerebral  origin  being  crossed. 

Cerebral  syphilis  often  causes  paralysis  of  the  cranial  nerves ;  the  nerves 
invaded  are  in  order  of  frequency :  the  third  nerve,  the  sixth  nerve,  the 
fourth  nerve,  the  facial,  etc.  These  syphilitic  paralyses  are  generally  rapid 
in  their  development ;  they  become  confirmed  within  the  space  of  a  few 
hours. 

3.  Disorders  of  vision  are  frequent  and  early.  Their  importance  leads  me 
to  describe  them  in  detail.  In  the  first  place  I  shaU  mention  amblyopia  and 
amaurosis,  due  to  lesions  of  the  optic  nerves.  These  lesions  are  generally 
bilateral  and  rapid  in  their  evolution.  The  ophthalmoscope  reveals  optic 
neuritis.  The  optic  disc  is  hyperasmic,  and  the  central  veins  are  enlarged 
and  tortuous.  The  arteries,  on  the  contrary,  are  diminished  in  size,  and  are 
partially  covered  by  exudate. 

The  disc  has  lost  its  clear  outline,  being  enlarged  and  prominent.  Later 
it  is  swollen,  and  surrounded  by  small  haemorrhages,  which  are  elongated  so 
that  the  radial  disposition  of  the  nerve  fibres  appears  prominently.  The 
process  may  extend  beyond  the  disc  to  the  retina  (neuro-retioitis).  At  this 
stage  the  optic  neuritis  may  be  cured.  If  the  lesion  progresses,  it  ends  in 
atrophy ;  the  papiUa  is  flattened,  and  the  red  tint  gives  place  to  a  whitish- 
grey.  The  arteries  become  atrophied.  Several  theories  have  been  pro- 
pounded to  explain  the  pathogenesis  of  optic  neuritis  of  intracranial  origin. 
It  has  been  attributed  to  vascular  stasis  (De  Graefe)  ;  to  infection  (Leber) ; 


DISEASES  OK  THE  BRAIN  1387 

to  excess  of  intracranial  tension,  with  a  j)ressing  backwards  of  the  cercDro- 
spinal  fluid  into  the  intervaginal  space  of  the  optic  nerve  (Schmidt)  :  to 
lyinphatic  oedema,  analogous  to  the  oedema  of  the  cerebral  tissue,  of  which 
the  optic  nerve  is  the  prolongation  (Parinaud).  The  fibrous  ring  through 
which  the  optic  nerve  passes  is  said  to  favour  strangulation  and  oedema  in 
the  same  manner  as  a  ligature  placed  on  the  limbs ;  whence  the  name 
"  oedematous  neuritis  "  (Parinaud). 

Optic  neuritis,  especially  when  associated  with  other  symptoms,  is  of 
great  diagnostic  value  as  to  the  existence  of  an  intracranial  tumour  ;  but  it 
gives  no  indication  regarding  the  situation  of  the  tumour.  It  is  quite  other- 
wise with  primary  atrophy  of  the  optic  nerves,  which  is,  besides,  very  much 
rarer  in  the  case  of  cerebral  tumours.  This  atrophy,  which  generally  is 
partial,  gives  rise  to  various  kinds  of  hemianopia. 

Homonymous  hemianopia  is  the  loss  of  the  left  or  right  half  of  the  visual 
field  in  both  eyes.  It  is  related  to  the  destruction  of  one  of  the  cortical  visual 
centres  or  of  one  of  the  quadrigeminal  tubercles,  or  of  one  optic  tract.  The 
tumour  is  seated  on  the  opposite  side  to  the  affected  half  of  the  visual  field. 
Temporal  hemianopia  is  the  loss  of  the  external  half  of  the  field  of  vision  of 
each  eye  ;  it  follows  a  lesion  of  the  anterior  or  posterior  angle  of  the  chiasma 
— that  is  to  say,  a  lesion  affecting  both  crossed  bundles  of  the  optic  nerves 
at  the  same  time  (tumours  of  the  pituitary  region).  Nasal  hemianopia  is 
the  loss  of  the  two  internal  halves  of  the  field  of  vision ;  it  is  the  index  of  a 
lesion  of  the  two  direct  bundles,  affecting  the  two  lateral  angles  of  the  chiasma 
at  the  same  time. 

Homonymous  hemianopia,  generally  due  to  a  central  lesion,  has  well- 
defined  symptoms :  sudden  or  rapid  evolution ;  loss  of  both  corresponding 
halves  of  the  field  of  vision,  without  peripheral  constriction  ;  preservation  of 
the  central  keenness  of  sight  on  account  of  the  integrity  of  the  macular 
bundle ;  whilst  the  other  varieties  of  hemianopia,  temporal  or  nasal,  present 
variable  characters.  Given  the  seat  of  the  lesions  causing  hemianopia,  it 
will  be  understood  that  the  ocular  troubles  are  often  associated  with  troubles 
resulting  from  lesions  of  the  neighbouring  cranial  nerves — anosmia  (lesion 
of  the  olfactory  lobes),  diplopia  (lesion  of  the  motor  nerves  of  the  eye). 

The  ocular  paralyses  which  may  be  noticed  in  cerebral  tumour  show 
constant  symptoms — paralytic  strabismus,  diplopia,  etc.  These  s}Tnptoms 
themselves  present  variable  characteristics  according  as  the  lesion  is  seated 
in  the  nerve  trunks,  in  their  roots,  in  the  nuclei  of  origin,  or,  higher  still,  in 
the  cerebral  cortex. 

4.  Epileptiform  convulsions  are  common  in  cerebral  tumours.  They  take 
two  distinct  forms  :  in  the  one  form  the  convulsions  have  all  the  character- 
istics of  a  true  attack  of  epilepsy ;  in  the  other  the  convulsions  are  dis- 
sociated and  partial,  being  limited  to  one  limb  or  to  one  side  of  the  body. 


1388  TEXT-BOOK  OF  MEDICINE 

This  form  of  epilepsy  was  well  described  in  1827  by  Bravais,  and  later  by 
Jackson  (Jacksonian  epUepsy).  In  this  form  of  partial  epilepsy  the  patient 
does  not  lose  consciousness.  The  convulsions  commence  in  the  arm,  and 
extend  thence  to  the  head  and  to  the  leg,  or  they  may  commence  in  the  face, 
and  extend  to  the  arm  and  the  leg  ;  in  rarer  cases  they  commence  in  the 
leg,  and  then  attack  the  arm  and  the  face.  Certain  sudden  movements,  such 
as  the  forced  flexion  of  the  wrist  or  of  the  foot,  may  bring  on  the  convulsive 
attack,  and  the  same  manoeuvre  at  the  commencement  of  the  convulsions 
may  sometimes  stop  them.  General  epilepsy,  a  variety  of  symptomatic 
epilepsy,  is  valueless  in  localizing  the  seat  of  the  tumour,  whilst  partial 
epilepsy,  or  monospasm  in  the  arm  or  in  the  leg,  is  always  the  index  of  a 
tumour  seated  at  a  fixed  point  of  the  cortical  motor  zone.  This  question 
wiU  be  discussed  under  Cerebral  Localization  and  Jacksonian  Epilepsy. 

Large  tubercles  of  the  brain,  exostoses  of  the  cranial  vault,  syphilitic 
gummata  of  the  dura-mater  and  of  the  cortical  regions,  are  the  most  common 
causes  of  epileptiform  convulsions.  This  syphilitic  epilepsy  will  be  studied 
later. 

I  have  just  enumerated  the  most  common  symptoms  of  cerebral  tumours  ; 
there  are  others  which,  though  more  rare,  are  none  the  less  of  great  impor- 
tance :  these  are  aphasia,  exaggerated  slowing  of  the  pulse,  syncope,  apo- 
plectiform attacks,  coma,  and  mania. 

The  aphasia  may  be  transitory  or  permanent ;  it  appears  alone,  or  is 
associated  with  hemiplegia.  It  may  even  show  itself  as  an  isolated  pheno- 
menon at  the  commencement  of  cerebral  syphilis.  Aphasia  in  cerebral 
tumour  is  generally  due  to  the  compression  of  the  nutrient  artery  of  the  third 
frontal  convolution. 

Coma  is  one  of  the  most  curious  manifestations  of  cerebral  tumours,  and 
I  am  speaking  not  only  of  coma  following  epileptiform  and  apoplectiform 
attacks,  or  of  coma  associated  with  the  gradual  and  increasing  troubles  of 
cerebral  oedema  and  hydrocephalus  :  but  I  also  allude  to  early  coma,  which 
sometimes  supervenes  suddenly,  especially  in  syphilitic  lesions  of  the  brain, 
and  which  is,  as  it  were,  an  isolated  manifestation  of  them,  calculated,  when 
we  are  not  forewarned,  to  upset  the  diagnosis. 

Diagnosis— Prognosis — -Treatment. — After  what  we  have  said  concern- 
ing the  evolution  of  cerebral  tumours,  and  the  many  complications  which  they 
produce,  we  see  that  they  are  generally  announced  by  prodromata,  such  as 
vertigo,  headache,  and  vomiting,  and  confirmed  by  paralytic  and  convulsive 
troubles  :  incomplete  hemiplegia,  monoplegia,  Jacksonian  epilepsy ;  amau- 
rosis, retinitis,  and  paralysis  of  the  cranial  nerves.  There  are  cases,  however, 
in  which  the  onset  of  the  symptoms  (aphasia,  coma)  gives  no  warning,  and 
the  diagnosis  then  presents  serious  difficulties. 

The  conditions  usual  to  the  development  of  tumours  are  not  realized  in 


DISEASES  OF  THE  THIAIX  i:',89 

haomorrhagc  or  in  cerebral  ernbolLsin ;  they  are  more  like  the  symptoms  of 
cerebral  suftoinn<^  due  to  obiit.oratiiiy;  arteritis  and  athtToma.  There  is, 
nevertheless,  this  difFeren(;e — that  the  symptoms  of  the  prodromal  period  are 
less  frequent  and  less  pronounced,  whilst  the  intellectual  troubles  are  more 
marked  in  atheromatous  softening  than  in  cerebral  tumour.  Furthermore, 
cerebral  atheroma  is  at  times  associated  with  general  atheroma  (aorta, 
radial  artery,  femoral  artery,  etc.),  a  fact  of  some  value  in  diagnosis.  In 
every  case  the  patient's  history  must  be  carefully  examined  in  order  to 
discover  whether  the  tumour  is  syphilitic  or  tubercular. 

In  certain  cases  a  cerebral  tumour  may,  from  its  symptoms,  simulate 
meningitis ;  in  this  event,  lumbar  puncture  may  give  valuable  iufor- 
mation.  Nevertheless,  we  must  remember  that,  in  a  case  of  cerebral 
tumour,  the  cerebro-spinal  fluid  may  contain  cells  just  as  it  does  in 
meningitis.     The  following  case  is  an  example  in  point : 

A  mau  wa.«!  admitted  witli  intellectual  torpor  and  intense  headache  of  four  days' 
duration.  Next  day  vei-tijro  and  vomiting  appeared  ;  the  mental  torpor  wa.s  more 
nuii-ked,  and  we  found  incomplete  paralysis  of  the  levatores  palpebrarum,  and  of  the 
third  nerve  of  the  rig-ht  eye.  Two  days  later  he  had  attacks  of  Jacksonian  epilepsy 
every  qutirter  of  an  hour,  the  temperature  rose,  and  death  from  coma  followed. 

Lumhar  puncture,  performed  on  his  admission,  showed  lymphocvtes  of  variable 
sizes ;  the  cyto-diatrnosis  was.  therefore,  in  favour  of  tubercular  or  sy])liilitic  menin- 
gitis. And  yet  the  autopsy  revealed  an  enucleable  tumour  in  the  occii^ital  lobes.  It 
was  a  sarcoma  originating-  in  the  pia  mater.  The  cells  removed  by  puncture  and 
tliose  of  the  tumotu'  were  almost  identical ;  sarcomatosis  of  the  cei*ebro- spinal  fluid 
was,  therefore,  present.  CA'to- diagnosis  is  generally  negative  in  the  case  of  cerebral 
t\imo\u-.  and  yet.  in  view  of  several  exceptional  cases,  we  must  remember  that  cyto- 
diagnosis  may  reveal  cells  analogous  to  lymphocytes,  thereby  leading  us  to  think  of 
meningitis,  whexi,  as  a  matter  of  fact,  a  tumour  is  present. 

The  prognosis  of  cerebral  tumours  is  very  grave,  cancer  being  the  worst, 
and  a  syphilitic  tumouj  the  least  serious,  because  it  often  gives  way  to 
energetic  treatment.  I  cannot  here  discuss  surgical  treatment,  which  has 
made  considerable  progress  during  the  past  few  years.  Recovery  often 
depends  on  timely  operation. 


IX.  CEREBRAL  SYPHILIS— SYPHILITIC  ARTERITIS— 
GUMMATA  AND  SCLERO-GUMMATOUS  LESIONS— SYPHILITIC 
GENERAL  PSEUDO-PARALYSIS. 

In  order  to  simplify  the  question  of  cerebral  syphilis,  I  shall  divide  it  into  three  parts, 
as  I  did  in  my  lectures  at  the  Faculte  in  1892.  In  the  first  part  I  shall  study  syphilitic 
cerebral  arteritis,  which  appears  to  me  to  be  one  of  the  most  frequent  forms  of  cerebro- 
meningeal  syphilis.  In  the  second  part  I  shall  deal  with  the  sclero-gummatous  lesions 
of  the  brain  and  of  the  meninges.  In  the  third  part  the  mental  forms  of  syphihs,  general 
pseudo-paralysis,  and  parasx'phihtic  general  paralysis  will  be  described. 


1390  TEXT-BOOK  OF  MEDICINE 

Syphilitic  Cerebro-Meningeal  Arteritis — Obliterating  Arteritis, 
and  Arteritis  followed  by  Aneurysm. 

Pathological  Anatomy. — Syphilis  shows  a  weU-marked  preference  for  the 
arteries  of  the  brain,  and  amongst  these  arteries  it  selects  especially  those 
forming  the  circle  of  Willis  and  its  branches.  Anatomically  speaking,  these 
cases  of  syphilitic  arteritis  do  not  present  lesions  which  are  absolutely 
peculiar  to  them ;  they  have,  nevertheless,  a  family  likeness  which  sometimes 
allows  them  to  be  recognized,  either  with  the  naked  eye  or  under  the 
microscope.  They  are  often  symmetrical,  and  sometimes  limited  to  a 
segment  of  the  vessel. 

According  to  Lancereaux,  syphilitic  arteritis  is  primarily  a  periarteritis. 
According  to  other  writers  it  consists  in  a  sclero-gummatous  change  in  the 
walls  of  the  artery ;  the  lesion  commences  in  the  tunica  externa,  which  it 
sometimes  envelops  like  a  cuff,  and  spreads  into  the  middle  and  internal 
coats.  The  cellular  proliferation  may  be  so  great  that  the  lumen  of  the 
vessel  is  obstructed.  In  these  various  cases  the  obliteration  of  the  vessel 
is  completed  by  the  occurrence  of  thrombosis,  and  cerebral  softening  is 
the  consequence. 

Cornil  has  shown  that  syphilitic  arteritis  may  end  in  atheroiria ;  indeed, 
atheroma  is  not  uncommon.  Syphilitic  arteritis,  then,  has  many  points  in 
common  with  other  forms  of  arteritis,  and,  like  them,  may  end  in  oblitera- 
tion of  the  vessel,  or  in  dilatation,  aneurysm,  and  rupture.  In  two  cases 
under  my  care,  the  micro-biological  findings  were  very  interesting.  In  a 
woman  covered  with  papulo-ulcerative  syphilides,  and  suffering  from  hemi- 
plegia with  coma,  Sezary  and  Paillard  found  a  treponema  in  the  cerebro- 
spinal fluid.  In  a  man  suffering  from  syphilitic  psoriasis  and  right-sided 
hemiplegia,  which  proved  fatal,  Sezary  found  treponemata  in  the  walls  of 
the  cerebral  arteries. 

Moreover,  syphilis  causes  arteritis,  with  obliteration  or  dilatation  in 
the  superficial  arteries  of  the  limbs  and  of  the  face,  so  that  we  can  account 
de  visit  for  what  takes  place  in  the  brain.  Let  us  next  consider  syphilitic 
arteritis  with  dilatation,  aneurysm,  and  rupture  of  the  vessel ;  and  arteritis 
with  thrombosis  and  obstruction  of  the  vessel. 

1.  Syphilitic  Aneurysm. — This   group   includes    cases   of   syphilitic 

arteritis  ending  in  aneurysm,  rupture,  and  meningeal  hsemorrhage.     To 

quote  examples : 

Lancereaux  :  A  woman  was  taken  ill,  six  years  after  the  primary  infection,  with 
headache,  vertigo,  and  right  hemiplegia,  without  apoplexy.  After  transient  improve- 
ment, the  cerebral  symptoms  reappeared,  and  the  patient  died  of  apoplexy.  The  post- 
mortem examination  showed  subarachnoid  haemorrhage,  due  to  the  rupture  of  an 
aneurysm  of  the  right  Sylvian  artery,  before  the  origin  of  the  perforating  arteries. 
Several  branches  given  off  by  the  right  Sylvian  artery  showed  endarteritis,  with  an  ob- 
literating tendency. 


DISEASES  OF  THE  BRAIN  l:U)I 

Brault :  A  young  woman  was  taken  ill  with  early  oorobral  symptoms  ten  montljH 
after  being  infectocl  with  ayphilia:  hoadaoho,  amnesia,  aphaHia.  The  patient  rapidly 
bcoamo  cachoetie,  and  died  8udd(>n!y  from  apoplexy.  At  the  jjost-mortem  examina- 
tion considerable  m(>ninp;eal  hirmorrhase  was  disooverod.  It  was  eauHed  by  a  nij)turcd 
aneurysm  of  the  left  itit»Mnal  carotid  at  its  point  of  entry  into  the  cranium.  The  right 
internal  carotid  was  attacked  byarteritis  at  a  corresponding  point.  Histological  examina- 
tion showed  that  the  three  coats  of  the  di-soased  segment  had  lo.st  their  proper  structure. 
They  were  uniformly  composed  of  embryonic  tissue.  The  internal  elastic  lamina  alone 
remained.  At  another  point,  near  the  aneurysm,  the  lumen  of  the  artery  was  almost 
obliterated  by  the  thickening  of  its  walls  and  by  a  large  bud  on  the  endarterium. 

These  cases  show  that  aneurysm  is  not  rare  when  syphilis  affects  the 
cerebral  arteries.  These  aneurysms  are  situated,  in  order  of  frequency,  in 
the  basilar  trunk,  the  Sylvian  arteries,  and  the  internal  carotid  arteries.  In 
many  cases  we  find  multiple  lesions  in  the  same  subject:  a  ruptured  aneurysm, 
an  aneurysm  in  process  of  formation,  endarteritis  with  an  obliterating 
tendency,  and  arteries  with  complete  transformation  of  their  walls.  It  must 
be  remarked  that  these  arterial  lesions  do  not  occur  only  in  the  tertiary 
stage ;  we  also  meet  with  them  soon  after  infection — eleventh  month  (Spill - 
mann),  tenth  month  (Brault),  and  eighth  month  (Spillmann). 

2.  Obliterating  Endarteritis. — The  second  group  comprises  cases  of 
arteritis  which  block  the  vessel,  and  which  may  cause  death  with  or  without 
cerebral  softening,  according  to  the  intensity  and  the  duration  of  the  process. 

GefTrier :  A  patient  suffering  from  syphilis  was  admitted  to  hospital  for  severe 
headache,  which  persisted  in  spite  of  large  doses  of  iodide  of  potassium.  A  few  months 
later  the  pains,  which  had  improved  for  a  time,  became  much  worse ;  they  were  accom- 
panied by  giddiness,  vertigo,  and  mental  torpor.  The  patient  could  not  walk  without 
losing  his  balance.  Delirium  set  in,  and  was  soon  followed  by  coma  and  death  in  the 
sixth  month  after  the  primary  infection.  The  post-mortem  examination  revealed 
syphilitic  lesions  of  the  basilar  trunk,  of  both  Sylvian  arteries,  of  the  anterior  cerebral, 
and  of  the  posterior  commmiicating  arteries.  The  basilar  trunk  was  filled  with  a  very 
adherent  clot,  which  commenced  in  the  vertebral  arteries.  The  cerebral  matter  nowhere 
showed  either  softening  or  haemorrhage.  The  histological  examination  showed  that  in 
certain  places  the  normal  elements  of  the  arterial  coats  had  almost  disappeared,  and 
were  replaced  by  embryonic  tissue.  At  certain  points  aneurysmal  pockets  had  formed. 
In  the  Sylvian  artery  granulations  projected  into  the  lumen  of  the  vessel.  Elsewhere 
the  endarteritis  presented  the  characters  of  typical  atheroma.  It  is  important  to 
remember  that  this  patient  was  not  an  alcoholic.  In  this  case  death  was  caused  by  the 
complete  obUteration  of  the  basilar  tmnk  before  cerebral  softening  had  time  to  develop. 

Mauriac  :  A  patient,  six  months  after  infection,  was  seized  with  severe  headache, 
weakening  of  memory,  embarrassment  of  speech,  awkwardness  of  the  hands,  unsteady 
gait.  A  few  days  later  the  patient  lost  consciousness.  Complete  hemiplegia  of  the 
left  side  declared  itself  and,  after  some  improvement,  death  from  coma  eight  months 
after  infection.  At  the  post-mortem  examination  scattered  lesions  were  found  in  the 
arteries  at  the  base  of  the  brain.  The  carotid  arteries  were  whitish  and  tliickened. 
The  right  Sylvian  artery  was  attacked  -with  arteritis,  and  its  principal  branches 
were  completely  obUterated  by  clots.  An  obhterating  clot  also  existed  in  the  right 
anterior  cerebral  artery.  Methodical  sections  of  the  brain  and  of  the  mesencephalon 
showed  no  focus  of  softening.  Here,  also,  the  obhteration  of  the  vessels  was  so  rapid 
that  death  supervened  before  necrobiosis  had  time  to  develop. 


1392  TEXT-BOOK  OF  MEDICINE 

I  shall  next  give  some  cases  of  syphilitic  obliterating  arteritis  in  which 
death  was  preceded  by  cerebral  softening. 

Joflfroy :  A  man  was  taken  ill  seven  years  after  infection  witli  headache,  transient 
aphasia,  and  numbness  of  the  right  arm.  A  month  later  right  facial  hemiplegia  and 
temjjorary  paralysis  of  the  right  arm  made  their  appearance  ;  during  the  nest  few 
months  inabihty  to  work,  giddiness,  and  vomiting  ;  a  short  time  after  this,  loss  of 
consciousness,  coma,  and  death.  At  the  post-mortem  examination  the  basilar  trunk 
was  found  to  be  thickened,  indurated,  and  contaraed  an  adherent  clot,  f  inch  in  length. 
The  left  Sylvian  artery  and  both  posterior  cerebral  arteries  were  the  seat  of  arteritis. 
The  histological  examination  revealed  lesions  of  endarteritis  with  the  projecting  buds, 
described  by  Heubner ;  the  lesions  of  periarteritis  were  less  advanced.  In  the  brain 
there  were  three  foci  of  softening  on  the  left  side :  in  the  internal  frontal  convolution 
in  front  of  the  paracentral  lobe,  and  in  the  foot  of  the  third  frontal  convolution. 

In  a  case  quoted  by  Mauriac  a  youth,  eight  years  after  infection,  was  taken  iU  with 
cerebral  symptoms  and  paralysis  of  the  right  arm.  He  improved  under  treatment,  but, 
four  years  later,  hemiplegia  occurred  on  the  right  side,  and  was  followed  by  secondary 
contracture  of  the  right  arm,  albuminuria,  cachexia,  and  death.  The  post-mortem 
examination  showed  arteritis  of  the  arteries  of  the  base,  with  softening  of  the  left  corpus 
striatum  and  secondary  degeneration  of  the  pyramidal  tract. 

In  some  cases,  then,  we  can  foUow  step  by  step  the  process  of  syphilitic 
obliterating  arteritis,  terminating  in  death,  with  or  without  cerebral  softening, 
dependent  on  the  severity,  the  extent,  and  the  duration  of  the  obliterating 
process. 

3,  Cerebral  Haemorrhage. — The  third  group  includes  the  less  common 
cases  in  which  syphilis  does  not  attack  the  large  arteries  at  the  base  of  the 
brain,  or  the  branches  given  ofi  directly  from  them,  but  the  superficial  or 
deep  arterioles  of  smaller  calibre.  In  the  cortical  or  central  portions  of  the 
brain  it  may  thus  cause  smaU  foci  of  softening,  consequent  on  obliteration 
of  the  arterioles,  or  miliary  aneurysms  that  cause  cerebral  haemorrhage, 
comparable  at  aU  points  with  ordinary  cerebral  haemorrhage.  Schwostek's 
case  is  a  remarkable  instance. 

In  a  young  man  of  twenty-four  years  of  age  the  secondary  compHcations  were  slight, 
but  three  years  later  very  grave  cerebral  symptoms  appeared  :  acute  pains  in  the  fore- 
head and  nape  of  the  neck,  vertigo,  and  uncertainty  in  walking.  These  symptoms 
were  soon  followed  by  hemiplegia  of  the  left  side,  with  coma  and  an  apoplectiform 
condition.  Death  was  the  consequence  thereof.  At  the  post-mortem  examin action 
syphihtic  arteritis  had  affected  the  arteries  at  the  base  of  the  brain,  and,  on  examining 
the  brain,  it  was  found  that  a  haemorrhage  had  partially  invaded  the  lenticular  nucleus, 
the  external  capsule,  the  claustrum,  and  the  ventricles. 

The  cerebellum  may  be  the  seat  of  hsemorrhage  or  of  softening,  conse- 
quent on  syphilitic  disease  of  the  cerebellar  arteries.  In  such  a  case  the 
patient  suffers  from  the  symptoms  given  in  the  section  on  the  Diseases  of 
the  Cerebellum. 

In  order  to  simplify  the  description,  I  have  divided  the  arterial  lesions  of 
cerebral  syphilis  into  several  categories.     There  are,  as  a  matter  of  fact,  cases 


DLSI<:ASES  ok  THh:  brain  139:i 

in  which  these  lesions  are  independent,  and  affect  the  types  which  I  have 
just  described  ;  but  in  other  cases  the  lesions  are  associated,  and  the  resulting 
clinical  tvpo  is  less  distinct.  As  we  know  the  various  forms  of  the  patho- 
logi(^al  process  in  sypliilitic  arteritis  of  the  cerebral  vessels,  we  shall  find  it 
easier  to  describe  the  clinical  picture. 

Symptoms  -Apoplexy.  -The  attack  of  apoplexy  may  be  the  consequence 
of  s\[)hilit  ic  cerebral  arteritis.  The  cases  already  quoted  prove  that  apoplexy 
and  death  have  been  caused  by  the  rupture  of  an  aneurysm,  or  by  the  more 
or  less  extensive  obliteration  of  a  large  artery.  In  the  former  case  the 
apoplexy  is  due  to  a  meningeal  haemorrhage  ;  it  is  lightning-like  in  its  action. 
I  n  the  latter  case  it  is  due  to  more  or  less  extensive  cerebral  ischsemia,  and  it 
is  not  so  rapid.  The  apoplexy  may  even  be  due  to  true  cerebral  haemorrhage. 
Syphihtic  apoplexy  differs  little,  as  far  as  the  unmediate  sjTnptoms  are  con- 
cerned, from  the  attack  of  ordinary  apoplexy,  but  it  is  widely  differentiated 
therefrom  by  its  precursory  signs.  The  attack  of  ordinary  apoplexy,  in  fact, 
generally  takes  the  individual  during  apparently  excellent  health.  He  is 
struck  down  during  his  sleep,  or  in  the  midst  of  his  work,  without  any 
warning.  It  is  not  so  in  s}T)hilitic  apoplexy.  The  latter  is  generally  the 
residt  of  more  or  less  intense  and  varied  cerebral  s}Tiiptoms,  which  date  back 
to  a  more  or  less  distant  period.  Headache,  so  to  say,  is  never  absent. 
Vertigo,  giddiness,  transient  sight  troubles,  obnubilation,  temporary  dis- 
orders of  speech  and  intelligence,  mental  weakness,  paresis  of  a  monoplegic 
or  hemiplegic  nature,  are  the  signs,  and  by  their  union  and  their  idiosyncrasy 
are  the  index  of  the  cerebral  disorder  which  is  going  on,  and  which  is  too  often 
the  herald  of  multiple  complications,  the  most  dangerous  of  which  is  the 
attack  of  apoplexy. 

Hemiplegia. — Hemiplegia  is  one  of  the  most  frequent  complications,  not 
only  of  syphilitic  obUterating  arteritis,  but  also  of  cerebral  syphilis  in  general. 
For  the  time  being  we  have  only  to  consider  hemiplegia  consequent  on 
obliterating  arteritis.  Syphilitic  arteritis  having  for  its  seat  of  election 
the  Sylvian  artery,  the  symptoms  of  hemiplegia  following  on  this  arteritis 
vary  according  to  the  degree  and  extent  of  this  obliteration.  As,  however, 
the  obliteration  of  the  artery  is  most  often  gradual,  it  is  quite  exceptional  for 
the  resulting  hemiplegia  to  strike  the  patient  as  rapidly  as  in  hemiplegia 
consequent  on  ordinary  cerebral  haemorrhage. 

In  order  to  give  an  idea  of  this  syphilitic  hemiplegia,  I  cannot  do  better 
than  quote  a  case  in  my  ward. 

A  man  who  had  suffered  from  syphilis  for  about  twelve  years  had  been  troubled 
for  some  time  with  severe  headache  at  night.  On  November  27,  1891,  ho  felt  a  sUght 
paresis  in  the  right  leg,  but  he  nevertheless  continued  his  work.  Next  day  the  paresis 
became  worse,  and  was  followed  by  paresis  of  the  right  arm.  During  the  afternoon  of 
the  same  day  his  speech  was  less  distinct,  and  on  the  morning  of  the  next  day  facial 
hemiplegia  appeared.     During  the  next  few  days  these  troubles  became  more  marked, 


1394  TEXT-BOOK  OF  MEDICINE 

and  the  hemiplegia  was  quite  definite  on  December  1.  On  December  2  I  noticed  total 
hemiplegia  of  the  right  side,  with  deviation  of  the  tongue  and  incomplete  aphasia. 
During  the  following  days  the  symptoms  grew  worse.  On  December  5  the  hemiplegia 
and  the  aphasia  became  total.  There  was  neither  hemiansesthesia  nor  epileptiform 
convulsions.  We  could,  therefore,  assert  that  the  patient  was  suffering  from  end- 
arteritis of  the  left  Sylvian  artery,  the  obUterating  process  having  invaded  the  vessel 
beyond  the  origin  of  the  perforating  arteries ;  and  as  the  obUteration  was  gradual,  the 
hemiplegia  and  the  aphasia  did  not  become  complete  until  the  ninth  day.  These 
symptoms  proved  that  the  branches  from  the  trunk  of  the  Sylvian  artery,  going  to  the 
foot  of  the  third  convolution,  and  to  the  ascending  frontal  and  parietal  convolutions, 
no  longer  fiunished  a  proper  supply  of  blood  to  these  regions.  The  question  as  regards 
prognosis  was  whether  these  regions  were  or  were  not  in  a  state  of  necrobiosis.  In  any 
case,  active  treatment  was  instituted  from  the  moment  of  the  patient's  admission. 

Whilst  the  right  hemiplegia  commenced  to  improve,  however,  we  witnessed  the 
commencement  of  left  hemiplegia.  This  left  hemiplegia  also  ran  a  slow  course.  It  com- 
menced in  the  left  arm  and  invaded  the  left  leg.  The  facial  paralysis  being  double,  the 
patient  experienced  such  difficulty  in  mastication  and  deglutition  that  ahmentation  became 
very  difficult.  This  left  hemiplegia  proved  that  the  Sylvian  artery  on  the  right  side,  hke 
its  fellow  on  the  left,  was  attacked  at  a  symmetrical  point  by  obhterating  endarteritis. 
Symmetry  of  the  lesions  is,  by  the  way,  common  in  the  history  of  syphihtic  disease 
of  the  cerebral  arteries.  The  active  treatment,  and  the  chance  of  intervening  before 
the  ischsemia  of  the  cerebral  regions  ended  in  necrobiosis,  gave  us  the  satisfaction  of 
witnessing  progressive  improvement  in  the  double  hemiplegia.  Abihty  to  write,  wiiich 
was  absolutely  impossible  at  the  time  of  the  patient's  admission,  not  only  on  account  of 
intellectual  troubles  but  on  account  of  true  motor  agraphia,  gradually  reappeared. 
The  difficulty  in  deglutition  hkewise  improved ;  the  aphasia,  which  had  been  absolute 
for  twenty-four  hours,  gradually  disappeared.  At  the  end  of  a  few  weeks  the  move- 
ments in  both  hands  reappeared,  the  patient  commenced  to  walk,  and  after  two 
months  very  marked  improvement  in  this  double  syphihtic  arteritis  was  obtained. 

The  example  above  quoted  might  serve  as  a  type,  but  all  cases  are  far 
from  being  alike.  According  to  the  localization  of  the  obliterating  arteritis 
the  symptoms  may  vary  and  reveal  themselves  by  complete  hemiplegia,  with 
or  without  aphasia ;  by  incomplete  hemiplegia ;  by  monoplegia ;  and,  finally, 
by  aphasia,  which  may  be  isolated  or  associated  with  paralytic  troubles. 
Each  one  of  these  kinds  exists.  I  might  quote  several  cases  in  which  they 
are  found  complete  in  every  detail.  In  one  case  we  find  that  the  hemiplegia 
has  remained  incomplete  ;  in  another  case  we  may  find  total  hemiplegia, 
unamenable  to  treatment  and  followed  by  secondary  contractures,  which 
proves  that  the  arterial  obliteration  has  been  complete,  and  of  such  a  dura- 
tion as  to  allow  necrobiosis  of  the  corresponding  region,  with  secondary 
degenerative  lesions. 

Aphasia. — Amongst  the  symptoms  of  which  I  have  just  spoken  there  is 
one  to  which  I  desire  to  refer — aphasia,  the  complete  history  of  which  has 
been  given  in  one  of  the  preceding  sections.  Syphilitic  aphasia  often  opens 
the  scen^  of  the  cerebral  complications.  It  may  or  may  not  be  associated 
with  hemiplegia  of  the  right  side  ;  it  may  appear  as  an  isolated,  initial,  and 
transitory  symptom.  It  may  supervene  in  the  shape  of  a  fit,  which  lasts  for 
some  minutes  or  for  some  hours ;    it  may  be  subject  to  recurrences.     As  a 


DISEASES  OF  THE  BRAIN  i:{9r, 

type  of  syphilitic  aphasia  without  hemiplegia,  I  recall  the  case  of  Tarnowski, 
which  is  quoted  in  the  admirable  treatise  of  Fouriiier  on  cerebral  sv^jhilis. 
Other  cases,  referring  to  the  various  types  of  syphilitic  aphasia,  will  be  found 
in  the  same  work.  Charcot  has  published  a  most  interesting  case  of  syphilitic 
aphasia.  The  patient  was  seized  with  progressive  hemiplegia  on  the  right 
side,  motor  aphasia,  and  word- blindness.  The  motor  aphasia  disappeared 
later,  but  the  word- blindness  persisted.  The  cerebral  lesion,  consequent 
on  syphilitic  arteritis  of  the  left  Sylvian  artery,  was  localized  by  Charcot  in 
the  psychomotor  region,  in  Broca's  convolution,  and  in  the  lobule  of  the 
angular  g\Tus. 

Diagnosis. — I  must  now  deal  with  the  differential  diagnosis  of  hemiplegia 
and  aphasia  consequent  on  the  syphilitic  obliteration  of  the  Sylvian  arteries. 
Apart  from  some  exceptional  cases,  this  form  of  hemiplegia  is  never  sudden 
and  complete  from  the  outset ;  it  is  preceded,  sometimes  at  a  remote  period,  by 
more  or  less  obstinate  and  severe  headache,  vertigo,  obnubilation,  amnesia, 
transitory  aphasia,  and  twitchings  or  heaviness  in  one  foot  or  in  one 
hand ;  these  symptoms  may  be  associated  with  one  another  or  may  follow 
on  one  another,  improving  and  reappearing  in  inJ&nite  variety.  Such  a  con- 
dition of  things  does  not  exist  in  ordinary  cerebral  haemorrhage,  or  in 
obliteration  of  the  cerebral  arteries  by  embolism.  The  syphilitic  process 
resembles,  though  with  more  marked  shades,  the  lesions  of  cerebral  atheroma 
in  patients  suffermg  from  alcoholism  and  gout,  and  in  old  people.  T\Tien  a 
patient  is  taken  ill  with  hemiplegia  which  has  required  two  or  three  days  to 
become  complete,  and  when  for  some  weeks  or  months  he  has  complained  of 
violent  headache  (worse  at  night),  of  transient  aphasia,  of  vertigo,  etc.,  we 
must  immediately  think  of  syphilitic  hemiplegia.  If  this  general  or  dis- 
sociated hemiplegia  has  been  preceded,  or  if  it  is  accompanied,  by  more  or 
less  limited  Jacksonian  epilepsy,  or  by  partial  contractures,  it  is  very  probable 
that  the  syphilitic  hemiplegia  is  caused  by  a  cortical  lesion  of  the  motor 
centres.  If,  however,  these  hemiplegic  or  aphasic  symptoms  havs  neither 
been  preceded  nor  accompanied  by  localized  contractures,  or  by  Jacksonian 
epilepsy,  and,  a  fortiori,  if  the  hemiplegia  invades,  though  unequally,  both 
sides  of  the  body,  it  may  almost  certainly  be  said  that  syphilitic  obliterating 
arteritis  is  the  cause. 

Sometimes,  however,  the  diagnosis  remains  uncertain.  It  is  then  that 
lumbar  puncture,  by  revealing  marked  l}Tnphoc}'tosis  (twelve  times  out  of 
thirteen  cases — Widal  and  Lemierre)  turns  the  balance  in  favour  of  the 
syphilitic  nature  of  the  hemiplegia,  and  induces  us  to  commence  active 
treatment  (Widal  and  Lemierre).  In  other  patients  the  presence  of  Argyll- 
Robertson's  sign  will  remove  all  doubts.  It  will  also  allow  us  to  affirm  the 
specific  nature  of  the  disease  (Babinskd).  Besides,  even  in  non-hemiplegic 
patients  who  show  only  Argyll-Robertson's  sign,  the  cerebro-spinal  fluid  is 


1396  TEXT-BOOK  OF  MEDICINE 

rich  in  lymphocytes,  as  the  researches  of  Babinski,  and  Widal  and  Lemierre 
have  shown. 

The  existence  of  lymphocytosis  in  syphilitic  hemiplegia  shows  once  more 
the  importance  of  the  meningeal  irritation  in  the  nervous  manifestations  of 
syphilis. 

The  prognosis  of  syphilitic  cerebral  arteritis  is  very  grave.  It  is  more 
easy  to  treat  a  sclero-gummatous  cerebro-meningeal  lesion  than  arteritis. 
To  begin  with,  the  gmnma  or  the  sclero-gummatous  lesion  is  more  clearly 
localized,  invading  only  a  relatively  restricted  region,  and  the  tissue  is  easily 
modified  by  mercury  and  iodide  of  potassium,  whereas  arteritis  is  by  nature 
more  diffuse,  and  invades  several  arteries  or  several  segments  of  arteries. 
These  lesions  are  obstinate,  and  less  accessible  to  treatment.  Relapse  in 
arteritis  is  frequent,  and  a  patient  whose  condition  has  been  improved  or 
apparently  cured  is  seized  a  few  months  later  with  fresh  cerebral  troubles. 
Sometimes  even  when  the  patient  appears  to  be  so  much  better  that  recovery- 
may  be  hoped  for,  the  improvement  stops,  and  persistent  troubles  appear 
(secondary  contractures,  embarrassment  of  speech,  and  weakening  of  the 
intellect). 

Finally,  let  us  remark  that  syphilitic  cerebral  arteritis  does  not  always 
exist  in  a  state  of  purity  ;  in  too  many  cases  it  is  accompanied  or  followed  by 
complications  which  are  due  to  rupture  of  an  aneurysm,  to  sclero-gumm.atou8 
lesions,  or,  finally,  to  symptoms  of  general  pseudo-paralysis.  It  would  be 
wrong  to  consider  syphilitic  cerebral  arteritis  as  the  appanage  of  late  syphilis. 
The  cases  previously  quoted  prove  that  fairly  often  syphilitic  arteritis,  with 
all  its  consequences,  appears  early,  within  one  or  two  years  of  the  primary 
infection. 

Treatment. — In  every  case  of  syphilitic  cerebral  arteritis  antisyphilitic 
treatment  must  be  immediately  adopted.  The  mercurial  preparations  and 
iodide  of  potassium  must  be  administered  in  large  doses,  and  without  delay. 
I  say  without  delay,  because  a  delay  of  a  few  days  may  allow  the  necrobiosis 
of  the  brain  to  become  irremediable.  We  must  act  as  soon  as  the  first 
precursory  symptoms  appear.  As  regards  mercurial  treatment,  sub- 
cutaneous injections  of  biniodide  and  inunction  of  mercurial  ointment  seem 
to  me  the  most  certain  means.  About  a  drachm  of  mercurial  ointment  is 
rubbed  in  daily,  and  at  the  same  time  chlorate  of  potassium  is  given.  The 
patient  must  be  most  careful  to  cleanse  the  mouth,  so  as  to  prevent  the 
appearance  of  gingivitis  or  of  mercurial  stomatitis,  which  interferes  with  the 
exhibition  of  mercury. 

The  undoubted  superiority  of  injections  of  biniodide  leads  me  to  recom- 
mend them  in  preference  to  all  others.  This  method  is,  moreover,  applicable  in 
all  cases  of  cerebral,  spinal,  lar}'ngeal,  pulmonary,  naso-buccal,  and  cutaneous 
syphilis.     The  reader  wiU  find  fuU  details  in  the  appendix  on  Therapeutics. 


DISEASES  OF  THE  BRAIN  1307 

With  the  nierfury  we  give  iodide  of  potassium  in  increasing  doses 
Rigorous  treatment  is  an  indispensable  condition  of  success.  It  is  better 
to  give  large  doses,  although  they  may  have  to  be  suspended  from  time  to 
time,  than  to  give  small  doses.  Instead  of  giving  mercury  and  iodide  at 
the  same  time,  they  may  be  gi>'en  alternately,  mercury  being  administered 
for  a  fortnight,  and  then  iodide  for  another  fortnight;  but  mercury  is  very 
much  better  than  iodide.  Brilliant  success  sometimes  rewards  our  efforts, 
but  a  favourable  prognosis  must  not  be  too  readily  given,  because  we  might 
run  the  risk  of  a  mistake.  The  arterial  lesions  of  syphilis  are  amongst  those 
which  sometimes  resist  the  best  directed  specific  treatment,  as  I  have  already 
remarked  and  as  I  once  more  point  out ;  and  even  when  they  appear  cured, 
or  almost  cured,  a  relapse  of  the  disease  is  to  be  feared. 

Cerebral  Gummata — Sclero-Gummatous  Syphilis  of  the  Brain 
and  of  the  Meninges. 

Pathological  Anatomy. — Let  us  examine  separately  the  lesions  of  the 
meninges  and  those  of  the  brain.  In  the  meninges,  as  elsewhere,  we  find 
circumscribed  gimimata,  or  diffuse,  sclerotic  gummatous  tissue.  The  gum- 
mata vary  in  size  from  a  millet-seed  to  a  hazel-nut.  They  are  usually 
found  on  the  base  of  the  brain  and  on  the  hemispheres,  and  especially 
the  motor  regions.  Sclero-gummatous  meningitis  is  very  common.  The 
patches  of  meningitis  have  the  look  of  yellowish  fibro-caseous  tracts  covering 
one  or  two  convolutions  ;  they  are  sometimes  thick  enough  to  form  a  tumour. 
They  bind  the  meninges  together  and  the  meninges  to  the  brain.  The 
adhesion  is  such  that  the  cerebral  matter  is  torn  on  attempting  to  decorticate 
the  brain.  The  sclero-gummatous  lesions  have  the  same  seats  of  election  as 
the  gunmiata. 

In  the  brain  the  gummatous  tissue  likewise  presents  itself  in  the  form  of 
diffuse  infiltration,  or  of  a  circumscribed  gumma.  Diffuse  gummatous 
encephalitis  penetrates  into  the  nerve  tissue  as  an  interstitial  infiltration. 
Circumscribed  gummata  are  not  common ;  they  vary  in  number  and  size  ; 
they  occupy  the  central  ganglia,  the  peripheral  portions  and  the  base  of  the 
brain  in  the  neighbourhood  of  the  sella  turcica.  It  is  interesting  to  know 
that  the  cerebral  gummata  are  much  more  frequent  in  the  frontal  lobe  than 
in  the  area  of  Rolando.  In  Herber's  figures  we  find  ten  cases  of  gummata 
in  the  frontal  lobe,  whereas  we  find  only  two  in  the  motor  convolutions 
(Rolando's  zone  and  the  paracentral  lobule),  whence  we  may  conclude 
a  priori  that  Jacksonian  epilepsy,  following  on  lesions  of  Rolando's 
area,  is  due  to  tuberculoma,  glioma,  etc.,  much  more  often  than  to 
syphiloma. 

From  the  anatomical  and  histological  point  of  \-iew  it  would  seem  that 
confusion  could  hardlv  be  possible  between  the  gumma  and  other  tumours, 
II.  '  89 


1398  TEXT-BOOK  OF  MEDICINE 

suet  as  glioma,  tuberculoma,  or  a  cyst  undergoing  degeneration,  and  yet 
there  are  cases  where  this  confusion  has  occurred,  as  in  the  following  case 
from  Herber's  thesis. 

A  man  suffered,  from  violent  headache,  especially  at  night.  He  had  nausea,  stra- 
bismus, and  diplopia.  Chauffard  foim.d  paralysis  of  the  external  rectus  of  the  right  eye. 
The  ophthalmoscope  revealed  double  haemoretinitis,  having  aU  the  characteristics  of 
syphihs.  Though  the  patient  denied  sjrphihs,  mercury  and  iodide  of  potassium  were 
given,  notable  improvement  resulting.  The  man  left  the  hospital,  but  returned  a  fort- 
night later,  the  headache  being  worse  than  ever.  The  same  treatment  was  again 
administered.  Shortly  afterwards  fits  of  dizziness  and  violent  dehrium  supervened. 
Two  attacks  of  epilepsy  soon  occurred,  and  the  patient  was  carried  off  by  a  third  attack, 
more  severe  than  the  first. 

The  diagnosis  of  cerebral  syphihs  appearing  certain  (and  everything  pointed  to  it 
being  correct),  the  following  were  the  results  of  the  post-mortem  examination :  (1)  A 
soft  gumma  was  found  in  the  white  matter,  at  the  foot  of  the  first  frontal  convolution. 
Its  contents  were  caseous  and  yellowish  in  its  upper  part ;  its  lower  part  was  cystic ; 
the  peripheral  zone  was  transparent  and  vitreous.  (2)  At  the  junction  of  the  anterior 
and  the  middle  third  of  the  first  frontal  convolution,  under  the  grey  matter,  a  small, 
soft,  transparent  tumour  was  discovered,  having  the  look  of  vitreous  degeneration,  and 
surrounded  by  a  zone  of  white  indurated  matter.  The  two  tumours  looked  like 
gummata. 

The  histological  examination  showed  that  the  diagnosis  made  during  life  and  at 
the  post-mortem  examination  was  erroneous.  It  was  not  a  question  of  syphiloma, 
but  of  ghoma.  "  The  histological  characters,"  says  PhiMppe,  "  left  no  doubt  as  to 
the  nature  of  these  tumours.  They  were  ghomata  of  the  mixed  type  in  which 
the  fibriUse  and  the  ceUs  had  developed  in  equal  proportions.  In  aU  the  sections  ex- 
amined the  ghoma  had  invaded  the  cortex  and  the  white  matter,  though  to  a  greater 
extent  in  the  latter." 

In  a  patient  at  the  Hotel-Dieu  who  died  from  a  syphihtic  gumma  of  the  frontal  lobe 
the  following  was  the  result  of  the  histological  examination  made  by  Jolly  :  The  sections 
of  the  tumour  showed  that  the  cerebral  tissue  was  almost  completely  replaced  by 
connective  tissue  of  new  formation,  fairly  homogeneous,  and  containing  but  few  ceUs. 
In  places  there  were  masses  of  rounded  ceUs  with  a  large  nucleus.  These  masses  most 
often  surrounded  the  vessels.  They  were  elongated  or  ramified,  dividing  the  newly- 
formed  tissue  into  lobules.  In  the  vertical  sections  of  the  meninges  the  dura  mater 
was  but  httle  altered.  Below  there  was  a  thick  adherent  and  vascular  connective 
layer,  which  corresponded  to  the  thickened  pia  mater.  Numerous  dilated  vessels 
were  surrounded  by  a  mass  of  rounded  cells  with  deeply  stained  nuclei.  These  vessels, 
surrounded  by  lymphatic  hyaline  tissue,  passed  down  at  right  angles  from  the  surface 
into  the  midst  of  the  pathological  tissue.  At  certain  points  the  tissue  of  the  tumour 
was  homogeneous,  necrosed,  and  lacking  in  cells.  It  did  not  take  the  stain.  These 
points  corresponded  to  the  caseous  islets  visible  to  the  naked  eye.  It  was,  therefore, 
not  a  question  of  a  ghoma,  an  epithelioma,  a  smaU-ceUed  sarcoma,  or  a  tuberculoma, 
which  is  more  limited  and  caseous.     It  was  a  gummatous  tumom:. 

The  gummatous  lesions  in  the  brain  and  its  membranes  give  rise  to 
meningeal  sclerosis,  with  obstruction  of  the  small  vessels  in  the  cortex,  and 
to  more  or  less  extensive  cerebral  softening  from  compression  and  thrombosis 
of  the  vessels.  It  is  even  probable  that  the  process  commences  with  a  lesion 
of  the  arterioles  (syphilitic  arterio-sclerosis),  and  extends  from  them  to  the 
connective  elements  and  to  the  tissue  of  the  organ. 


DISIOASER  OF  TtFE  BRAIN  1309 

Symptoms.  -A  giunma  may  be  presoiit  for  a  long  while  in  certain  regions 
of  the  hraiii  witlioiit  caiLsiiig  any  aymptorii.  In  my  clinical  lectures*  I  have 
quoted  the  case  of  a  patient  who  during  Ih*;  long  evolution  of  a  gumma  of  the 
frontal  lobe  felt  nothing.  The  lesion  suddenly  revealed  itself  by  an  attack 
of  Jacksonian  ei>ilepsy,  and  at  that  time  the  lesion  had  advanced  so  far  that 
in  a  few  days  it  was  fatal,  in  spite  of  all  treatment.  How  are  we  to  explain 
that  a  cerebral  lesion  may  remain  latent  for  so  long  a  time  ?  It  depends  on 
the  situation  of  the  lesion.  In  the  brain  some  regions  are  more  tolerant  than 
others.  This  toleration  is  not  to  be  envied,  because  the  patient,  unaware  of 
the  danger,  lives  in  false  security,  without  following  any  treatment. 

Nothing  is  more  common  than  paralyses  of  the  third  and  sixth  nerves, 
because  these  nerves,  before  entering  the  orbit,  run  for  a  long  way  at  the 
base  of  the  skull  in  contact  with  the  meninges.  This  region  is  precisely  a 
seat  of  election  of  gummatous  cerebro-meningeal  lesions  (Fournier).  I  do 
not  say  that  all  the  syphilitic  palsies  which  affect  the  oculo-motor  and  facial 
nerves  are  due  to  a  lesion  at  the  base  of  the  brain.  In  some  cases  these 
paralyses,  especially  when  they  are  partial,  may  be  due  to  a  lesion  of  the 
cortex ;  but,  in  proportion  as  the  question  is  better  understood,  it  will  be 
found  that  many  of  these  cases  of  paralysis  are  due  to  peripheral  neuritis, 
and  have  nothing  to  do  with  central  lesions. 

Syphilitic  paralysis  of  peripheral  origin,  and  probably  of  a  toxic  nature, 
deserves  recognition.  It  supervenes  rapidly,  is  usuaDy  transient,  and  some- 
times dissociated ;  it  may  occur  in  the  second,  or  even  in  the  first  year  of  the 
infection.  Accordingly,  in  a  syphilitic  patient  sufEering  from  deviation  of 
the  mouth,  facial  hemiplegia,  ptosis,  strabismus,  and  diplopia,  we  must  not 
be  in  a  hurry  to  make  the  grave  diagnosis  of  a  syphilitic  lesion  at  the  base  of 
the  brain,  because  the  paralysis  may  be  due  to  peripheral  neuritis  ;  but  if 
the  third  nerve  is  paralyzed  as  a  whole,  and  a  fortiori  if  the  other  motor  nerves 
of  the  eye  are  also  affected,  and  if  these  symptoms  have  gradually  become 
more  marked,  and  have  been  accompanied  by  vertigo  and  headache,  with  or 
without  direct  or  crossed  hemiplegia,  a  sclero-gummatous  lesion  of  the  base 
of  the  brain  can  be  diagnosed.  Syphilitic  new  growths  are  common  in  the 
interpeduncular  space,  whence  the  third  pair  of  nerves  emerge  ;  it  is  also  not 
an  uncommon  thing  to  find  double  paralysis  of  the  common  oculo-motor. 
nerves.  We  may  likewise  be  certain  of  a  sclero-gummatous  lesion  at  the  base 
of  the  brain  if  a  syphilitic  patient  has  diminution  or  loss  of  sight,  optic 
neuritis  with  nocturnal  headache,  which  may  or  may  not  be  accompanied  by 
vomiting  and  epileptiform  attacks. 

Here,  as  in  all  cerebral  tumours,  the  different  varieties  of  hemianopia 
described  under  Polioencephalitis  may  be  obser%'ed.  Often,  in  conclusion, 
the  examination  with  the  ophthalmoscope  reveals  a  chorio-retinitis,  which 

*  Dieulafoy,  Clinique  Medicale  de  VHotd-Dieu,  1903,  T"'  le9on. 

89—2 


1400  TEXT-BOOK  OF  MEDICINE 

has  considerable  value  in  establishing  the  diagnosis  of  syphilis.  As  regards 
the  examination  of  the  fundus  oculi,  the  condition  of  the  ophthalmic  artery- 
may  give  an  idea  of  the  condition  of  the  cerebral  arteries  from  which  it 
arises. 

We  have  said  that  the  sclero-gummatous  lesions  have  as  their  seat  of 
election  the  cortical  motor  zone.  Hemiplegia  and  partial  epilepsy  are  the 
two  great  symptoms  accompanying  these  localizations.  The  paralysis 
takes  the  form  of  hemiplegia  or  of  monoplegia  on  the  side  opposite  to  the 
lesion.  The  face,  arm,  and  leg  may  be  paralyzed,  as  in  ordinary  hemiplegia. 
More  often  the  arm  only  is  attacked,  or  the  arm  and  the  face,  or  the  leg  alone. 
These  paralyses  are  rarely  complete,  the  power  of  movement  not  being 
absolutely  lost ;  in  many  cases  we  find  paresis  rather  than  paralysis.  Hemi- 
plegia is  hardly  ever  present  from  the  outset ;  the  paralysis  sets  in  slowly 
and  progressively.  It  is,  for  a  longer  or  shorter  period,  preceded  by 
weakness,  numbness  of  the  hand,  twitchings,  and  heaviness  of  the  foot  and 
leg ;  for  some  time  the  patient  complains  of  being  unable  to  grasp  objects, 
and  of  being  awkward.  He  notices  that  his  leg  gives  v/ay  ;  he  stumbles 
against  the  steps  when  going  upstairs,  or  he  finds  some  hesitation  in  his 
speech.  These  prodromata  are  the  herald  ol  paralysis.  If  severe  nocturnal 
headache  is  added  to  these  prodromata,  it  is  evident  that  the  hemiplegic 
troubles  resulting  from  a  syphilitic  lesion  of  the  motor  area  do  not  resemble 
the  hemiplegia  which  accompanies  cerebral  haemorrhage  ;  it  is  even  slower, 
more  dissociated,  and  more  incomplete  than  the  hemiplegia  consequent 
on  the  obliteration  of  the  Sylvian  artery  by  syphilitic  endarteritis.  Finally, 
as  we  shall  see,  this  hemiplegia,  by  virtue  of  the  cortical  lesion,  is  often 
associated  with  partial  epilepsy. 

Jacksonian  epilepsy  constitutes  one  of  the  most  frequent  symptoms  of 
gummatous  lesions  in  the  motor  area.  This  partial  epilepsy  appears  on  the 
side  opposite  to  the  lesion,  and  presents  several  types. 

(1)  In  the  facial  type  the  convulsions  are  limited  to  the  face  and  to  the 
neck.  They  attack  the  commissures  of  the  lips,  the  orbicularis  palpebrarum, 
tlie  motor  muscles  of  the  eye  and  of  the  tongue,  and  the  sterno-mastoid. 
Jerking  of  the  arm  may  also  be  present.  (2)  In  the  brachial  type,  which  is 
more  common,  the  aura  commences  in  one  of  the  fingers.  The  convulsions 
involve  the  hand,  arm,  and  shoulder,  and  sometimes  the  face  and  the  neck. 
(3)  In  the  crural  type,  which  is  the  least  common,  the  aura  commences  in 
the  foot,  and  the  convulsions  stop  at  the  hip. 

The  topography  of  the  cerebro-meningeal  lesion  may  be  diagnosed  by 
the  type  of  the  epilepsy  :  facial  type — lesion  of  the  lower  extremity  of  the 
cortex  of  the  two  ascending  convolutions ;  brachial  type — lesion  of  the 
middle  portion  of  the  ascending  frontal  convolution  ;  crural  type — lesion  of 
the  upper  part  of  the  ascending  convolutions  and  of  the  paracentral  lobule  ; 


DISEASES  OF  THE  BRAIN  MOl 

lingual  Ir,  po — lesion  of  the  lower  part  of  tlic  ascemliiig  convoluti(tii  la  Iho 
neighbourhood  of  the  foot  of  the  third  frontal  convolution. 

In  Jaeksonian  ejiilcpsy  loss  of  consciousness  may  Ijc  absent  or  incom- 
plete, or  it  may  only  supervene  when  the  convulsive  attack  has  commenced. 
After  the  attack  the  patient  may  suffer  from  diplopia,  dysphasia,  amnesia, 
or  vertigo.  Under  some  circumstances  the  attack  of  partial  epilepsy  may 
be  stopped  by  placing  a  ligature  above  the  seat  of  the  aura. 

Partial  epilepsy  is  often  preceded  or  followed  by  transient  paralysis 

(hemiplegia,  monoplegia) ;  in  some  cases  the  convulsive  attack  lays  hold  of 

the  limbs,  which  are  almost  completely  paralyzed.     The  fits  of  Jacksonian 

epilepsy  may  be  isolated,  or  may  be  repeated  several  times  a  day. 

A  patient  who  had  been  suffering  from  syphilis  for  several  years  came  into  my 
ward  at  the  Neckor  Hospital  for  hemiplegia  of  the  right  side  without  aphasia.  The 
hemiplegia  affected  the  hmbs,  the  lower  part  of  the  face,  and  the  tongue.  It  super- 
vened gradually',  and  was  accompanied  by  violent  headache  and  intellectual  torpor. 
From  the  time  of  his  admission  into  the  hospital  the  patient  had  fits  of  partial  epilepsy. 
These  tits  consisted  of  a  tonic  stage,  lasting  some  seconds,  and  of  a  clonic  stage,  lasting 
half  a  minute.  The  whole  fit  did  not  last  a  minute.  It  supervened  suddenly,  without 
any  initial  cry,  pallor  of  the  face,  or  any  aura.  It  commenced  in  the  right  hand,  spread 
to  the  face,  to  the  neck,  and  sometimes  to  the  leg  on  the  same  side,  and  then  terminated. 
During  the  tit  the  patient  never  had  stertorous  respiration,  the  sahva  was  not  blood\% 
and  the  tongue  was  not  bitten.  In  a  few  days  as  many  as  400  fits  could  be  counted 
in  the  twenty-four  hours.  They  were  often  subintrant,  as  in  the  status  epilepticus,  but 
they  were  never  accompanied  by  a  rise  in  temperature.  The  fit  sometimes  supervened 
when  the  patient  had  his  mouth  full  of  food.  Mastication  was  stopped  for  a  few  seconds, 
and  the  fit  having  passed  over,  the  patient  continued  eating.  Further  details  are  given 
under  Jacksonian  Epilepsy. 

Under  some  circumstances  the  sclero-gunmiatous  lesions  produce,  not 
partial  epilepsy,  but  temporary  or  permanent  contractures,  which  are  at 
times  very  painful.  The  cortical  lesions  of  s}^hilis  which  cause  the  troubles 
just  described  may  be  the  origin  of  secondary  degeneration,  with  late 
contracture,  hemichorea,  and  athetosis. 

In  some  cases  the  sclero-gummatous  lesions  cause  paraphasia  or  aphasia 
by  their  localization  in  Broca's  convolution.  The  aphasia  may  occur  alone, 
or  may  be  associated  with  monoplegia  or  hemiplegia  of  the  right  side. 

Finally,  there  are  some  cases  in  which  the  sclero-gummatous  lesions 
produce  the  syndrome  described  under  the  name  of  glosso-labio-lar}Tigeal 
pseudo-paralysis.  Incessant  flow  of  the  saliva  through  the  half-open  lips, 
difficulty  in  mastication  and  deglutition,  paralysis  of  the  tongue,  increasing 
difficulty  in  the  articulation  of  words,  are  the  symptoms  present.  For  further 
details  as  to  the  topography  of  the  lesions,  I  refer  the  reader  to  the  section 
dealing  with  glosso-labio-laryngeal  paralysis. 

In  short,  the  cerebro-meningeal  sclero-gimimatous  lesions  may  provoke 
paralysis  of  the  cranial  nerves,  including  disturbances  of  hearmg  and  of 
sight  (amblyopia,  amaurosis) ;  their  most  common  symptoms  are  special 


1402  TEXT-BOOK  OF  MEDICINE 

forms  of  paralysis,  hemiplegia,  monoplegia,  contractures,  epileptiform  fits. 
The  epileptiform  fit  assists  most  in  the  cortical  topographical  diagnosis  of 
the  lesion,  and  allows  us  to  eliminate  the  hypothesis  of  hemiplegia,  or  of 
monoplegia,  consequent  on  obliterating  endarteritis  of  the  Sylvian  artery. 

These  symptoms,  which  depend  solely  on  the  situation  of  the  lesion,  are 
accompanied  by  others  which  are  common  to  all  forms  of  cerebral  syphilis, 
such  as  headache,  which  is  worse  at  night,  vertigo,  intellectual  torpor,  etc. 

The  prognosis  in  cere bro -meningeal  sclero-gummatous  lesions  is  not  as 
grave  as  in  the  other  forms  of  cerebral  syphUis.  The  lesions  are  cortical, 
and  do  not,  like  endarteritis  of  the  large  trunks,  cause  large  foci  of  softening ; 
and,  again,  they  are  more  accessible  to  treatment  than  the  interstitial  and 
diffuse  lesions  which  lead  to  the  mental  forms  of  cerebral  syphilis.  The 
epileptic  or  epilepto-paralytic  form  has  not  therefore  a  very  grave  prognosis. 
"It  is,"  says  Fournier,  "  one  of  the  forms  which  yields  best  to  treatment, 
and  is  most  easily  cured  when  attacked  in  time  by  the  specific  treatment." 

Treatment. — The  treatment  has  been  described  under  Syphilitic  Cerebral 
Arteritis. 

Intellectual  Troubles— Syphilitic  General  Pseudo-Paralysis. 

We  now  come  to  one  of  the  most  delicate  and  most  controversial 
questions.  Is  or  is  not  cerebral  syphilis  capable  of  causing  general 
paralysis  ?  Before  replying  to  this  question  let  us  proceed  methodically. 
It  is  well  known  that  cerebral  syphilis  is  often  the  cause  and  the  origin  of 
the  most  varied  intellectual  troubles.  These  troubles  may  arise  from  deep 
foci  of  softening  due  to  obliterating  arteritis,  and  spreading  to  the  frontal 
convolutions  which  preside  over  the  mental  faculties.  They  may  likewise  arise 
from  the  cortical  lesions  ending  in  sclero-gummatous  meningo-encephahtis. 
Finally,  they  may  be  caused  by  the  lesions  of  diiTuse  interstitial  sclerous 
encephaHtis. 

Following  Foumier's  example,  I  shall  divide  the  intellectual  troubles  of 
cerebral  syphilis  into  two  groups.  In  the  fiist  group  I  include  the  phenomena 
of  exaltation  and  cerebral  excitation,  with  relatively  acute  conditions  of 
delirium  or  mania.  The  patients  are  excited,  loquacious,  and  restless. 
They  sleep,  but  they  have  haUucinations.  Some  of  them  commit  acts  of 
violence,  and  utter  expressions  significant  of  mental  trouble,  "but  they  are 
conscious  of  it,  because  they  are  not  incoherent,  like  patients  suffering  from 
general  paralysis. 

The  patients  of  the  second  group,  instead  of  being  excited,  are  depressed. 
Their  intelligence  is  weak  and  their  memory  fails.  They  are  less  fit  for 
work,  and  suffer  from  "  intellectual  asthenia,"  which  may  be  accompanied 
neither  by  incoherence  nor  by  delirium.  They  certainly  have  some  idea  of 
their  condition,  being  aware  of  their  intellectual  weakness,  but  they  do  not 


OTREASES  OF  TIFR  BRATN  140?! 

trouble  about  it,  and  the  tranquil  apathy  with  which  they  accept  their 
condition  sufficiently  proves  their  mental  decay.  In  some  patients  these 
s^Tnptonis  are  very  marked ;  the  intellectual  depression  is  associated  with 
incoherence,  and  the  disease  ends  in  dementia. 

In  certain  circimistances  the  symptoms  are  cerebro-spinal.  Within 
a  few  weeks  or  days  an  individual  who  has  had  syphilis  is  taken  ill  with 
headache,  vertigo,  embarrassment  of  speech,  ptosis,  numbness  and  heavi- 
ness in  the  legs,  anaesthetic  patches  on  the  buttock  or  on  the  thighs,  and 
difficulty  in  micturition.  Walking  soon  becomes  difficult;  the  patellar 
reflex  is  abolished ;  the  sexual  functions  are  lost,  and  the  patient  suffers  from 
cerebral  excitation  or  depression — in  a  word,  the  disease  is  cerebro-spinal, 
and  in  part  resembles  the  picture  of  the  slow  and  progressive  invasion  of 
tabes  dorsalis.  These  cases  led  Fournier  to  assign  to  syphilis  a  large 
oetiological  share  in  the  pathogenesis  of  tabes  dorsalis  and  of  cerebral 
tabes. 

The  cerebral  or  cerebro-spinal  symptoms  just  described  do  not  give  rise 
to  a  well-defined  type.  In  another  type,  however,  the  nature  and  course  of 
the  symptoms  recall  the  picture  of  general  paralysis.  It  is  to  this  form  of 
cerebral  syphilis  that  Fournier  has  given  the  name  of  syphilitic  general 
pseudo-paralysis. 

The  symptoms  of  this  form  are  described  in  the  article  on  General 
Paralysis.  It  is  certain  that  cerebral  syphilis  causes  an  affection  which 
simulates  idiopathic,  progressive,  chronic  peri-encephalitis.  The  clinical 
manifestations  are  similar,  and  the  anatomical  lesion  consists  in  a  diffuse 
s}^hiloma  of  the  cerebral  cortex  and  of  the  meninges.  Fournier  has  given 
the  excellent  name  of  cerebral  tabes  to  the  depressing  form  of  this  general 
pseudo-paralysis. 

It  has  been  asked  whether  syphilis  is  capable  of  producing  true  general 
paralysis.  It  would  then  have  an  important  part  in  the  setiology  of  tabes 
dorsalis,  of  cerebral  tabes,  and  of  cerebro-spinal  tabes. 

This  opinion,  of  which  Fournier  was  almost  the  only  defender,  and 
whicb  was  for  a  long  time  contested,  is  now  held  in  Germany,  as  well  as  in 
France,  and  it  appears  certain  that  syphilis  is  one  of  the  most  important 
factors  in  the  production  of  general  paralysis  and  of  general  pseudo-paralysis. 
This  does  not  mean,  of  course,  that  syphilis  may  not  be  much  assisted  bv 
other  factors  :  heredity,  sexual  or  alcoholic  excesses,  worry,  grief,  and  brain 
fag  play  some  part.  It  may  be  the  syphilitic  factor  alone  would  have 
remained  indefinitely  in  the  latent  condition.  Nevertheless  its  aetiological 
part  is  considerable,  and  at  times  predominant. 

In  any  event  the  fact  remains  certain,  from  the  point  of  view  of  the 
prognosis,  that  of  all  the  forms  of  cerebral  syphilis  the  mental  one  is  the 
most  serious  and  the  most  difficult  to  cure. 


1404  TEXT-BOOK  OF  MEDICINE 

Hereditary  Cerebral  Syphilis. 

Early  or  late  hereditary  syphilis  causes  the  most  varied  pathological 
conditions  in  the  nervous  system.  "  Numerous  cerebral  conditions  in 
childhood  and  in  youth,  vaguely  put  down  to  meningitis  or  encephalitis,  are 
in  reality  nothing  but  the  more  or  less  late  manifestations  of  hereditary 
syphilis "  (Fournier).  These  manifestations  include :  intellectual  torpor 
bordering  on  hebetude ;  repeated  attacks  of  severe  headache,  labelled 
migraine  or  growing  pains ;  vertigo,  giddiness,  and  changes  of  character, 
wrongly  looked  upon  as  hysterical ;  finally  and  especially,  the  various  forms 
of  epilepsy,  masked  forms,  nocturnal  incontinence  of  urine,  nocturnal 
vomiting,  "petit  mal,  and  grand  mat.  We  cannot  too  often  think  of  early 
or  late  hereditary  syphilis  manifesting  itself  in  childhood  or  in  youth, 
because  it  is  the  cause  of  many  ills,  and  is  often  amenable  to  specific 
treatment. 

Summary. — To  facilitate  the  description,  I  have  divided  the  study  of 
cerebral  syphilis  into  three  parts.  In  some  clinical  cases,  which  are  fairly 
numerous,  this  somewhat  artificial  division  holds  good.  Some  patients,  for 
instance,  have  obliterating  arteritis;  others  have  only  paralysis  or  con- 
vulsions due  to  gummatous  lesions ;  while  others  finally  suffer  from  the  mental 
form,  with  intellectual  troubles,  and  more  or  less  complete  general  paralysis. 
In  other  circumstances,  however,  these  various  manifestations  of  cerebral 
syphilis  are  associated  or  succeed  one  another.  They  may,  indeed,  spread 
to  the  spinal  cord,  when  they  become  cerebro-spinal.  Of  these  various  forms, 
the  one  most  amenable  to  treatment  is  the  epUeptic  or  epilepto-paralytic 
form  ;  the  one  most  rebellious  to  treatment  is  the  mental  form.  In  a  case 
of  cerebral  syphUis  mercury  and  iodide  of  potassium  must  be  at  once  given 
in  large  doses.  I  prefer  injections  of  biniodide  of  mercury.  Every  efiort 
must  be  made  to  favour  the  tolerance  of  these  remedies.  Careful  attention 
to  the  mouth  will  avoid  or  retard  the  appearance  of  mercurial  gingivitis. 
By  the  intensive  treatment  we  often  succeed  in  limiting  the  disease.  And 
yet,  even  in  case  of  success  we  must  watch,  as  Fournier  says,  for  relapses. 
Kecrudescences  sometimes  supervene  even  when  recovery  seems  assured. 
Recurrences  are  too  often  met  with  when  the  cure  seems  definite.  In  spite 
of  these  disappointments,  we  must  not  be  discouraged,  and  as  long  as  the 
syphilitic  process  is  in  an  active  stage  we  must  make  every  effort  to  fight  it. 

X.  GENERAL  PARALYSIS— CHRONIC  MENINGO- 
ENCEPHALITIS. 

General  paralysis  was  for  a  long  time  regarded  as  a  simple  complication 
supervening  during  the  course  of  madness.  Such  was  the  opinion  of  Esquirol, 
Calmeil,  and  Parchappe,  and  this  explains  the  name  of  general  paralysis  of 


DISEASKS  OK  TIIK   I'.HAIN  UOr. 

the  insane  given  to  tliis  disease.  Bayle,  in  1820,  opj)osc(l  this  vicnv,  luit 
Haillai«,fer  {h'fmiti'h-  gave  to  general  ])aralysis  th»^  |)0:;i(i(»n  whicli  it  occiii)it.'.s 
to-day,  by  showint^  that  it  is  a  definite  morbid  entity,  in  which  the  rnot(»r 
disorders  play  at  least  as  large  a  part  as  the  psycliic  trouMis. 

Pathological  Anatomy.  -  The  lesions  of  giMioral  ])aralysis,  which  were  at 
first  thought  to  be  limited  to  the  meninges  and  the  brain,  in  most  cases  occupy 
the  whole  extent  of  the  nervous  centres.  On  opening  the  skull  the  meninges 
are  found  to  be  thickened,  especially  over  the  frontal  loijes  (chronic 
nieningitis).  The  dura  mater  is  adherent  to  the  cranium,  and  the  pia  mater 
to  the  brain.  The  brain  matter  exposed  by  the  removal  of  the  meninges  is 
rough,  bleeding,  and  ulcerated  (Calmeil).  The  convolutions  are  atrojihied, 
the  brain  is  diminished  in  size,  and  the  cavity  of  the  ventricles  is  enlarged. 
On  scraping  the  cortical  layer  with  the  handle  of  a  scal^icl,  indurated  lamella? 
or  ridges  of  the  white  matter  are  detached  (Baillarger).  The  surface  of  the 
fourth  ventricle  (Joire)  and  of  the  lateral  ventricles  is  studded  with  granula- 
tions (sclerotic  tissue),  and  these  various  changes  (ridges,  lamellae,  granula- 
tions) are  simply  the  result  of  a  diffuse  chronic  encephalitis  affecting  chiefly 
the  frontal  lobes. 

Under  the  microscope  we  see  that  the  nerve  cells  are  atrophied  and 
reduced  to  a  vitreous  mass,  in  which  neither  a  nucleus  nor  a  nucleolus  is  any 
longer  distinguishable ;  or  else  they  are  granular,  pigmented,  and  stain 
badly.  The  cellular  processes  are  broken,  and  the  nerve  fibres  only  exist 
in  small  numbers  ;  in  their  place  we  find  numerous  granular  bodies. 

The  walls  of  the  arteries  are  thickened,  and  the  proliferated  neuroglial 
elements  seem  in  certain  cases  to  smother  the  nerve  cells.  The  starting- 
point  of  the  lesions  is  the  subject  of  controversy.  The  theory  of  cerebral 
sclerosis  commencing  around  the  vessels  may  not  be  true  in  all  cases,  if  we 
accept  the  researches  of  Pierret,  Friedman,  Klippel,  and  Joffroy.  According 
to  them  the  theory  of  primary  parenchymatous  encephalitis  is  far  more 
probable. 

Interstitial  encephalitis,  ependymitis,  and  periencephalitis  are  represented 
by  analogous  lesions  in  the  spinal  cord,  where,  indeed,  we  find  diffuse  peri- 
ependymal and  peripheral  myelitis,  as  well  as  the  changes  of  chronic 
meningitis.  In  other  cases  we  do  not  find  diffuse  lesions  of  the  spinal  cord, 
but  combined  scleroses  (Ra\Tnond)  in  the  posterior  columns,  lesions  identical 
with  those  of  tabes.  The  relation  of  tabes  and  general  paralysis  is  discussed 
under  Locomotor  Ataxy. 

The  nerves  themselves  may  be  attacked  by  chronic  neuritis.  During  life 
the  symptoms  noticed  are  patches  of  anaesthesia,  muscular  atrophy  limited 
to  a  group  of  muscles,  or,  finally,  one  of  the  secondary  trophic  lesions 
common  to  peripheral  neuritis. 

The  other  viscera  present  various  lesions,  but  not  one  of  them  seems  to  be 


1406  TEXT-BOOK  OF  MEDICINE 

in  undisputed  relation  with  the  anatomical  changes  in  the  brain  and  in  the 
meninges.  « 

Symptoms. — In  order  to  facilitate  the  description  it  is  customary  to 
divide  general  paralysis  into  three  periods  of  indeterminate  duration  :  the 
first  period  is  called  prodromal ;  the  second  is  the  stationary  stage  ;  and  the 
third  is  the  terminal,  paralytic,  and  cachectic  period. 

At  the  commencement,  psychic  or  motor  troubles  predominate.  Amnesia 
is  one  of  the  most  frequent  symptoms.  "  Weakening  of  the  memory  is,  with 
deHrium,  one  of  the  most  characteristic  symptoms  of  general  paralysis" 
(Luys).  "  Memory  is  the  first  of  the  faculties,  sometimes  the  only  one,  which 
is  attacked  at  the  onset "  (Ball).  "The  patient  loses  the  faculty  of  self- 
control  "  (Dupre).  According  to  circumstances,  the  patient  becomes  melan- 
choly, or  else  irascible  and  violent — so  much  so  as  to  strike  without  reason  the 
people  who  are  about  him.  One  patient  wiH  be  seized  with  an  all-devouring 
activity.  He  walks  the  whole  day  long  without  stopping,  and  conceives  a 
thousand  projects,  which  are  most  often  unrealizable.  Another  patient  will 
indulge  in  reckless  extravagance,  and,  without  reason,  purchase  several 
dozen  watches  or  a  number  of  suits  of  clothes.  In  some  subjects  we  meet 
with  perversion  of  the  moral  faculties.  One  man  obstinately  refuses  to  pay 
for  an  article  which  he  has  just  bought,  or  steals  without  a  motive  ;  another 
man  gives  himseK  up  to  indecent  acts  in  public,  although  his  sexual  passions 
are  weakened.  These  facts  are  most  important  from  a  medico-legal  point 
of  view,  because  the  patient  has  sometimes  to  appear  in  court,  and  it  is  the 
physician's  duty  to  decide  whether  his  patient  is  or  is  not  responsible. 

In  many  cases  motor  troubles  open  the  scene.  How  often,  do  we  not 
meet  with  a  quavering  speech,  awkwardness  in  the  hand,  a  modification  in 
the  writing,  or  inequality  of  the  pupils,  in  people  who  so  far  show  no  trace 
of  intellectual  troubles,  and  in  whom  we  can  foretell  six  months  or  a  year  in 
advance  the  appearance  of  other  complications. 

Sometimes  the  commencement  of  the  disease  reveals  itself  by  apoplecti- 
form or  epileptiform  attacks,  loss  of  consciousness,  or  transitory  hemiplegia, 
and  the  psychic  troubles  break  out  after  one  or  more  congestive  attacks. 
The  attacks  are  sometimes  ushered  in  by  fits  of  ophthalmic  migraine. 

Disturbances  in  the  organs  of  the  senses  sometimes  precede  aU  the  other 
symptoms  ;  amblyopia  and  diplopia  have  been  noticed.  Voisin  has  insisted 
on  the  bluntmg  or  on  the  abolition  of  the  sense  of  smell,  which  often  precedes 
the  usual  symptoms. 

In  the  stationary  stage  the  disease  assumes  several  forms.  Its  most 
common  form  is  characterized  by  defirium  of  grandeur.  The  patient  lives 
in  a  condition  of  continual  satisfaction ;  he  believes  himself  to  be  an  Emperor, 
the  Pope,  or  God.  He  is  possessed  of  millions,  and  wishes  to  distribute  them 
to  those  who  are  around  him.     He  owns  palaces  built  out  of  precious  stones. 


DISEASES  OF  THE  BRAIN  1407 

Nothing  on  earth  equals  his  strength,  his  beauty,  or  his  power.  His  ideas, 
however,  are  not,  like  those  of  the  monomaniac,  ambitious,  connected,  and 
well  co-ordinated  ;  they  are,  on  the  contrary,  mobile  and  contradictory 
(Falret) ;  and  whilst  the  patient  suffering  from  general  paralysis  is  talking 
to  you  of  his  splendour,  ask  hira  his  calling,  and  he  will  artlessly  tell  you 
"  I  am  a  cobbler  "  (Magnan). 

In  certain  patients  hypochondriasis  dominates  the  scene.  He  believes 
himself  to  be  dead,  or  fancies  that  he  is  persecuted  ;  he  refuses  all  food  for 
fear  of  poison  ;  he  has  hallucinations  and  ideas  of  suicide. 

In  the  midst  of  these  symptoms  (exalted  and  hypochondriac  forms) 
some  patients  have  attacks  of  acute  mania — their  fury  necessitates  the 
application  of  the  strait-jacket.  The  attack  then  disappears,  and  the 
general  paralysis  continues  its  progressive  course  (Baillarger). 

Speech  troubles  often  show  themselves  from  the  first ;  in  some  cases  they 
are  the  only  symptom  of  the  onset.  The  change  in  speech  is  so  character- 
istic that  it  alone  would  suffice  to  establish  the  diagnosis.  When  a  patient 
suffering  from  paralysis  wishes  to  speak,  there  is  a  kind  of  tremor  in  the 
muscles  of  the  lips ;  the  speech  is  hesitating,  and  participates  in  the  tremor 
of  the  lips  and  tongue.  The  motor  troubles  depend  on  the  inco-ordination 
and  the  weakening  of  the  movements  ;  it  is  a  kind  of  ataxy  mixed  with 
paresis.  The  patients  are  less  clever  in  manual  work,  and  their  gait  becomes 
tottering.  In  certain  cases  the  want  of  co-ordination  predominates,  and  the 
disease  assumes  for  a  time  the  symptoms  of  locomotor  ataxy  (see  section  on 
Tabes). 

As  the  disease  progresses,  the  intellectual  and  paralytic  troubles  become 
more  pronounced,  and  are  sometimes  complicated  by  epileptiform  or 
apoplectiform  attacks,  with  a  rise  in  temperature  and  transitory  hemiplegia. 
Contractures  and  paralyses  may  also  be  observed  in  the  form  of  special 
attacks  (Magnan). 

The  sensory  nervous  system  is  but  little  affected  in  general  paralysis. 
Anaesthesia  is  more  common  than  liyperaesthesia.  Visceral  pains  analogous 
to  those  of  locomotor  ataxy  have  been  noticed  (Teissier). 

Inequality  of  the  pupils  (Baillarger)  is  a  frequent  symptom  often  observed 
in  the  first  period.  It  sometimes  disappears  during  the  remissions,  but 
reappears  afterwards.  The  pupU  reflexes  are  sometimes  sluggish  or 
abolished,  as  far  as  light  or  accommodation  are  concerned  ;  at  times  they 
correspond  to  AjgyU-Robertson's  sign.  At  the  commencement  of  the  disease 
the  paralysis  of  the  pupil  is  often  associated  with  paralysis  of  the  accommo- 
dator  muscle  (Parinaud,  BaUet).  Internal  ophthalmoplegia  is  the  result. 
The  optic  nerve  is  very  rarely  atrophied  ;  the  motor  nerves  of  the  eye  are 
rarely  affected. 

Hflematoma  auris  is  conmion  in  general  paralysis.     It  is  situated  between 


1408  TEXT-BOOK  OF  MEDICINE 

the  cartilage  and  the  perichondrium,  and  attributed  by  some  writers  to 
injury,  by  others  to  vascular  trouble. 

In  women  the  development  of  general  paralysis  most  frequently  results 
in  irregularity  or  suppression  of  menstruation,  which  function  may  return 
during  the  remissions  of  the  disease.  The  terminal  period  of  general 
paralysis  is  characterized  by  the  mental  decay  of  the  individual.  "  The 
patients,  who  are  constantly  soiled  by  urine  or  faeces,  defsecate  incessantly, 
and  plunge  their  hands  into  the  excrement,  with  which  they  cover  every- 
thing. They  are  practically  isolated  from  the  external  world,  merely  leading 
a  vegetative  existence  "  (Magnan).  Some  reach  the  end  of  their  existence, 
being  conscious  of  their  decay ;  their  intelligence  is  weakened,  but  they  are 
not  insane. 

Course — Duration. — General  paralysis  commences  with  motor  or  with 
psychic  troubles,  according  as  the  lesion  affects  the  motor  convolutions  or 
the  psychic  convolutions.  In  other  cases,  however,  the  lesion  announces 
itself  by  spinal  symptoms  (inco-ordination,  pains,  paresis,  and  trophic 
troubles),  which  precede  the  intellectual  troubles  by  several  years ;  in  other 
words,  the  lesions  of  the  nervous  system  in  general  paralysis  are  sometimes 
ascendmg,  sometimes  descending,  and  often  involve,  from  the  outset,  the 
major  portion  of  the  nerve  centres.  Sometimes  the  lesion  is  limited  for  a 
time  to  the  optic  nerves  (amaurosis)  and  to  the  motor  nerves  of  the  eye 
(ptosis,  strabismus,  diplopia). 

The  course  of  the  disease  is  slow  and  progressive.  It  is  interrupted  by 
exacerbations,  and  by  remissions  which  vary  from  a  few  months  to  two  and 
three  years.  These  remissions  may  appear  spontaneously,  or  may  be  due 
to  an  intercurrent  disease,  to  a  traumatism,  to  a  surgical  afiection,  or  to 
copious  suppuration.  In  its  rapid  form  the  disease  may  last  less  than  a  year. 
The  general  duration  varies  from  one  to  six  years  ;  there  are  exceptional 
cases  in  which  the  remissions  prolong  the  existence  indefinitely. 

iEtiology — Diagnosis. — General  paralysis  attacks  adults  from  thirty  to 
forty-five  years  of  age.  It  may,  however,  appear  at  the  age  of  fourteen 
years  in  the  form  of  juvenile  general  paralysis  (Charcot).  Males  are  usually 
attacked,  and  heredity  plays  a  considerable  part  in  its  development.  Alco- 
holism, excess  of  work,  prolonged  grief — in  a  word,  congested  conditions  of 
the  brain — favour  chronic  meningo-encephalitis.  The  existence  of  a  general 
pseudo-paralysis  due  to  alcohol,  lead,  etc.,  has  been  admitted ;  but  at  present 
these  cases  of  pseudo-paralysis  are  more  usually  placed  under  true  general 
paralysis.  According  to  the  setiological  factor,  and  according  to  the  soil  in 
which  the  disease  evolves,  certain  difEerences  in  the  symptomatology  and 
in  the  course  are  observed,  but  the  very  essence  of  the  disease  appears  to  be 
the  same.  The  nerve  elements  may  be  damaged  by  toxic  products  of  various 
origins,  but  their  mode  of  reaction  is  said  to  be  the  same,  no  matter  what 


DTSKASES  OK    TIIK   MK\I\  1400 

agorit  is  the  cause,  furthermore,  as  far  as  syphilis  is  concerned,  it  seems 
that  the  virus  of  svphilis  is  more  apt  in  certain  cases  to  jiroduce  (ujrehral 
lesions.  This  fact  would  explain  the  cases  reported  by  Morel-Lavallee,  in 
which  live  men  who  had  contracted  syphilis  from  the  same  source  ail  died 
frtun  syphilitic  general  paralysis. 

S}^)hilis  is  intimately  associated  with  the  history  of  general  paralysis. 
The  setiological  relations  of  these  two  diseases  have  been  discussed  recently 
at  the  Academic  de  Medecine.  According  to  Fournier,  these  two  affections 
stand  to  one  another  in  the  relation  of  cause  and  effect,  for  the  following 
reasons  :  (1)  Statistics  show  that  syphilis  is  very  common  in  general  para- 
lytics, the  proportion,  according  to  certain  writers,  being  90  per  cent. 
(2)  Many  s^^hilitic  persons  become  general  paralytics  without  any  other 
cause  to  be  found  save  syphilis.  (3)  General  paralysis  is  more  rare  in  women, 
except  in  districts  where  syphilis  is  raging.  (4)  General  paralysis  is  rare  in 
the  country,  where  s}'philis  is  equally  rare.  (5)  Syphilis  is  more  common  in 
general  paralytics  than  in  other  insane  persons.  (G)  Tabes,  which  is  undoubt- 
edly of  syphilitic  origin  in  many  cases,  is  often  associated  with  general 
paralysis.  (7)  In  general  paralysis,  as  in  tabes,  we  find  lymphocytosis  of  the 
cerebro-spinal  fluid  and  Argyll-Robertson's  pupil,  which  is,  according  to 
Babinski,  a  sign  of  syphilis. 

In  spite  of  these  arguments,  Joffroy  does  not  think  that  s}'philis  causes 
general  paralysis,  and  insists  on  the  fact  that  syphilis  is  common  among  the 
Moors,  while  general  paralysis  is  very  rare.  Lancereaux  and  CornQ  oppose 
Fournier's  opinion  by  pathological  arguments,  and  deny  that  the  lesions  of 
general  paralysis  run  the  same  course  as  s}'philitic  lesions  of  the  nerve  centres. 
Ra}Tnond  answers  this  argument  by  a  collection  of  cases  showing  the  frequent 
coexistence  of  both  varieties  of  lesion  in  the  same  individual. 

I  shall  attempt  a  brief  review  of  the  pathogenesis.  It  is  certain  that 
general  paralysis,  like  tabes,  appears,  practically  speaking,  only  in  persons 
who  have  had  syphilis.  Theory  is  not  of  much  moment.  The  view  I  hold  is 
that  people  are  not  exposed  to  the  risk  of  paralysis  or  of  tabes  unless  they  are 
syphilitic.  I  readily  admit  that  general  paralysis  runs  a  fatal  course,  a 
fact  not  in  agreement  with  the  usual  course  of  syphilitic  lesions.  I  also 
admit  that  specific  treatment  has  no  hold  upon  confirmed  tabes  or  general 
paralysis.  But,  in  spite  of  everything,  I  state  the  following  aphorism — a 
person  who  is  not  syphilitic  will  have  neither  general  paralysis  nor  tabes. 

Fournier,  in  his  communication  to  the  Academic,  has  stated  the  date 
at  which  general  paralysis  appears  ;  it  is  between  six  and  twelve  years 
after  the  primary  infection,  the  maximum  being  the  tenth  year.  Accord- 
ingly, he  advises  cures  de  renjorcement  with  mercurial  treatment,  beginning 
in  the  fifth  year  after  infection,  and  carried  out  for  several  years. 

Cases  of  ambitious  and  melancholic  monomania  are  distinguished  from 


1410  TEXT-BOOK  OF  MEDICINE 

general  paralysis  in  that  they  have  not,  like  it,  mobile  and  contradictory 
ideas.  General  paralysis  must  be  distinguished  from  senile  dementia, 
insular  sclerosis,  alcoholism,  and  cerebral  softening. 

As  in  the  case  of  tabes,  lymphocytosis  of  the  cerebro-spinal  fluid  is  the 
rule  in  patients  suffering  from  general  paralysis  (Widal,  Sicard,  and  Ravaut). 
Sometimes,  indeed,  at  the  moment  of  certain  exacerbations  lymphocytosis 
may  give  place  to  polynucleosis  (Widal  and  Lemierre). 

Treatment. — During  the  prodromal  period  the  patient  must  avoid 
fatigue,  work,  and  excitement  of  every  kind.  A  quiet  country  life,  walks  in 
the  open  air,  absolute  abstention  from  alcohol ;  milk  diet,  together  with 
ordinary  food ;  laxatives,  and  blisters  to  the  nape  of  the  neck,  such  are  the 
usual  methods.  Treatment  with  mercury  yields  no  results,  and  Ehrlich's 
salvarsan  is  contra-indicated.  The  periods  of  excitement  must  be  con- 
trolled by  the  use  of  the  douche,  valerian,  and  bromides. 

At  a  more  advanced  period  it  is  generally  necessary  to  place  the  patient 
in  an  asylum,  "  either  because  the  maniacal  excitement  reaches  an  excessive 
degree,  in  which  case  the  patient  becomes  dangerous  to  others,  or  because  the 
melancholia  is  accompanied  by  refusal  of  food  and  impulse  to  suicide  " 
(G.  BaUet  and  P.  Blocq). 


XI.  SYPHILITIC  NECROSIS  AND  PERFORATION  OF  THE 

VAULT  OF  THE  SKULL— DIAGNOSIS  FROM  TUBERCULOSIS 

AND  FROM  CANCER. 

The  following  section  is  based  upon  two  of  my  clinical  lectures  :  * 

Clinical  case  :  A  young  woman  was  admitted  for  a  perforation  in  the  right  parietal 
bone.  The  perforation  formed  an  oval  hole  as  large  as  a  sixpence.  The  edges  were  clean- 
cut,  and  the  external  orifice  was  bounded  by  the  scalp,  which  was  neither  ulcerated  nor 
adherent.  At  the  bottom  of  the  hole  the  dura  mater  was  exposed,  and  the  pulsations 
of  the  brain  were  evident.  The  perforation  was  covered  with  a  dressing  in  order  to 
prevent  infection. 

About  eighteen  months  before  she  had  felt  a  boss  on  the  bone.  The  tumour  caused 
neither  pain  nor  ill-health.  Six  months  later  it  was  as  large  as  a  hazel-nut,  and  the 
pain  was  so  acute  that  Delannoy  operated.  The  txunour  resembled  a  cyst.  During 
the  exploration  pmiilent  fluid  made  its  exit,  and  the  surgeon  found  osteitis  of  the 
subjacent  bone.  As  he  concluded  that  the  abscess  was  secondary  to  tubercular  osteitis, 
the  bone  was  scraped.  No  rehef  followed  the  operation  ;  the  wound  suppurated  freely., 
and  other  tumours  appeared. 

The  patient  suffered  fi'om  severe  headache,  insomnia,  and  wasting.  As  drugs 
gave  no  relief,  a  further  operation  was  ■  performed.  The  affected  bone  was  exposed,  a 
sequestrum  was  removed,  and  the  friable  edges  of  the  bone  were  trimmed  with  forceps. 
The  dura  mater,  studded  with  granulations,  was  scraped.    In  spite  of  tbe  operation  the 

♦  Dieulafoy,  Clinique  Medicale  de  VHotd-Dieu,  1906,  !■*  et  2""  le90ns. 


DltShiASES  OF  THE  BRAIN  1411 

wound  coutimuMl  In  Hii|i|mrato,  find  tlio  iKiiidHuht)  was  moat  Hnvoro,  fmjjeci.illy  at  nii»ht. 
Tho  juitiont  could  noitlinr  cat  nor  Hloop.     Vomiting  was  frotjuonl. 

Tho  fingers  of  tlio  loft  hand  now  bocarao  fixed  in  Iho  semi  flfxod  position  ;  a  con- 
traoturo  of  the  face  caused  deviation  of  tho  mouth,  incroanofl  at  tim^H  by  spasms.  Tho 
picture  was  ono  of  Jacksonian  epilepsy. 

With  this  knowledge  it  was  easy  to  reconcile  tho  symptom  and  (Ihi  lesion.  Stimula- 
tion of  the  motor  cortex  on  tho  right  side  had  caused  permanent  contracture  of  tho 
fingers  of  tho  left  hand  and  Jacksonian  epilepsy  of  tho  face.  This  syndrome,  including 
the  attacks  of  vomiting,  was  not  due  to  the  sequestrum,  because  it  had  been  removed 
months  before  ;  it  was  the  result  of  moningo-encephalitis  of  the  Rolandic  area. 

Her  condition  was  very  grave,  when  LetuUe  diagnosed  the  lesion  as  syphilitic,  and 
at  once  gave  injections  of  biniodide  of  mercury.  After  tho  fourth  injection  the  patient 
felt  better  than  she  had  done  for  a  long  time,  and  after  ten  or  twelve  injections  the 
symptoms  yielded.  The  injections  were  alternately  suspended  and  administered. 
Further  destruction  of  the  cranium  was  prevented,  and  the  loss  of  substance  began  to 
fill  up. 

Syphilitic  necrosis  of  the  cranium  is  by  no  means  rare.  Wallet,  in  1897, 
collected  forty-six  cases,  and  I  have  succeeded  in  finding  others,  making  a 
total  of  eighty  cases,  of  which  I  shall  make  use  in  the  present  discussion. 

Pathological  Anatomy. — Syphilis  attacks  the  bones  of  the  cranial  vault 
in  the  following  order  :  frontal,  parietal,  temporal,  and  occipital.  This  is 
true  for  the  initial  lesions,  but  untreated  cranial  syphilis  rarely  remains 
limited  to  a  single  bone.  From  the  cases  and  specimens  I  have  examined,  I 
find  that  a  large  part  of,  or  even  the  entire,  cranial  vault  may  be  invaded  by 
syphilis  in  the  absence  of  proper  treatment.  The  lesions  are  at  first  confined 
to  a  single  bone,  usually  the  frontal  or  the  parietal,  but  untreated  syphilis  of 
long  duration  may  affect  both  surfaces  of  the  vault  in  various  regions. 
When  the  cranial  vault  falls  a  victim,  syphilis  gains  a  firm  hold,  and  as  a  rule 
grants  no  truce  unless  effective  treatment  steps  in.  And  when  we  see  the 
destruction  wrought  by  syphilis  upon  the  cranial  vault,  we  ask  how  life 
could  have  been  compatible  with  such  lesions. 

On  examination  of  the  two  tables  of  the  skull  we  find  the  bone  eaten 
away  and  perforated  ;  in  some  parts  the  bone  is  destroyed,  in  others  exostoses 
are  present.  Some  skulls  resemble  old  plates  of  ivory  carved  in  relief,  others 
have  a  worm-eaten  appearance  ;  some  resemble  a  row  of  teeth,  in  others 
the  bone  is  hollowed  out  and  tunnelled ;  some  skulls  are  full  of  holes  like  a 
sieve,  while  others  resemble  a  macaroon-mill  (Foumier) ;  in  some  i^.pecimens 
we  find  sequestra  of  every  size  and  shape ;  some  skulls  have  perforations 
with  circular,  polycyclical  edges,  others  resemble  a  map  of  islands ;  lastly, 
skuUs  are  seen  with  astounding  losses  of  substance. 

The  Figures  65  to  70  show  some  of  these  skulls. 

We  are  now  clear  as  to  the  different  pathological  varieties  of  necrosis 
and  perforation  of  the  skull  due  to  syphilis.  How  are  these  lesions  produced  ? 
In  the  first  place,  the  cranial  bones  are  composed  of  a  compact  inner  and 
outer  table,  separated  by  spongy  tissue,  called  diploe.     Externally,  the 


1412  TEXT-BOOK  OF  MEDICINE 

convex  surface  is  covered  by  periosteum,  which  takes  part  in  the  formation 
and  natrition  of  the  bone  ;  internally,  the  concave  surface  is  lined  by  the 
dura  mater,  which  is  considered  to  be  an  internal  periosteum. 

The  gumma  originates  in  the  periosteum  close  to  the  outer  table,  or  in 
the  dura  mater  close  to  the  inner  table ;  it  rarely  originates  in  the  diploe. 
The  syphiloma  is  at  first  composed  of  an  accumulation  of  embryonic  cells, 
producing  a  nodular  tumour.  Tha  granulations  are  often  as  large  as  a  pin's 
head  ;  they  are  due  to  an  agglomeration  of  nodules. 


Fig.  65. — Syphilitic  Skull.     Dupuytren  Museum  (No.  593,  New). 

The  skull-cap  looks  like  old  ivory  sculptured  in  relief.  Some  parts  of  the  skull  are 
eaten  away,  while  others  stand  out  Mke  kidneys,  bridges,  tunnels,  arabesques, 
and  branches  of  coral. 

The  osseous  gumma,  says  Cornil,  appears  as  a  soft  reddish  vegetation, 
which  is  but  little  vascular,  semitransparent,  and  of  variable  size  ;  it  pene- 
trates the  table,  and  forms  a  cavity  at  the  expense  of  the  bone,  which  is 
absorbed  by  a  process  of  rarefying  osteitis.  A  centre  of  osteitis  develops 
in  contact  with  the  gumma ;  the  bone  appears  to  melt  away  under  the  attack 
of  the  specific  lesion. 

A  characteristic  figure  (Fig.  69),  reproduced  from  Ziegler's  work,  shows 
gummatous  osteitis  of  the  parietal  bone.     The  gumma  has  begun  in  the 


DISEASES  OF  THE  BRAIN  111;! 

deep  layer  of  the  periosteum  :  on  f  lie  otio  side  ii;  proji'cis  towards  the  exterior; 
on  the  other  siile  it  has  invaded  the  outer  table,  which  has  been  absorbed, 
and  it  is  beginning  to  eat  away  the  diploe. 

Two  foci  of  gummatous  osteitis  may  exist :  tho.  one  starts  from  the 
periosteum,  the  other  from  the  dura  mater  ;  the  two  foci  grow  to  meet  each 
other  in  the  form  of  a  cone,  and  perforation  of  the  bone  may  result. 

Tlie  syphiloma  in  its  course  nearly  always  provokes  exuberant  and  rarefy- 
ing osteitis.  While  one  portion  of  the  bone  disappears,  other  parts  of  the 
bone  become  thickened  and  condensed,  so  that  we  see  side  by  side  bone  in 
process  of  disappearing  and  hypertrophied  eburuated.  bone,     fn  a  section 


^>». 


^  ..4  ,jy 


Fig.  66. — Syphilitic  Skull.     Dupuytren  Museum  (No.  339,  A). 

The  whole  skull-cap  is  affected.  In  front  much  loss  of  substance ;  in  other  parts  small 
circular  perforations.  The  outer  table  is  destroyed  to  a  large  extent.  Eburnated 
projections  are  seen  at  certain  spots. 

"  we  are  struck  by  the  contrast  between  condensation  and  rarefaction ; 
numerous  small  holes,  as  large  as  a  pin's  head,  are  surrounded  by  a  zone  of 
condensing  osteitis  as  hard  as  ivory  "  (Poulet).  Whether  the  bony  lesion 
is  small  or  large  we  find  these  inverse  processes — rarefaction  of  the  bone  and 
ivory  exostoses. 

Syphilitic  osteitis  has  been  said  to  describe  a  kind  of  spiral.  "  The 
gummatous  bud,  arising  in  the  periosteum,  penetrates  the  bone  through  a 
narrow  aperture,  which  is  not  larger  than  a  pin's  head ;  it,  then,  describes  a 
helix  in  the  spongy  tissue  "  (Poulet). 

We  have  seen  how  the  bones  of  the  skull-cap  are  eaten  away  and  hyper- 
H.  90 


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trophied  by  gummatous  osteitis,  which  causes  both  condensation  and  rare- 
faction. We  have  now  to  see  how  the  osteitis  results  in  perforation  of  the 
bone.  It  does  so  by  the  various  processes  just  enumerated.  Foci  of 
osteitis  hollow  out  pits  in  the  bone,  and  lead  to  gradual  perforation  by 
molecular  necrosis.  In  other  cases  the  perforation  is  produced  through  the 
meeting  of  two  foci,  the  one  superficial  and  the  other  deep. 

I  think  that  the  perforation  usually  results  from  the  falling  out  of  small 
or  large  sequestra.    Foci  of  osteitis  gradually  isolate  a  portion  of  the  bone, 


Fig.  67. — Syphilitic  Skull.    Val-de-Grace  Museum. 

Very  extensive  loss  of  substance,  affecting  the  anterior  and  middle  portion  of  the  skull 
as  far  as  the  occipital  bones.  The  bones  are  everywhere  eaten  away  and  sur- 
mounted here  and  there  by  bosses  of  ebumated  bone. 


which  necroses ;  the  sequestrum  is  finally  detached  in  one  or  in  several 
pieces,  and  a  perforation  in  the  bone  results.  Accordingly,  the  sequestra 
and  the  perforations  show  great  variety  in  size  and  shape.  The  preceding 
plates  show  skulls  with  incredible  losses  of  substance. 

Laqueau  relates  the  case  of  a  man  who  had  necrosis  of  nearly  the  whole  of  the  skull. 
A  crucial  incision  was  made  from  the  frontal  eminence  to  the  upper  angle  of  the  occipital 


DTSKASRS  OF  THE  BRAIN  1413 

bonn,  nnil  lioiii  oiu*  parietal  «>iuin<'iico  to  the  other.  The  operator  removed  in  three 
weeks  hoth  parietal  lK)tU's,  the  greater  part  of  the  upper  angle  of  the  oceipitaJ  and  the 
upper  two-thinJs  of  the  frontal  hone.     The  patient  Burvived  for  some  months. 

I  should  like  to  mention  one  mode  of  perforation.  We  find  circinate  and 
polycvclioal  foci  of  gummatous  osteiti.s,  exactly  similar  in  shape  to  certain 
syphilides  of  the  sldn.  Wliile  I  was  examining  a  skull  from  Fournier's 
collection,  I  discovered  this  circinate  osteitis  in  the  act  of  causing  sequestra- 
tion and  perforation  of  the  bone.  In  order  to  appreciate  the  specimen,  it  is 
necessary  to  hold  up  the  skull  and  examine  its  inner  surface  wliilc  the  outer 


^mB 


t, 


Fig   68. — Syphiutic  Skull  :  From  Professor  Foxjrnier's  Collection. 

The  lesions  are  situated  on  the  concave  aspect  of  the  skull.     The  centres  of  osteitis 
have  a  circinate  and  polycycUcal  form,  which  we  shall  study  later. 

surface  is  in  a  good  light ;  the  rays  of  light  passing  -through  the  minute  pores 
of  ths  gummatous  foci,  which  have  perforated  or  are  in  process  of  perforation, 
show  the  details  of  the  necrotic  process. 

At  several  points  on  this  skull  I  have  found  annular  or  circinate  foci  of 
osteitis.  The  centre  of  the  focus  is  somewhat  opaque  ;  this  is  the  portion 
of  the  bone  which  is  destined  to  form  the  sequestrum,  and  around  the 
sequestrum  we  find  several  small  holes  in  the  form  of  a  ring,  and  not 
larger  than  the  point  of  a  needle,  which  allow  the  rays  of  light  to  pass  through 
them.     We  might  well  speak  of  it  as  an  opaque  stone  surrounded  by  a  circle 

90—2 


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of  small  diamonds  ;  the  central  sequestrum  is  kept  in  place  merely  by  some 
bony  filaments.  The  picture  is  even  more  clear  if  we  examine  the  circinate 
focus  with  a  lens,  the  skull  being  held  in  the  same  position  as  regards  the 
light. 

At  another  point  in  this  skuU  we  see  a  loss  of  substance  due  to  gummatous 
osteitis ;  the  polycyclical  edges  resemble  the  polycyclioal  edges  of  certain 


ii.tt'«-»'.>t  ^i."-^    V  5j;y^«mt, 


Fig.  69. — Gumma  of  the  Skull, 


a,  External  periosteum  ;  h,  outer  table ;  c,  diploe  ;  d,  inner  tabic  ;  e,  dura  mater  ;  /,  centre 
of  syphilitic  infection  ;  g,  carious  bony  trabeculse. 

cutaneous  syphilides.  In  the  centre  of  the  focus  we  see  a  toothed  sequestrum 
which  has  been  isolated  by  peripheral  osteitis,  and  which  is  connected  some- 
what like  a  peninsula  to  the  bank  of  bone  by  a  thin  pedicle.  At  other  parts 
of  the  skull  the  osteitis  has  taken  a  semilunar  form,  and  the  sequestrum  is 
in  part  isolated  in  the  loss  of  substance.     And,  lastly,  at  other  points  the 


Fig.    70. — Syphilitic  Osteitis  of  the  Skull. 

sequestrum  has  disappeared,  leaving  an  oval  or  irregular  perforation,  with 
toothed  edges. 

These  various  lesions  are  seen  in  the  above  photograph,  which,  how- 
ever, does  not  do  justice  to  the  delicate  points  of  the  specimen. 

In  the  foregoing  varieties  I  have  only  considered  the  cranial  syphiloma 
which  starts  in  the  bone  and  the  periosteum  ;  there  are,  however,  cases, 


DISEASES  OK    TIIK  liKAIN  I  117 

says  Maiiriac,  in  wliicU  llu*.  Ifsiim  comnienco.s  in  the  scalp.  "Cutaneous 
tubercles  and  subcutaneous  gummata  break  down,  iiliorate,  and  reach  the 
pcM-iosionm  ;  the  affection  tlicn  spreads  like  the  pei-forafing  or  scqjiginous 
process  seen  in  certain  syphilides." 

A  case  of  this  nature  has  boon  published  by  Hobbs  and  Broustot.  A  woman  was 
suffering  from  ulo(!ratod  •iummalu  of  tho  scalp,  the  jn-ocoss  running'  a  rapid  courso, 
somewhat  like  phagoda-na  ;  thoguniinata  sproad  from  tiio  skin  to  tho  bones,  from  tlio 
l)one3  to  tlio  meninges,  and  tho  patient  died.  Tiio  autopsy  showorl  that  tho  distiaso  had, 
in  a  short  space  of  time,  destroyed  the  outer  table  and  eaten  tiirough  tho  whole  thick- 
ness of  the  skull.  This  ease  proves  that  gummata  of  tho  scalp  and  of  tlu!  forehead  must 
bo  watched  for  and  treated,  because  they  may  be  the  starting-points  of  a  most  serious 
osteosypiiiloma. 

Cranial  sequestra  present  interesting  features  :  the  outer  table  disappears 
by  exfoliation,  and  the  inner  table  opposes  a  marked  resistance.  Some 
sequestra  are  surroimded  by  a  line  of  demarcation,  which  finally  frees  the 
necrosed  fragment  of  bone.  This  process  of  elimination  lasts  for  months  ; 
it  niay  last  indefinitely  if  the  sequestrum  is  set  in  a  wide  circle  of  hypertro- 
phied  bone ;  the  surgeon  is,  then,  obliged  to  remove  it  with  the  aid  of  the 
gouge  and  mallet.  The  sequestrum,  when  exposed  to  the  air,  becomes  of  a 
blackish-green  colour.  The  surface  of  the  syphilitic  sequestra  often  has  a 
worm-eaten  appearance,  while  the  tubercular  sequestra  are  rather  smooth 
and  polished. 

The  cranial  syphiloma  may  become  infected  and  suppurate.  Sometimes 
the  abscess  projects  under  the  scalp  ;  at  other  times  it  burrows  between  the 
skull  and  the  dura  mater,  forming  the  so-called  button-hole  abscess.  The 
sequestra  keep  up  abundant  foetid  suppuration. 

The  meninges  and  the  brain  may  participate  in  the  specific  process ; 
the  dura  mater  is  sometimes  the  seat  of  a  gummatous  infiltration.  Pachy- 
meningitis, with  granulations,  is  often  seen.  In  the  case  of  Hobbs  and 
Broustet  the  thickened  dura  mater  was  converted  into  fibrous  tissue,  com- 
posed of  large  parallel  fibres,  in  the  midst  of  which  nodular  gummata  were 
present.  Abscess  of  the  brain  and  lesions  between  the  cerebrum  and  the 
meninges  have  been  noted  in  several  cases. 

A  specimen  in  the  Saint-Louis  Museum  shows  the  surface  of  the  dura 
mater  exposed  by  the  falling  out  of  a  sequestrum,  and  covered  with  a 
circinate  eruption.  Mauriac  quotes  similar  cases.  It  is  indeed  remarkable 
that  cranial  syphilis  shows  this  circinate  form  in  the  skin,  the  bone,  and  the 
dura  mater. 

Qcatrization  of  the  bony  lesions  takes  place  in  the  following  manner  : 
If  the  external  table  only  has  been  destroyed,  a  simple  depression  is  left ; 
if,  however,  the  whole  thickness  of  the  skuU  has  been  destroyed,  the  scar 
mats  together  the  scalp,  the  bone,  and  the  dura  mater. 

Brief  mention  must  be  made  of  the  cranial  lesions  of  hereditary  syphilis. 


1418  TEXT-BOOK  OF  MEDICINE 

Some  are  the  result  of  deformities  which  commence  shortly  after  birth, 
and  give  rise  to  the  natiform  skull,  to  the  forehead  with  lateral  bosses,  to 
the  keel-like  forehead,  and  to  the  Olympian  brow  (Fournier).  Others 
supervene,  as  the  first  manifestation  of  syphilis,  at  a  more  or  less 
advanced  period  of  life,  and  comprise  rarefying  osteitis  and  overgrowth 
of  bone. 

1  shaU  now  give  a  short  summary  of  the  lesions  of  cranial  syphilis. 
Syphilis  of  the  cranial  vault,  unless  arrested  by  timely  treatment,  has  a 
tendency  to  perforate  the  skull.  The  lesions  may  predominate  either  on 
the  exterior  or  on  the  interior  of  the  skull.  Whether  these  lesions  are  small 
or  large,  we  nearly  always  find,  side  by  side,  a  double  process,  ending,  on 
the  one  hand,  in  absorption  and  destruction  of  the  bone,  and,  on  the  other 
hand,  in  overgrowth  and  eburnation  of  the  neighbouring  bony  tissue.  The 
cranial  syphiloma  starts  in  gummatous  granulations,  which  originate  in  the 
periosteum  near  the  outer  table,  or  in  the  dura  mater  near  the  inner  table. 
In  some  cases  the  syphiloma  commences  in  the  skin,  and  then  spreads  to 
the  bone.  The  perforations  are  produced  in  different  ways  :  sometimes  the 
gmnmatous  buds  perforate  the  bone  right  through'';  at  other  times  two 
gummata,  one  on  the  inner  table,  the  other  on  the  outer  table,  meet  one 
another,  and  establish  the  perforation.  In  many  cases,  whether  the  focus 
of  osteitis  is  or  is  not  circinate,  a  certain  number  of  gummata  isolate  a 
fragment  of  bone  ;  this  fragment  forms  one  or  several  sequestra,  and  more 
or  less  considerable  loss  of  substance  results.  The  meninges  and  the  brain 
may  participate  in  the  syphilitic  process. 

Symptoms. — ^For  the  sake  of  clearness  in  description  let  us  separate  the 
cases  in  which  the  gumma  arises  in  the  outer  table,  thus  forming  a  visible 
tumour,  from  the  cases  in  which  the  syphiloma  arises  in  the  inner  table, 
thus  escaping  observation.  In  the  first  stage  of  the  external  syphiloma 
pain  and  swelling  are  the  only  indications  of  the  lesion,  and  even  the  pain 
is  not  a  constant  symptom.  Absence  of  pain  is  not  enough  to  exclude 
the  diagnosis  of  gummatous  osteosyphiloma.  In  the  presence  of  an 
indurated  or  softened  cranial  tumour  we  should  be  wrong  to  exclude 
syphilis  on  the  ground  that  the  lesion,  if  syphilitic,  must  be  painful. 
And  yet  it  must  be  said  that  the  absence  of  pain  is  exceptional ;  the 
pericranial  syphiloma  causes  pain,  which  is  sometimes  excessive,  especi- 
ally at  night,  and  the  headache  commonly  extends  over  the  whole  of  the 
cranium. 

As  the  syphiloma  projects  externally,  it  forms  a  tumour,  which  is  not 
movable,  because  it  starts  from  the  bone.  The  tumour  is  hard  at 
first  and  somewhat  spread  out ;  later  it  softens  at  the  centre,  and  an 
abscess  may  result.  This  condition  lasts  for  months.  Nevertheless,  the 
osteosyphiloma,  even  though  it  is  fluctuating,  may,  under  proper  treat- 


DISEASES  OK  Till-:  BRAIN  1410 

raent,  end  nt'itln'r  in   iilcciatidii   iiur   in   al)sc<>ss.      I  inav  (|U()tp,  a  (^ast-  from 
Fournier : 

A  young  woman  who  sutTuroil  from  sovero  headaclie  bad  a  frontal  ostoo-syphiloma, 
which  was  fluctuating  in  tho  oontre.  In  spito  of  this  advancod  lesion  there  was  no 
ulceration,  and  recovery  followed  mixed  treatment. 

The  syphiloma  adheres  to  the  skin,  which  grows  thin ;  an  opening  then 
forms,  through  which  purulent  liquid  makes  its  exit.  An  oval  or  circular 
idceration,  with  clean-cut  edges,  sanious  floor,  and  purulent  secretion, 
results.  The  edges  are  sometimes  limited  by  indurated  bone.  The  bottom 
of  the  ulcer  is  filled  in  by  the  bone,  which  is  attacked  by  osteitis  or  necrosis. 
The  ulcerations  may  be  smaller  than  a  sixpence  or  larger  than  a  crown- 
piece.     It  is  not  uncommon  to  see  several  ulcerated  osteosyphilomata. 

Galtier-Boissi^re  has  reported  the  case  of  a  patient  who  had  on  the  left  side  of  the 
frontal  bone  an  ulcerated  osteosyphiloma  as  large  as  a  pigeon's  egg.  Two  years  later 
(tile  first  ulceration  being  still  unhealed)  an  osteosyphiloma,  wliich  ulcerated,  appeared 
on  the  right  side  of  the  forehead.  Intense  headache  was  present.  Later  another 
osteosyphiloma  appeared  in  the  middle  of  the  forehead.  Finally  two  other  growths 
appeared  above  the  right  and  left  orbits,  and  perforated  the  bone  so  that  the  pulsations 
of  the  brain  could  be  seen.     These  lesions  were  much  improved  by  mixed  treatment. 

In  this  destructive  process  the  necrosis  is  sometimes  limited  to  the 
outer  table  of  the  bone,  wliich  is  eliminated  by  exfoliation,  the  inner  table 
forming  a  rampart;  or  the  whole  thickness  of  the  bone  is  necrosed,  with 
the  formation  of  a  sequestrum,  which  may  be  movable,  or  may  be  set  in  a 
ring  of  hypertrophied  bone.  When  the  sequestrum  is  eliminated  spon- 
taneously, or  when  it  is  removed  by  the  surgeon,  the  thickened  dura  mater  is 
exposed,  and  the  brain  is  seen  pulsating  at  the  bottom  of  the  wound. 

I  have  just  said  that  the  pericranial  gumma  usually  begins  as  a  small 
painful  tumour.  We  must  not,  however,  confound  this  formidable  tertiary 
lesion  with  the  bem'gn  tumour  of  the  periosteum  seen  in  the  secondary  stage. 
Some  patients  suffer  early  in  the  secondary  stage  from  periostitis  of  the  skull, 
tibia,  clavicle,  etc.  The  cranium  is  one  of  the  seats  of  election  ;  this 
periostitis  is  circumscribed  and  very  painful ;  slight  pressure  may  cause  the 
patient  to  cry  out  from  pain.  The  patches  of  periostitis  at  times  project 
slightly ;  at  other  times  they  form  hard  nodes,  about  as  large  as  a  shilling. 
These  nodes  resolve  in  two  or  three  weeks  under  appropriate  treatment. 
They  differ,  therefore,  in  several  points  from  the  gummatous  osteosyphiloma. 

I  have  so  far  considered  the  pericranial  osteosyphiloma  which  reveals 
itself  by  pain  and  swelling.  When  the  tumour  is  endocranial,  swelling  is 
absent,  or,  if  it  does  occur,  it  is  after  a  long  period,  when  the  lesion  has  ex- 
tended through  the  bone  to  the  surface.  In  the  endocranial  syphiloma  we 
have  no  swelling  to  help  us,  and  we  must  rely  on  the  pain  alone. 

A  patient  complains  of  headache,  which  has  been  growing  worse  for  some 


1420  TEXT-BOOK  OF  MEDICINE 

weeks  ;  tlie  wliole  head  is  painful,  and  yet  the  pain  is  more  severe  at  certain 
points.  Methodical  percussion  of  the  head  reveals  the  most  painful  region, 
but  the  most  exact  examination  does  not  show  any  swelling.  An  important 
point  is  that  the  pain  is  worse  at  night,  and  prevents  sleep  in  spite  of  every 
remedy,  such  as  aspirin,  veronal,  antipyrin,  pyramidon,  or  morphia.  Inquiry- 
justifies  the  exclusion  of  Bright' s  disease  as  the  cause  of  the  headache.  In 
answer  to  questions  the  patient  admits  syphilis  ;  he  also  shows  some  stigmata. 
Examination  of  the  mouth  may  reveal  a  patch  of  leucoplasia  on  the  cheeks. 
The  increase  of  the  pain  at  night  and  the  failure  of  non-specific  drugs 
complete  the  diagnosis,  and  show  that  the  patient  is  suffering  from  a  syphilitic 
lesion  of  the  cranium.  As,  however,  no  sign  of  meningeal  or  ceiebral 
mischief  has  so  far  appeared,  it  is  probable  that  the  lesion  is  still  limited  to 
the  bone.  In  any  case  an  injection  of  biniodide  of  mercury  is  given  daily.  . 
After  six  or  seven  injections  improvement  sets  in,  the  headache  disappears, 
sleep  returns,  and  the  success  of  the  treatment  proves  the  correctness  of 
the  diagnosis.  I  am  quite  convinced  that  many  syphilitic  headaches  are 
the  result  of  an  endocranial  osteosyphiloma,  of  which  the  only  symptom  for 
the  time  being  is  pain,  cerebral  symptoms  and  pericram"al  tumour  being 
absent.  We  must  be  on  the  watch  for  this  endocranial  syphiloma,  because 
mercurial  treatment  is  necessary  before  the  patient  is  exposed  to  grave 
dangers. 

We  must  not,  however,  ascribe  to  osteosyphiloma  every  pain  in  the  head 
which  a  syphilitic  patient  may  have  sooner  or  later  after  infection.  I  do 
not  refer  to  painful  periostitis  in  the  secondary  stage.  I  merely  mention  the 
early  headache  which  accompanies  the  secondary  fever  and  syphilides. 
I  wish,  however,  to  insist  on  certain  intracranial  lesions  of  which  headache 
is  so  often  the  forerunner. 

Syphilitic  arteritis  of  the  cerebral  vessels,  occurring  at  an  early  or  remote 
date  after  the  primary  infection,  is  often  ushered  in  by  acute  headache. 
In  some  cases  patients  have  suffered  from  severe  headache  without  other 
signs,  and  have  died  suddenly  from  rupture  of  a  syphilitic  aneurysm  of  the 
circle  of  WiUis.  In  other  cases  patients  have  suffered  from  severe  headache 
without  other  signs,  and  have  been  stricken  with  hemiplegia  due  to  obliterat- 
ing arteritis  of  the  Sylvian  artery.  Intracranial  arteritis  is,  then,  the 
cause  of  intense  headache,  which  may  be  the  herald  of  an  approaching 
catastrophe.  In  gummatous  lesions  of  the  meninges  and  of  the  brain  head- 
ache may  be  the  chief  feature  ;  its  importance  is  very  great.  In  short,  head- 
ache, especially  when  it  is  paroxysmal  and  more  severe  at  night,  is  a  sign 
which  must  always  disturb  the  patient  and  his  physician.  It  is  often 
accompanied  by  important  signs,  such  as  vertigo,  vomiting,  tingling  in  the 
fingers,  paralysis,  contractures,  etc.  ;  but  in  some  cases  the  headache  remains 
for  a  time  the  chief  feature,  and  overshadows  the  other  signs.     Gummatous 


DISEASES  OF  TilK   I'.KAIN  14l'1 

osteitis  of  the  deep  surface  of  the  akiUl-cap  may  cause  transient  or  intense 
headache.  I  admit  that  it  is  often  difHcult  to  say  whetlier  the  headache  is 
due  to  a  bony  lesion,  to  arteritis,  or  to  meningitis,  but  the  therapeutic  indica- 
tion in  each  case  is  to  give  promptly  injections  of  mercury. 

Our  description  has  so  far  been  confined  to  osteosyphiloma  which  does  not 
encroach  upon  the  nuuiin^cs  or  the  cerebral  convolutions.  The  meninges 
and  the  brain,  however,  may  be  alTected  by  the  osteosyphiloma  ;  sometimes 
these  organs  are  compressed  by  an  exostosis,  a  sequestrum,  or  an  abscess ; 
at  other  times  they  are  the  scat  of  pachymeningitis  or  ence])halitis.  Tn  ord(^r 
to  simplify  the  description,  let  us  take  the  cases  in  which  tlie  lesion  is  limited 
to  one  lobe  of  the  brain. 

Let  us  begin  with  the  frontal  lobe,  whi(;h  is  most  frequently  affected. 
We  should  naturally  expect  lesions  of  the  frontal  lobe  to  excite  troubles 
having  a  definite  relation  to  the  functions  of  tjiis  lobe,  such  as  weakening  of 
the  memory,  loss  of  mental  power,  etc.  Observation  shows  that  such  is  not 
always  the  case. 

For  example,  Fournier  has  published  a  case  of  osteosyphiloma  with 
encephalitis  of  the  right  frontal  lobe. 

A  woman  who  had  had  syphiUs  many  years  before  suffered  from  headache  and 
swelUng  of  the  frontal  bone.  The  tumour  became  painful ;  its  diameter  measured 
3^  inches.  The  intellect  was  but  Uttle  affected  ;  memory  and  speech  were  intact. 
Mercury  and  iodides  produced  marked  improvement,  and  recovery  seemed  probable, 
when  the  patient  died  of  haemorrhagic  smallpox.  At  the  autopsy  the  antero-lateral 
fossa  of  the  frontal  bone  was  found  to  be  riddled  with  hollows  ;  the  surface  of  the  bone 
was  worm-eaten  ;  the  dura  mater  was  much  thickened,  and  showed  two  patches  of 
gummatous  infiltration  ;  the  brain  was  adherent  to  the  meninges. 

In  some  cases  with  lesions  in  the  frontal  lobes  intellectual  troubles  are 
absent,  and  motor  disturbances  predominate. 
The  following  case  is  quoted  by  Wallet : 

A  man,  six  years  after  the  chancre,  was  seized  with  violent  frontal  headache,  which 
became  worse  at  night.  For  a  year  the  headache  was  the  only  symptom.  At  intervals 
of  some  weeks  the  patient  had  three  attacks  of  epilepsy,  followed  by  incomplete  paralysis 
on  the  left  side.  Later  a  large  frontal  tumour  appeared ;  it  opened  and  gave  exit  to  a 
quantity  of  pus.  Mauclaire  removed  some  sequestra.  The  aperture  in  the  bone 
was  as  large  as  a  crown  piece,  and  the  brain  could  be  seen  pulsating  at  the  bottom  of 
the  wound.  Inimction  of  mercury  and  iodide  of  potassium  were  ordered.  The  troubles 
ceased,  and  the  aperture  began  to  fill  up.  In  this  case  the  frontal  lobe  was  attacked 
by  a  syphilitic  lesion,  but  yet  intellectual  disturbance  was  absent.  It  Avas  simply  a 
question  of  epilepsy  and  paralysis. 

Verchefe's  case  also  deserves  mention : 

A  woman  who  had  had  gummatous  osteitis  in  different  regions  of  the  body  suffered 
fiDui  an  osteosypliiloma  to  the  right  of  the  median  fine  of  the  frontal  bone.  A  seques- 
trum formed  and  was  removed  by  the  patient.  Later  another  osteosyphiloma 
appeared  in  the  frontal  region.  When  Verchere  saw  the  patient,  he  found  two  deep 
holes,  the  edges  of  which  were  clean  cut  and  blended  with  the  thickened  bones.      One 


1422  TEXT-BOOK  OF  MEDICINE 

aperture  was  situated  near  the  eyebrow ;  the  other  was  close  to  the  roots  of  the  hair. 
The  end  of  a  black  sequestrum  could  be  seen  between  the  dura  mater  and  the  thickened 
frontal  bone.  It  was  bathed  in  foul-smeUing  pus.  One  night  the  patient  was  seized 
with  hemiplegia.  She  could  not  raise  her  heel  from  the  bed ;  the  arm  hung  helpless. 
Verchere  performed  craniectomy,  and  removed  a  sequestrum  as  large  as  a  crown -piece. 
Next  day  the  headache  and  the  paralysis  had  disappeared,  and  recovery  set  ia. 

In  this  case  the  frontal  lobe  was  affected,  and  yet  no  intellectual  troubles 
were  seen ;  motor  disorders  were  alone  present.  Therefore,  hemiplegia  and 
epilepsy,  including  Jacksonian  epilepsy,  may  be  caused  by  lesions  of  the 
frontal  lobes.  I  have  given  further  proofs  of  this  point  in  a  paper  read  at 
the  Academic  de  Medecine  (October  22,  1901); 

Let  us  now  consider  the  symptoms  present  when  the  parietal  lobe  is 
involved.  Invasion  of  the  Rolandic  area  determines  contractures,  paralysis, 
and  Jacksonian  epilepsy  on  the  side  opposite  to  the  lesion.  In  the  case 
quoted  at  the  beginning  of  this  section  contractures  affected  the  left  hand, 
and  partial  epilepsy  attacked  the  face. 

A  patient  of  Troisier  had  had  on  the  scalp  early  nodes,  cured  by  treatment  with 
mercury.  Later,  attacks  of  Jacksonian  epilepsy  uivolved  the  right  arm  and  the  right 
side  of  the  face.  There  was  severe  headache  on  the  left  side  of  the  cranium.  One  day 
the  patient  had  a  right  hemiplegia,  without  loss  of  consciousness.  The  hemiplegia 
only  lasted  twenty  minutes,  and  was  accompanied  by  some  disturbance  of  speech.  The 
headache  was  contiauous,  and  worse  at  night.  The  attacks  of  hemiplegia  returned 
several  days  in  succession.  Mercurial  treatment  was  given,  and  the  cerebral  troubles 
finally  disappeared.  Troisier  expressed  the  opinion  (which  I  endorse)  that  these  cerebral 
troubles  were  due  to  intracranial  syphihtic  exostoses,  compressiag  the  parietal  lobe. 

Lancereaux  has  published  the  following  case : 

A  woman  had  on  the  right  frontal  bone  an  osteosyphiloma,  which  ulcerated  and 
exposed  a  sequestrum.  Convulsions,  followed  by  left  hemiplegia,  appeared  a  Kttle  later. 
The  frontal  bone  presented  three  large  apertures,  from  which  thick  foetid  pus  escaped. 
The  convulsions  recurred  and  the  patient  died.  The  autopsy  revealed  a  sequestrum 
3  inches  by  4  inches.  The  underlying  dura  mater  was  ulcerated.  The  ascending  frontal 
and  parietal  convolutions  were  destroyed  by  gangrene. 

In  short,  contractures,  hemiplegia,  and  Jacksonian  epilepsy  are  the  usual 
symptoms  when  lesions  of  the  Rolandic  area  are  associated  with  osteo- 
syphiloma of  the  parietal  bone. 

Many  cases  do  not  conform  to  a  set  description  ;  these  cases  concern 
osteosyphilomata  starting  from  the  outer  or  inner  table,  spreading  in  various 
directions,  and  causing  necrosis  of  the  cranial  vault  without  perforating  it. 
Headache,  vertigo,  dizziness,  mental  weakness,  disorders  of  speech,  amnesia, 
vomiting,  contractures,  paralysis,  and  epileptiform  convulsions  occur  in 
succession  or  in  combination,  inducing  cachexia. 

Evolution. — The  gummatous  osteosyphiloma  of  the  cranium  is  a  tertiary 
lesion.  In  a  general  way  the  term  "  tertiary  "  awakens  the  idea  of  syphilitic 
lesions  appearing  many  years  after  infection.     In  the  majority  of  cases  the 


DISEASES  OF  THE  BRAIN  1423 

tertiary^  troubles  appear  live,  ten,  twenty,  or  even  thirty  years  after  the 
chancre.  This  rule  is,  however,  far  fnnii  being  absolute,  and  it  is  liable  to 
numerous  exc(']»tions.  Many  so-caHtMl  tertiary  lesions  a])pear  within  a  year 
of  infection ;  so-called  nuili^nant  syi)iiilis  may  pn!maturely  engender 
gumraata  and  phagedajnic  lesions.  A  case  in  point  is  the  cerebral  arteritis 
which  in  the  first  year  may  end  in  an  aneurysm,  or  in  obliteration  of  an 
artery,  with  all  its  consequences. 

Syphilitic  necrosis,  as  considered  in  this  section,  is  also  essentially  a 
tertiary  manifestation ;  it  may,  however,  occur  early  in  the  first  or  second 
year  after  the  infection.  The  following  case,  related  to  me  by  Critzman  and 
Nattan-Larrier,  is  a  proof : 

A  man,  forty-fivo  years  of  age,  suffered  in  January,  1901,  from  a  chancre  of  the 
tongue,  followed  by  typical  roseola.  In  February  syphilitic  iritis  made  its  appearance. 
In  April  papular  syphilides  appeared  on  the  scrotum,  and  were  soon  followed  by  epididy- 
mitis. Injections  of  benzoate  of  mercury  relieved  these  troubles.  In  May  the  face 
and  the  neck  were  invaded  by  an  eruption  of  papulo-squamous  syphilides.  In  spite  of 
continuous  treatment,  the  patient  noticed  in  April,  1902,  a  swelling  in  the  right  parietal 
region.  The  tumour  broke  down  and  gave  exit  to  a  putty-like  substance  while  the 
patient  was  in  Portugal,  where  he  took  no  medicine.  On  his  return  to  Paris  a  deep 
suppurating  ulcer  was  present.  In  spite  of  treatment  with  grey  oil,  the  necrosis  went 
on,  and  several  small  sequestra  were  removed.  In  January,  1903,  the  irmer  table 
necrosed,  and  a  large  sequestrum  formed.  The  patient  begged  for  operation.  Legueu, 
on  February  26,  removed  a  sequestrum  as  large  as  a  florin.  Daily  injections  of  biniodide 
of  mercury  arrested  the  necrosis,  and  a  scar  formed  over  the  dura  mater.  In  this  case 
perforation  of  the  skull  took  place  within  fourteen  months  from  the  appearance  of  the 
chancre. 

In  a  case  of  Vedrennes'  the  osteosyphiloma  appeared  six  weeks  after  the  chancre. 
An  abscess  symptomatic  of  necrosis  of  the  frontal  bone  appeared  on  the  forehead.  The 
headache  was  intense,  ulceration  set  in,  and  seven  months  later  sequestra  from  the 
outer  table  were  removed.  The  following  year  aphasia  came  on,  with  paralysis  on  the 
right  side,  deUrium,  and  convulsions.  The  patient  was  unconscious,  the  respiration 
was  jerky,  the  pulse-rate  140,  the  Mmbs  flaccid,  and  the  only  hope  lay  in  trephining. 
A  disc  of  bone  was  removed  over  the  necrosed  area.  The  patient  came  to  and  answered 
questions.  Several  sequestra  were  removed.  The  patient  recovered,  and  his  intelli- 
gence appeared  to  be  intact,  since  he  could  play  chess  ;  but  the  aphasia  and  the  paralysis 
persisted. 

Diagnosis. — Two  cases  may  present  themselves.  In  the  first  case  the 
osteosyphiloma  may  be  on  the  irmer  table,  and  escape  observation  because 
no  tumour  is  present.  In  tliis  event  progressive  headache,  paroxysms  of 
pain  at  night,  and  a  definite  area  of  pain  on  percussion  are  important 
signs  in  a  case  of  syphilis  ;  they  lead  to  a  suspicion  of  the  existence 
of  deep  osteosyphiloma,  and  furnish  good  reason  for  prompt  injection  of 
mercury. 

Let  us  now  pass  on  to  the  differential  diagnosis  of  osteosyphiloma 
forming  a  tumour  on  the  surface  of  the  cranium.  Sebaceous  cysts  and 
lipomata  present  but  little  resemblance  to  osteosyphiloma.     The  distinc- 


1424 


TEXT-BOOK  OF  MEDICINE 


tion  between  osteosvpliiloma  and  osteotuberculoma,  however,  demands 
attention. 

Tlie  osteotuberculoma  is  ushered  in  by  more  or  less  acute  pain  ;  fever  is 
absent ;  the  headache  is  sometimes  very  severe,  and  may  be  worse  at  night. 
After  some  weeks  a  swelling  appears  and  rapidly  grows  to  the  size  of  a 
hazel-nut,  of  a  walnut,  or  of  an  egg.  The  tumour  breaks  down  in  the  centre, 
and  an  abscess  forms.  The  pus  contains  clots,  and  is  sometimes  foetid. 
Fungoid  growths  are  common.  Exploration  with  the  probe  reveals  bare 
bone.  A  sequestrum  is  separated  by  the  line  of  demarcation  which  occurs 
between  the  dead  and  the  li\nng  tissue.  The  removal  of  the  sequestrum 
exposes  the  dura  mater,  thickened  and  covered  by  tubercular  granulations. 
The  tubercular  sequestrum  is  smooth,  and  usually  comprises  the  whole 
thickness  of  the  bone. 

The  tubercular  skull  differs  anatomically  from  the  syphilitic  skull,  as  we 
can  readilv  see  from  the  figures  shown  in  this  section.     The  syphihtic  skull  is 


Figs.    71  and  72. — Tubeectjlae  Skulls.     Val-de-Grace  Museum. 

These  tTvo  crania  show  tubercular  perforations  with  much  loss  of  substance.  Around 
the  perforations,  and  also  over  the  whole  skull-cap,  the  bone  is  as  smooth  as  in 
a  normal  skull.     No  roughness,  no  projections,  and  no  eburnated  bosses  are  seen. 

more  or  less  rugged ;  the  tubercular  skull  is  smooth  and  uniform.  In  the 
tubercular  skull  the  loss  of  substance  is  often  more  marked  on  the  inner  than 
on  the  outer  table,  and  the  edge  is  bevelled.  The  bone  around  the  tubercular 
perforation  is  smooth ;  we  do  not  see  rarefying  osteitis,  eburnated  bosses,  and 
osteophytes,  as  in  the  s}^hilitic  skuU. 

The  foregoing  considerations  give  the  anatomical  diagnosis  when  we  have 
the  specimen.  How  are  we  to  decide  clinically  whether  an  ulcerated  tumour 
of  the  skuU  is  syphilitic  or  tubercular  ? 

Headache,  growing  worse  at  night,  is  present  in  both  cases.  Pulmonary 
tuberculosis  is  in  favour  of  osteotuberculoma,  but  mischief  in  the  lungs  is 
absent  in  most  cases.    OsteosyphHoma  is  probable  if  the  patient  has  recently 


DISEASES  OF  THE  BRAIN  1425 

sliowii  other  maiiifrstatious  of  syphilis.  Pus  coritiiiniii^'  clots  and  fungous 
growths  are  in  favour  of  a  tubercular  lesion.  In  doubtful  cases,  however, 
we  must  cxaniino  for  Koch's  bacillus,  and  make  inoculatioas  in  the  guinea- 
pig.  On  the  other  hand,  injections  of  biniodide  of  mercury  will  speedily 
clear  up  the  diagnosis,  because  a  syphilitic  lesion  is  almost  certain  to  show 
prompt  improvement. 

Cranial  osteosyphiloma  should  not  be  mistaken  for  osteomyelitis  of  the 
bones  of  the  skull-cap.  The  latter  occurs  in  yoimg  persons.  The  temperature 
is  high,  103°  to  104°  F. ;  the  course  of  the  disease  is  very  rapid  ;  in  a  few  days 
the  skin  becomes  red  and  ulcerates,  the  wound  suppurates,  and  the  bone 
necroses.  This  acute  process,  which  may  speedily  induce  delirium  and 
coma,  differs  absolutely  from  the  evolution  of  the  osteosyphiloma. 

Hydatid  cyst  of  the  cranial  bones  somewhat  resembles  cranial  osteo- 
syphiloma.    Keate  reports  the  following  case  : 

A  girl,  eighteen  years  of  age,  had  a  tumour  as  large  as  a  small  orange  on  the  fore- 
head. The  operation  showed  that  it  was  due  to  a  hydatid  ;  the  cavity  in  the  bone  was 
roughened.     The  patient  recovered. 

Cases  of  this  kind  are  common  in  foreign  countries,  especially  in  the 
Argentine  Republic.  The  hydatid  develops  in  the  frontal  sinuses,  between 
the  dura  mater  and  the  temporal  or  parietal  bone,  or  at  other  parts  of  the 
skull.  The  cyst,  as  it  grows,  affects  both  the  bones  and  the  brain.  The 
bone  in  contact  with  the  cyst  is  rough,  and  reduced  through  the  loss  of  the 
inner  table  to  a  thin  parchment-like  layer.  Vegas  and  Cranwell  have  found 
small  perforations..  Bony  projections  have  also  been  met  with.  In 
Antonin's  case  the  right  parietal  bone  presented,  at  the  insertion  of  the 
tumour,  a  firm  crust  of  a  circular  shape  ;  on  the  inner  surface  of  the  crust 
there  were  small  stalactites  of  bone,  the  bone  between  them  being  composed 
solely  of  the  outer  table.  The  right  cerebral  hemisphere  was  compressed, 
and  showed  a  depression  at  the  fissure  of  Rolando  ;  the  convolutions  were 
flattened,  but  softening  was  absent. 

"WTiat  are  the  symptoms  of  hydatid  cysts  of  the  skull,  and  how  can  we 
distinguish  them  from  osteosyphiloma  ?  After  a  latent  period  the  disease 
Is  ushered  in  by  certain  indefinite  symptoms,  such  as  headache,  loss  of 
appetite,  and  wastmg  ;  deformity  of  the  skull  and  cerebral  symptoms  then 
appear.  A  swelling  in  the  frontal,  parietal,  or  other  region  indicates  the 
appearance  of  a  cranial  lesion,  but  gives  no  information  as  to  the  nature  of 
the  tumour.  C'ontractures,  paralysis,  and  epileptiform  convulsions  prove 
that  the  brain  is  involved,  but  they  do  not  indicate  the  nature  of  the  lesion. 
Owing  to  this  incomplete  information,  the  diagnosis  of  hydatid  cyst  is  very 
difficult,  because  the  same  s}'inptoms  may  exist  in  the  case  of  osteosyphiloma, 
I  know  only  of  two  ways  of  making  a  diagnosis  :  the  first  is  the  use  of  injec- 
tions of  biniodide  of  mercury,  which,  in  the  case  of  syphilis,  will  bring  about 


1426  TEXT-BOOK  OF  MEDICINE 

rapid  improvement,  showing  the  nature  of  the  mischief ;  the  second  is 
surgical  intervention. 

There  is  another  disease  which,  like  osteosyphiloma,  may  show  itself  by 
tumour  and  perforation  of  the  skull.  I  mean  fungus  of  the  dura  mater. 
The  growth  arises  in  the  dura  mater ;  the  bone  over  the  tumour  is  slowly 
absorbed,  and  finally  perforated. 

A\Tien  perforation  has  occurred,  the  growth  raises  the  skin  in  the  form 
of  a  rounded  or  nodular  tumour,  which  is  hard  at  first,  but  which  softens 
later.  The  skin  then  perforates,  and  the  tumour  expands  outwards  like  a 
mushroom.  In  this  stage  the  diagnosis  is  easy,  but  at  a  less  advanced  stage, 
when  the  tumour  is  covered  by  the  skin,  the  diagnosis  is  very  difficult,  and 
we  are  the  more  likely  to  think  of  osteosyphiloma,  because  headache,  vertigo, 
vomiting,  etc.,  occur  in  both  cases.  In  case  of  doubt  mercurial  treatment 
win  decide  the  point. 

Treatment. — The  treatment  of  cranial  osteosyphiloma  is  essentially 
medical,  although  surgical  intervention  is  at  times  necessary.  As  a  general 
rule,  whether  the  growth  is  large  or  small,  and  is  or  is  not  accompanied  by 
meningeal  and  cerebral  complications,  mercurial  treatment  is  imperative. 

Of  the  mercurial  preparations,  I  prefer  an  aqueous  solution  of  the 
biniodide.  While  the  injection  need  not  be  mtramuscular,  it  should  be  deep ; 
a  fold  of  the  skin  in  the  lumbar  or  gluteal  regions  is  pinched  up,  and  the 
needle  is  inserted  deeply  at  right  angles  to  the  surface.  The  susceptibility  of 
the  patient  is  tested  for  a  day  or  two  by  an  injection  of  ^g-  grain,  and  an 
injection  of  ^  grain  is  given  daily  for  twelve  days.  The  injections  are  then 
stopped  for  a  week,  when  a  fresh  series  is  given.  The  interval  between  the 
injections  should  be  gradually  increased.  If  the  whole  thickness  of  the  bone 
is  not  destroyed,  or  if  the  lesion  consists  only  of  gummatous  ulceration,  with 
superficial  osteitis,  the  pus  dries  up,  the  ulceration  fiUs  up,  and  recovery 
follows.  If,  however,  the  bony  lesion  is  deep,  if  a  fragment  of  bone  has 
necrosed,  if  a  sequestrum  is  in  process  of  formation,  or  if  the  suppuration  is 
extending  between  the  cranium  and  the  dura  mater,  surgical  intervention 
is  essential. 

Some  people  wiU  say  that,  before  resorting  to  an  operation,  we  may  wait 
and  attempt  a  cure  by  medical  measures.  I  do  not  hold  this  view ;  in  my 
opinion,  medical  and  surgical  treatment  should  be  associated  in  certain  cases. 
We  know  that  the  sequestrum  may  be  fixed  by  osteophytes  and  bridges  of 
bone,  so  resistant  that  the  surgeon  is  obhged  to  use  a  chisel  and  maUet  to 
free  it.  Under  these  conditions  the  sequestrum  may  remain  in  situ  for  an 
indefinite  period  in  spite  of  medical  measures  ;  valuable  time  is  lost  by  post- 
poning surgical  intervention. 

In  every  case  of  ulcerated  osteosyphiloma  the  physician  should,  I  think, 
appeal  to  the  surgeon  in  order  to  verify  the  exact  condition  of  the  subjacent 


DISEASES  OF  THE  BRAIN  1427 

bone,  aiui  to  ascerlaiii  the  possible  presence  of  a  sequestrum.  The 
sequestrum  induces  suppuration,  prevents  healing,  and  favours  the  onset  of 
intracranial  complications  ;  it  must  be  promptly  removed,  so  that  mercurial 
treatment  may  be  tflicacious. 

In  some  cases  the  dura  mater  is  thickened  and  covered  with  granulations, 
for  which  curetting  has  often  been  performed.  Although  this  operation  is 
practically  painless,  it  is  unnecessary,  because  the  pachymeningitis  will 
improve  under  mercurial  treatment. 

Medical  and  surgical  treatment  together  yield  remarkable  results  even 
in  very  grave  cases.  To  the  cases  already  quoted  in  this  section  I  would 
add  the  following  : 

In  a  woman  who  had  had  syphihs  a  tumour  appeared  on  the  right  side  of  the  fore- 
head. Some  months  later  the  tumour  ulcerated,  and  a  year  later  the  patient  was 
admitted  under  Bcsnier.  A  large  ulcer,  2  inches  in  diameter,  was  present  on  the  fore- 
heeid.  The  centre  was  occupied  by  a  blackish  sequestrum  ;  the  pus  was  abundant  and 
foetid.  Exploration  with  the  probe  showed  another  sequestrum.  Richelet  removed 
the  sequestra  and  fi'eed  the  adhesions.  The  wound  measured  4  inches  in  length  and 
3  inches  in  breadth.  The  exposed  dura  mater  was  covered  with  granulations.  The 
result  was  excellent. 

I  have  said  that  it  is  essential  to  begin  treatment  as  early  as  possible, 
but  it  is  also  essential  to  keep  on  with  this  treatment  in  spite  of  apparent 
cure.  We  must  not  forget  that,  in  addition  to  the  visible  lesion,  the  skull  is 
frequently  affected  by  deep  lesions  which  may  run  a  latent  course. 


XII.  CEREBRAL  LOCALIZATION. 

The  question  of  cerebral  localization  has  taken  such  an  important  place  in 
the  pathology  of  the  brain  as  to  deserve  a  special  section,  in  order  to  give  a 
general  survey. 

The  study  of  cerebral  localization  has  during  the  past  few  years  received 
a  considerable  impulse.  Physiology  opened  the  way,  and  pathology  followed 
it.  Experiments  have  been  made  on  animals,  the  brains  of  dogs  and  of 
monkeys  being  subjected  to  galvanic  and  faradic  currents  (Hitzig,  Ferrier, 
CarviUe,  and  Duret),  and  most  of  the  experimenters,  after  certain  contra- 
dictory results,  are,  however,  agreed  on  these  two  points  :  (1)  That  the  grey 
matter  of  the  cerebral  convolutions  is  experimentally  excitable  ;  (2)  that 
excitation,  limited  to  a  convolution,  or  to  a  still  more  restricted  portion, 
determines  movements  which  are  always  localized  in  a  certain  part  of  the 
body  (Ferrier). 

It  must  be  said,  however,  that  the  experimenters  did  not  all  obtain 
the  same  result  as  regards  the  exact  localization  of  the  motor  centres. 
Pathological  anatomy,  however,  furnished  facts  agreeing  with  physiological 
experiments  ;  the  topographical  diagnosis  made  during  life  was  frequently 


1428  TEXT-BOOK  OF  MEDICINE 

verified  at  the  post-mortem  examination,  and  the  cortical  motor  centres  have 
since  been  gradually  mapped  out. 

These  positive  ideas  gave  to  cerebral  pathology  an  accuracy  previously 
unknown.  If  a  patient  was  attacked  by  paralysis,  contracture,  or  con- 
vulsions limited  to  the  arm,  the  leg,  or  the  face,  the  cerebral  origin  of  the 
lesion  being  admitted,  it  became  possible  to  make  the  exact  topographical 
diagnosis  of  this  lesion.  Surgery  profited  thereby,  and  the  application  of 
the  trephine  was  no  longer  a  matter  of  chance.  In  the  following  pages 
we  shall  see  that  these  ideas  are  not  as  correct  as  we  have  been  wont  to 
think. 

The  question  of  cerebral  localization  includes  not  only  the  localization 
of  the  tumours  (syphiloma,  glioma,  tubercle),  but  also  the  localization  of 
the  vascular  lesions  which  may  produce  cerebral  softening  by  thrombosis 
or  by  embolism.  Given  an  arterial  obliteration,  can  the  seat  of  the  embolism 
or  of  the  thrombosis  be  diagnosed,  and  can  we  state  precisely  the  area  of 
the  consequent  softening  ?  We  may  feel  the  more  correct  in  so  doing 
since  researches  regarding  the  cerebral  circulation  in  France  (Duret) 
and  in  other  countries  (Cohnheim,  Heubner)  have  given  the  following 
conclusions  : 

1.  The  arteries  of  the  brain  are  not  anastomotic  ;  there  are  no  anasto- 
moses either  between  the  peripheral  arteries  and  the  central  ones  ;  in  other 
words,  these  arteries  are  terminal  (Cohnheim). 

2.  Certain  regions  in  the  brain  are  supplied  by  only  one  artery,  and  when 
this  artery  is  obliterated,  death  follows  in  the  area  supplied  by  it,  because  the 
artery  does  not  anastomose. 

These  data  being  given,  the  morbid  localization  could  not  then  fail  to  be 
precise ;  the  question,  however,  on  further  examination,  has  been  modified. 
In  the  first  place,  the  cerebral  arteries  are  not  deprived  of  anastomoses  at 
this  point  (Cadiat),  and  it  is  not  uncommon  to  see  the  small  arterioles 
anastomose  (Lucas).  These  anastomoses  may  establish  in  certain  cases 
a  collateral  circulation  that  prevents  the  death  of  the  affected  area.  In 
the  second  place,  further  researches  have  shown  that  an  area  supposed  to 
possess  only  one  artery  receives  its  blood  from  various  sources.  Contrary 
to  the  opinion  of  Duret,  Hallopeau  has  discovered  that  the  Sylvian 
artery  is  not  the  only  vessel  which  supplies  the  corpus  striatum ;  he  found, 
moreover,  either  a  branch  of  the  anterior  cerebral,  which  reached  the  lenti- 
cular nucleus  after  having  traversed  the  perforated  space,  or  a  branch  of  the 
anterior  choroidal ;  this  explains  why  the  internal  segment  of  the  corpus 
striatum  is  generally  spared  in  lesions  dependent  on  the  Sylvian  artery. 
The  "  arterial  territories  "  lose,  therefore,  some  importance,  but  the  question 
of  localization  has  none  the  less  acquired  great  accuracy.  With  regard  to 
this  we  may  say  that  in  most  cases  the  topographical  diagnosis  made  during 


DISEA8KS  OF  THE  BRAIN  1429 

life  has  been  proved  to  be  correct  at  the  post-mortem  examination  or  at  the 
operation.  In  the  following  paragraphs  I  shall  give  our  actual  knowledge 
with  regard  to  this  (piestiou  : 

1.  Localization  in  the  Cortex. 

Aphasia. — Until  the  recent  work  of  Murii;  the  lesion  which  produces 
ordinary  aphasia  was  placed  in  the  posterior  third  of  the  third  left  frontal 
convolution  (Broca's  convolution),  and  in  the  white  fibres  (inferior  pediculo- 
frontal  ])undles)  which  arise  in  this  cortical  centre. 

Agraphia  appears  to  be  due  to  lesions  of  the  foot  of  the  second  left  frontal 
convolution. 

Word-deafness  appears  to  coincide  with  the  lesions  of  the  first  left 
temporal  convolution,  especially  in  its  postero-superior  extremity,  and 
word-blindness  appears  to  be  due  to  the  lesions  of  the  left  inferior  parietal 
lobule  in  the  neighbourhood  of  the  angular  gyrus  (see  Section  V.). 

Paralysis.  —  The  following  account  concerning  the  localization  of 
paralyses  is  largely  taken  from  the  monograph  of  Charcot  and  Pitres,  and 
from  the  writings  of  Grasset : 

1.  All  cortical  lesions  of  the  cerebral  hemispheres  in  man  do  not  give  rise 
to  motor  disorders.  From  this  point  of  view  the  cortex  of  the  brain  may 
be  divided  into  two  distinct  parts — the  non-motor  zone,  in  which  destructive 
lesions  never  cause  permanent  paralysis ;  and  the  motor  zone,  in  which 
destructive  lesions  cause  permanent  paralysisof  the  opposite  side  of  the  body. 

2.  The  non-motor  zone  comprises  : 

(a)  The  prefrontal  region  of  the  brain  (orbital  lobe,  first,  second,  and 
third  frontal  convolutions). 

(6)  The  occipito-parietal  region  (occipital  lobe,  superior  and  inferior 
parietal  lobules). 

(c)  The  entire  temporo-sphenoidal  lobe. 

3.  The  motor  zone  comprises  only  the  ascending  frontal  and  parietal 
convolutions  and  the  paracentral  lobe  ;  perhaps  also  the  foot  of  the  frontal 
convolutio2is. 

•1.  Paralyses  caused  by  destructive  lesions  of  the  cortex  affect  various 
forms,  according  to  the  seat  and  to  the  extent  of  the  lesions.  Total  hemi- 
plegia of  cortical  origin  is  produced  by  extensive  lesions  of  the  ascending 
convolutions.  Partial  paralysis  is  produced  by  limited  lesions  of  the  same 
convolutions. 

Ajnongst  the  varieties  of  partial  paralysis  we  may  distinguish  : 

(a)  Brachio-facial  monoplegia,  due  to  lesions  of  the  inferior  half  of  the 
ascending  convolutions. 

(b)  Brachio-crural  monoplegia,  due  to  the  lesions  of  the  superior  half  of 
the  ascending  convolutions. 

"•  91 


1430  TEXT-BOOK  OF  MEDICINE 

(c)  Facial  and  lingual  monoplegia,  depending  on  very  limited  lesions  of 
the  inferior  extremity  of  the  motor  zone,  and  particularly  of  the  ascending 
frontal  convolution. 

(d)  Brachial  monoplegia,  dependent  on  very  limited  lesions  of  the  middle 
portion  of  the  motor  zone,  and  particularly  on  the  middle  third  of  the 
ascending  frontal  convolution. 

(e)  Crural  monoplegia,  due  to  lesions  of  the  paracentral  lobule. 

(/)  Paralysis  of  the  levator  palpebrae  superioris,  which  appears  to  depend 
on  a  limited  lesion  of  the  lobule  of  the  angular  gyrus  (Grasset,  Landouzy). 

5.  Total  or  partial  paralysis,  provoked  by  destructive  lesions  of  the 
cortex,  is  permanent,  and  is  accompanied  after  a  certain  time  by  secondary 
contracture  of  the  paralyzed  muscles  and  descending  degeneration  of  the 
pyramidal  tract. 

Contractures. — I  need  not  dwell  on  contractures  and  spasms  limited  to 
the  arm  and  to  the  leg.  They  have  the  same  localization  as  the  paralyses, 
only  in  one  case  we  have  to  deal  with  irritative  lesions  (contractures),  in  the 
other  with  destructive  lesions  (paralysis). 

Convulsions.— The  cortical  lesions  which  produce  convulsions  cannot  be 
localized  as  clearly  as  the  lesions  which  produce  paralysis.  On  this  subject 
Charcot  and  Pitres  are  of  the  following  opinion :  Irritative  lesions  of  the 
cortex  may  give  rise  to  epileptiform  convulsions  (partial,  Jacksonian,  or 
cortical  epilepsy).  These  convulsions  are  as  a  rule  quite  distinct  from  the 
convulsions  of  true  epilepsy.  They  commence  with  a  motor  aura,  and  may 
become  general,  or  may  remain  limited  to  one  half  of  the  body  (hemispasm), 
or  to  a  single  group  (monospasm). 

Lesions  capable  of  causing  epileptiform  troubles  are  seated  in  the  motor 
zone  itself  or  in  its  neighbourhood,  and  between  the  variety  of  partial 
epilepsy  and  the  topography  of  the  provoking  cortical  lesion  there  is  not 
always  the  constant  relation  that  is  found  between  paralyses  of  cortical 
origin  and  the  seat  of  the  destructive  lesions  which  give  rise  to  them. 

Numerous  observations  show  that  in  many  cases  partial  epilepsy  assumes 
the  following  types,  depending  on  clearly  defined  lesions  :  (1)  In  the  facial 
type  the  convulsions  are  limited  to  the  face  and  the  neck  ;  they  involve  the 
commissure  of  the  lips,  the  orbicularis  palpebrarum,  the  motor  muscles  of 
the  eye  and  tongue,  and  the  sterno-mastoid  ;  jerky  movements  of  the  arm 
are  sometimes  present.  (2)  In  the  brachial  type,  which  is  more  common, 
the  aura  commences  in  one  of  the  fingers  ;  the  convulsions  attack  the  hand, 
the  arm,  the  shoulder,  and  sometimes  the  face  and  the  neck.  (3)  In  the 
crural  type,  which  is  the  rarest,  the  aura  commences  in  the  foot,  and  the 
convulsions  stop  at  the  hip. 

The  topography  of  the  cerebro-meningeal  lesion  may  be  diagnosed  by 
the  type  of    the  epilepsy :    facial    type — inferior  extremity  of    the  two 


DISEASES  OF  THE  BKAIN  14^1 

asceuding  convolutiona  ;  brachial  type — middle  rejiiou  of  the  aaceiidiiig 
troii(;il  cunvohitioii ;  crural  tvpe — superior  region  of  tfie  ascending  convolu- 
tioiiij  and  of  the  puraceutrul  lobule  ;  lingual  type  iiiforior  region  of  the 
ascending  frontal  convolution  in  the  neighbourhood  of  the  foot  of  the  third 
frontal  convolution. 

For  further  details  I  would  refer  (lie  nM<|(>r  tf>  tho  ^.-.-tion  on  Jacksonian 
Epilepsy. 

2.  Localization  of  the  Central  Lesions. 

Localization  in  certain  central  parts  of  the  brain  is  extremely  precise  : 
thus  the  lesions  producing  hemianaesthesia,  accompanied  or  not  by  hemi- 
plegia, hemichorea,  etc.,  may  be  placed  with  certainty  in  the  posterior 
portion  of  the  posterior  segment  of  the  internal  capsule.  These  localizations 
have  been  described  under  Cerebral  Haemorrhage. 


XIIL  DISCUSSION  ON  MEDICO-SUKGICAL  ERRORS  REGARDING 
CEREBRAL  LOCALIZATION. 

In  the  previous  section  I  remarked  that  the  current  doctrines  of 
cerebral  localization  had  induced  physicians  and  surgeons  to  localize  in  the 
area  of  Rolando  the  lesions  (syphiloma,  tuberculoma,  glioma,  etc.)  which 
cause  certain  types  of  partial  epilepsy,  with  or  without  paralysis  of  the  con- 
vulsed parts.  Physicians  and  surgepns  confident  in  this  doctrine  have  been 
able  to  operate  on  the  region  of  the  skuU  corresponding  to  Rolando's  area. 

We  should  be  wrong,  however,  to  rely  too  much  on  these  localizations, 
because  certain  mistakes  have  been  made,  and  the  trephine  has  been  applied, 
but  the  expected  lesion  has  not  been  found.  I  wish  to  point  out  these  mis- 
takes, as  I  have  already  done  at  the  Academie. 

On  January  10  a  man  was  sent  into  the  Hotel-Dieu.  He  was  unable  to  give  ns 
any  information.  He  had  been  seen  by  Dr.  Maynau  on  the  night  of  January  5,  when 
he  answered  questions  with  difficulty.  The  previous  day  he  had  done  his  work  and 
had  eaten  well.  He  had  gone  to  bed,  and  since  that  time  he  had  lost  consciousness. 
His  wife  stated  that  about  midjoight  she  was  awakened  by  his  snoring.  She  shook  her 
husband,  who  was  unconscious.  It  was  impossible  to  awake  him  from  his  torpor. 
She  called  in  a  doctor,  who  noticed  that  the  patient  had  bitten  his  tongue,  and  that  he 
had  passed  his  urine  under  him.  He  immediately  thought  of  the  possibihty  of  an 
attack  of  epilepsy,  possibly  due  to  syphihs,  and  prescribed  Gibert's  syrup  and  iodide 
of  potassium. 

Next  morning,  Januaiy  6,  the  man's  brother  confirmed  the  hypothesis  of  syphihs, 
contracted  ten  years  previously.  The  patient  was  prostrate,  and  spoke  with  difficulty. 
He,  nevertheless,  showed  by  signs  that  he  understood  what  was  going  on  around  him. 

On  the  night  of  January  6  the  doctor  was  again  called  :  the  patient  ha,d  just  had 
an  attack  "to  which  there  was  no  ending."  He  was  in  a  comatose  condition,  the  breathing 
WAS  stertorous,  and  the  rectal  temperature  was  104°  P.  Suddenly  a  noisy  inspiration 
supervened  :  the  head  and  the  eyes  were  turned  to  the  right,  and  immediately  the 
right  arm,  and  then  the  right  leg,  were  thrown  into  convulsions.     It  was  an  attack  of 

Ui— 2 


1432  TEXT-BOOK  OF  MEDICINE 

Jacksonian  epilepsy.  About  ten  similar  attacks  took  place,  one  after  the  other,  and 
the  comatose  condition  persisted  from  one  o'clock  to  five  o'clock  in  the  morning.  On 
Wednesday,  the  9th,  the  patient  partially  regained  consciousness,  but  he  declined  to 
submit  to  the  prescribed  treatment,  and  he  was  sent  to  the  Hotel-Dieu  in  a  semi-comatose 
condition,  his  temperatixre  reaching  102°  F. 

When  I  saw  the  patient  on  Friday  morning,  the  fifth  day  of  the  disease,  I  could  not 
obtain  any  precise  answers  from  him,  and  yet  he  made  attempts  at  understanding, 
replying  by  gestures,  or  by  monosyllables.  His  tongue  showed  traces  of  having  been 
bitten.  The  limbs  on  the  right  side,  the  arm  particularly,  were  flaccid,  but  not  com- 
pletely paralyzed.  Sensibility  seemed  to  be  diminished  on  the  right  side  of  the 
body.  From  the  previous  evening  nine  convulsions  had  been  counted,  and  just  as  I 
was  examining  him  an  attack  of  partial  epilepsy  came  on.  He  suddenly  uttered  a 
muffled  growl.  His  face  and  lips  were  deflected  to  the  right,  the  right  hand  became 
contracted,  the  fingers  were  flexed,  and  in  a  few  moments  convulsions  appeared 
in  the  upper  hmb.  The  attack  did  not  remain  hmited  to  the  right  arm,  but  soon  invaded 
the  right  leg  (brachio-crural  type).  On  the  left  side  shght  communicated  movements 
were  noticeable.  During  the  crisis  the  patient  did  not  seem  to  have  lost  consciousness 
completely.  In  forty  seconds  the  convulsions  ceased ;  the  patient  remained  cyanosed, 
njid  the  breathing  was  laboured. 

Li  this  case  we  had  to  make  a  topographical  and  a  pathogenic  diagnosis.  The 
former  seemed  obvious.  The  hmitation  of  the  attack  to  the  right  side  of  the  body, 
with  marked  predominance  in  the  right  arm,  indicated  a  lesion  of  the  motor  cortex  on 
the  left  side.  This  locahzation  was  the  more  probable  because  paralysis  was  also 
present.  According  to  current  ideas,  the  lesion  should  attack  the  ascending  frontal  and 
parietal  convolutions,  and  as  the  leg  was  affected  after  the  arm,  it  was  probable  that 
the  lesion  was  in  the  middle  part  of  these  convolutions,  the  upper  region  and  the  para- 
central lobule  being  immune. 

In  case  of  surgical  intervention  I  should  have  indicated  the  left  motor  convolutions 
to  the  surgeon :  the  trephine  would  have  been  apphed  over  this  part  of  the  skull. 
There  was  not,  however,  any  question  of  operation.  As  the  patient  had  had  syphihs, 
everything  pointed  to  the  lesion  of  Rolando's  area  being  gummatous  or  sclero-gum- 
matous.  Injections  of  biniodide  of  mercury  were  given,  but,  in  spite  of  the  treatment, 
the  Jacksonian  attacks  continued  day  and  night.  In  twenty-four  hours  he  had  forty 
or  fifty  attacks. 

On  Saturday,  the  12th,  the  temperature  was  103-5°  F.  The  attacks  followed  one 
on  another,  and  the  patient  died  on  Sunday  night.  The  cranial  cavity  was  opened, 
and  the  Rolandic  area  on  the  left  side  was  examined.  Nothing  appreciable  was  found — 
no  tumour,  no  depression,  no  adhesions.  When  we  tried  to  remove  the  brain,  we 
noticed  that  the  dura  mater  was  adherent  to  the  pia  mater  over  the  anterior  portion 
of  the  left  frontal  lobe.  The  pia  mater  was  severed,  and  the  cerebrum,  cerebellum,  and 
bulb  were  removed. 

The  examination  of  the  brain  gave  the  following  information  :  Rolando's  convolu- 
tions were  healthy,  as  were  the  parietal,  occipital,  and  temporal  lobes.  The  only 
apparent  lesion  was  limited  to  the  left  frontal  lobe.  At  this  point  the  tissue  was  softer 
than  the  grey  matter  of  the  convolutions.     The  lesion  was  gummatous. 

The  gumma,  seen  from  the  external  surface  of  the  frontal  lobe,  occupied  the  anterior 
third  of  the  first,  second,  and  third  frontal  convolutions.  On  the  inferior  surface  of 
the  brain  the  lesion  occupied  the  oiiter  part  of  the  olfactory  convolutions  over  an  area 
of  3  centimetres.  On  making  a  median  horizontal  section  of  the  brain  we  found  that 
the  lesion  extended  to  within  IJ  centimetres  of  the  anterior  horn  of  the  lateral  ven- 
tricle. Its  Umits  were  clearly  defined.  The  brain  tissue  around  the  tumour  was  in 
no  wise  changed.  The  tumour  was  of  the  size  of  a  small  egg.  On  section,  its  tissue 
presented  the  following  aspect :  the  dura  mater  adhering  to  the  pia  mater  had  a  thick- 
ness of  1  to  2  millimetres.     The  newly-formed  subjacent  tissue  had  invaded  and  replaced 


DISEASES  OF  THE  BRATN  14:;:: 

tho  white  aiul  tlie  K'^'V  nmtlor.  This  (iHsuo  was  yellowish -lnown,  fairly  soft  arxi  friable, 
and  soiuowhat  rosoinhiinK  a>(ieniatous  connective  tiBsuo.  Jt  was  travcjrsed  by  whiter 
ami  more  resisting  filaments,  and  in  several  places  there  were  small  islets  of  cawioii.s 
asjH'it  and  consistency. 

We  had  now  to  decide  as  to  this  strange  case.  Tho  patient  had  suffered  from 
certibral  gunmia,  and  so  far  the  pathogenic  diagnosis  was  correct ;  but  we  had  locali/x-d 
the  lesion  in  Rolando's  area,  and  in  that  respect  the  topographical  diagnosis  was  wrong, 
because  the  lesion  occupied  the  frontal  lobe.  I  then  asked  myself  whether  this  case 
was  an  i.-^olated  one.  I  looked  the  question  up,  and  found  some  identical  cases.  Seeing 
♦  ho  importance  of  the  subject,  I  shall  quote  them  : 

Ijepine  has  published  a  case  entitled  "  Jacksonian  Epilepsy  ending  in  Death. 
Autopsy :  old  abscess  of  tho  anterior  lobe  of  the  brain."  An  old  woman  Avas  admitted 
for  Jacksonian  epilepsy  of  tho  limbs  on  the  left  side,  the  face  remaining  immune.  Besides 
the  attacks,  wliich  were  complicated  by  loss  of  consciousness,  he  noticed  sUght  jerks 
in  the  fingers  and  in  the  forearm,  and  rigidity  of  the  arm,  but  no  loss  of  consciousness. 
Did  not  these  convulsions  point  to  a  lesion  in  the  middle  portion  of  the  right  motor 
convolutions  ?  The  patient  died.  At  the  post-mortem  examination  Rolando's 
area  was  healthy.     An  old  encysted  abscess  was  found  in  the  first  right  frontal  con- 


FiG.   73. — TuMOTJK  IN  Frontal  Lobe. 

volution.  As  Lepine  remarks,  if  trephining  had  been  carried  out,  it  would  not  have 
exposed  the  lesion,  "  because,  reljTng  on  the  symptoms  in  the  attack,  we  should  have 
opened  the  skull  far  back  in  a  region  intermediate  to  the  centre  for  the  upper  hmb 
and  to  that  for  the  lower  hmb."  Lepine  and  myself,  in  our  respective  cases,  arrived  at 
the  same  erroneous  conclusion. 

In  another  case  Lepine  had  to  deal  with  a  syphilitic  patient  who  was  suffering 
from  cerebral  s3Tnptoms  :  ambitious  ideas,  amnesia,  Avith  strangeness  of  manner,  and 
attacks  of  Jacksonian  epilepsy  hmited  to  both  arms.  This  limitation  of  the  con- 
vulsive attacks  would  lead  us  to  place  the  cerebral  lesion  at  a  sjnimietrical  point  in 
the  Rolandic  area.  The  patient  died,  and  at  the  post-mortem  examination  two  gummata 
were  found  placed  SA^mmetrically,  not  in  the  convolutions  of  Rolando,  but  in  the  first 
convolution  of  the  two  frontal  lobes. 

Faguet  and  Lowitz  have  published  the  following  case  : 

A  woman  who  had  had  syphihs  was  seized  with  Jacksonian  epilepsy,  hmited  to 
the  left  side  of  the  body.  The  convulsions  commenced  in  the  hand,  spread  to  the  arm, 
attacked  the  mouth  and  the  upi^er  eyelid,  and  ended  in  the  lower  hmb,  always  on  the 
left  side.  The  convulsions  disappeared  in  the  foUoAving  order :  they  ceased  first  in  the 
face,  then  in  the  arm,  then  in  the  leg,  and  finally  in  the  hand      During  the  attacks 


1434  TEXT-BOOK  OF  MEDICINE 

the  patient  did  not  lose  consciousness.  Slemory,  intelligence,  and  speech  were  normal. 
Percussion  of  the  skuJl  over  the  psycho-motor  zone  caused  fairly  acute  pain. 

As  antisyphihtic  treatment  gave  no  result,  and  as  the  symptoms  pointed  to  a  lesion 
in  the  right  motor  convolutions,  Lannelongue  trephined  over  .the  lower  part  of  the 
fissure  of  Rolando.  The  dura  mater  was  laid  bare,  but  the  suspected  lesion  was  not 
found.  The  convulsions  continued,  and  the  patient  died.  The  post-mortem  ex- 
amination showed  that  the  motor  zone  was  healthy.  The  lesion,  a  gumma  of  the  size 
of  a  nut,  was  seated  in  the  posterior  third  of  the  second  right  frontal  convolution. 

The  following  case  is  taken  from  Chipault : 

A  man  who  had  already  had  some  cerebral  symptoms  was  seized  with  Jacksonian 
epilepsy,  locahzed  in  the  left  arm  and  left  leg.  The  convulsions  were  followed  by 
paralytic  symptoms.  Nevertheless,  nearly  every  morning  on  rising  the  patient  ex- 
perienced an  involuntary  extension  of  the  paralyzed  arm,  which  raised  the  coverlet 
of  the  bed.  The  forearm  and  the  hand  were  straight,  the  fingers  were  extended  and 
separated.  The  condition  lasted  a  moment.  When  the  patient  was  excited,  the 
paralyzed  hand  showed  rapid  tremor,  which  could  be  lessened  or  arrested  by  supporting 
the  hand.  As  these  symptoms  indicated  a  lesion  of  the  right  Eolandic  area,  the  trephine 
was  applied,  and  this  area  was  widely  exposed.  After  incision  of  the  dura  mater  no 
lesion  of  the  motor  area  could  be  seen.  Puncture  with  a  Pravaz  syringe  in  the  frontal 
and  then  in  the  ascending  parietal  convolution  gave  no  result.  An  incision  1  centi- 
metre long  and  2  centimetres  deep,  made  from  above  downwards  in  the  ascending  frontal 
convolution,  showed  nothing.  Three  weeks  later  the  patient  died.  At  the  post-mortem 
examination  a  gUoma  of  the  size  of  a  cherry  was  found,  but  in  the  second  right  frontal 
convolution. 

Crouzon  has  reported  the  following  case  : 

A  coachman,  who  had  fallen  unconscious  from  his  box,  was  brought  to  hospital. 
The  head  and  the  eyes  were  deviated  to  the  right.  The  Hmbs  showed  neither  paralysis 
nor  contracture.  Next  day  convulsions  appeared  in  the  face,  the  arm,  and  the  leg,  on 
the  left  side.  The  cutaneous  and  tendon  reflexes  were  normal.  Two  days  later  Jack- 
sonian epilepsy  was  typical  in  the  face  and  in  the  left  arm  (facio -brachial  type).  The 
patient  was  in  a  condition  of  coma.  Lumbar  puncture  gave  a  clear  hquid,  rich  in 
lymphocytes. 

The  clinical  evidence  pointed  to  a  lesion  in  the  right  motor  area,  and  an  operation 
was  performed.  After  incision  of  the  meninges,  which  were  healthy,  Rolando's  area 
and  the  neighbourhood  were  explored,  but.  contrary  to  all  expectations,  no  change 
was  found.  The  patient  died,  and  the  post-mortem  examination  showed  that  Ro- 
lando's area  was  normal.  The  lesion  which  had  caused  the  Jacksonian  epilepsy  was 
seated  at  the  apex  of  the  right  temporal  lobe.  This  lesion,  in  the  shape  of  an  adherent 
fibrous  patch,  was  probably  tubercular.     The  remainder  of  the  brain  was  healthy. 

Lucas-Championniere  showed  at  the  Societe  de  Chirurgie  a  tumour  of  the  right 
frontal  lobe.  It  was  as  large  as  a  tangerine  orange,  and  had  been  removed  from  a 
patient  suffering  from  Jacksonian  epilepsy  in  the  left  arm  (brachial  type).  This  locahza- 
tion  pointed  to  a  lesion  in  the  ascending  frontal  and  parietal  convolutions.  Nothing 
of  the  kind  was  present.  These  convolutions  were  absolutely  healthy,  and  the  lesion 
was  seated  in  the  frontal  convolutions. 

These  cases  furnish  valuable  information.  In  mv  patient  suffering  from 
Jacksonian  epilepsy  (brachio- crural  type)  I  had  made  the  natural  diagnosis 
of  a  cerebral  lesion  in  the  area  of  Eolando.  In  the  event  of  an  operation  the 
surgeon  would  have  trephined  at  this  spot,  but  he  would  have  found  nothing. 


DISEASES  OF  TIIK  BRAIN  1435 

because  the  post-mortem  examiiuitioii  sliownd  that  tho  lesion  was  seated  in 
the  frontal  lolje.  The  same  remark  applies  to  the  other  cases  just  quoted. 
•Tacksonian  epilepsy  in  Lopino's  patient  induced  him  to  diagnose  a  lesion  in 
Rolando's  area,  and  at  the  post-mortem  examination  it  was  seen  that  the 
lesion  was  seated  in  the  first  frontal  convolution.  .Tacksonian  e))ilepsv  in  the 
patient  of  Faguet  and  Lowitx  pointed  to  a  lesion  in  the  area  of  Rolando. 
The  trephine  was  applied,  and  nothing  was  found ;  the  post-mortem 
oxammation  showed  that  the  lesion  was  localized  in  the  second  frontal 
convolution.  In  Chipaidt's  patient  the  lesion  was  thought  to  be  in  the 
motor  area  ;  at  the  post-mortem  examination  it  was  discovered  that  the 
lesion  was  in  the  second  frontal  convolution. 

Jacksonian  epilepsy  in  Crouzon's  patient  (facio-brachial  type)  led  to  the 
diagnosis  of  a  lesion  in  Rolando's  area.  An  operation  was  performed,  and 
it  was  found  that  this  region  was  absolutely  healthy ;  at  the  post-mortem 
examination  it  was  seen  that  the  lesion  was  seated  at  the  apex  of  the 
temporal  lobe.  Jacksonian  epilepsy  in  the  patient  of  Lucas-Championniere 
(brachial  type)  led  to  the  diagnosis  of  a  lesion  in  Rolando's  area,  but  the 
operation  showed  that  this  region  was  healthy,  and  the  post-mortwn 
examination  proved  that  the  lesion  was  in  the  temporal  lobe. 

Accordingly,  a  lesion  (glioma,  syphiloma,  tuberculoma,  etc.)  in  the  frontal 
lobe,  remote  from  Rolando's  area,  may  cause  Jacksonian  epilepsy,  such  as 
we  are  accustomed  to  see  when  the  lesions  are  localized  in  Rolando's  convo- 
lutions. Physicians  and  surgeons  have  been  deceived  thereby.  It  must  be 
admitted  that  cases  of  this  kind,  which  are  relatively  numerous,  leave  some 
uncertainty  as  to  the  accuracy  of  the  topographical  diagnosis  of  the  cerebral 
lesions,  and  cause  legitimate  difficulty  when  the  question  arises  of  indicating 
the  area  of  the  brain  to  be  exposed. 

Is  there  no  symptom  by  which  we  can  say  that  in  one  case  Jacksonian 
epilepsy  is  caused  by  a  lesion  of  Rolando's  area,  and  in  another  case  by  a 
lesion  in  the  frontal  lobe  ?  It  would  seem  a  'priori  that  a  lesion  of  the 
frontal  lobe  would  produce  mental  troubles,  which  are  not  caused  by  lesions 
in  the  convolutions  of  Rolando  ;  but  this  hypothesis,  though  rational  in 
itself,  does  not  always  correspond  with,  the  actual  facts.  My  patient,  who 
had  a  lesion  in  the  frontal  lobe,  had  shown  neither  psychical  nor  intellectual 
troubles  when  he  was  attacked  with  Jacksonian  epilepsy ;  on  the  previous 
evening  he  was  in  good  health,  and  carried  out  his  duties  as  telegraph 
operator  without  any  failing  of  his  mental  faculties.  In  the  case  of  Faguet 
and  Lowitz  it  is  recorded  that  the  patient,  who  was  suffering  from  Jack- 
sonian epilepsy  caused  by  a  lesion  of  the  frontal  lobe,  "  had  no  intellectual 
trouble.  His  memory  was  perfect,  and  his  speech  was  normal."  In 
Chipault's  case  we  see  that  the  patient,  who  was  suffering  from  Jacksonian 
epilepsy  caused  by  a  lesion  of  the  frontal  lobe,  "  had  no  intellectual  troubles." 


1436  TEXT-BOOK  OF  MEDICINE 

The  absence  of  psychical  and  intellectual  troubles  cannot  therefore  serve  to 
difierentiate  between  Jacksonian  epilepsy  caused  by  a  Rolandic  lesion  and 
Jacksonian  epilepsy  due  to  a  frontal  lesion. 

Are  the  paralytic  symptoms  of  help  in  making  a  diagnosis  ?  We  know, 
as  a  matter  of  fact,  that  the  lesions  of  Rolando's  convolutions  cause  con- 
vulsions, and  also  give  rise  to  special  paralysis  ;  paralysis  or  paresis  of  the 
arm  and  of  the  leg  may  precede  the  attacks  of  Jacksonian  epilepsy,  may 
coexist  with  them,  or  may  survive  them.  jVIany  patients  suffering  from 
Jacksonian  epilepsy  of  the  upper  or  of  the  lower  limb  suffer  after  a  con- 
vulsive attack,  or  in  the  interval  between  the  attacks,  from  more  or  less 
lasting  paralysis  of  the  limbs  which  have  been  convulsed.  If  the  addition 
of  paralytic  troubles  were  peculiar  to  Jacksonian  epilepsy  of  Rolandic 
origin,  and  if  it  were  absent  in  Jacksonian  epilepsy  of  frontal  origin,  we 
should  have  a  valuable  aid  to  the  topographical  diagnosis. 

This  aid,  however,  is  wanting,  since  paralysis  may  be  associated  with 
Jacksonian  epilepsy  of  frontal  origin.  Thus,  my  patient  had  partial  paralysis 
in  his  arm  and  in  his  leg,  and  we  noticed  in  his  case  the  coexistence  of  paretic 
strmptoms  and  of  convulsions  ;  the  convulsive  attack  having  ended,  the 
paralytic  symptoms  became  the  chief  feature.  In  one  of  Lepine's  patients 
the  arm  and  the  left  leg  were  paralyzed  after  the  convulsions,  and  the 
paralysis  persisted  untU  death.  The  patient  of  Faguet  and  Lowitz  had 
flaccid  hemiplegia  in  the  interval  between  the  convulsive  attacks,  and  the 
paralysis  persisted  in  an  absolute  manner.  Chipault's  patient  had  paresis 
of  the  limbs  affected  by  Jacksonian  epilepsy,  and  the  arm  remained 
paralyzed. 

The  presence  of  paralysis  cannot  assist  as  in  differentiating  with  certainty 
between  Jacksonian  epilepsy  caused  by  a  Rolandic  lesion  and  Jacksonian 
epilepsy  caused  by  a  frontal  lesion. 

Therefore,  we  must  admit  Rolandic  and  frontal  Jacksonian  epilepsy, 
and  also  temporal  Jacksonian  epilepsy,  which  are  absolutely  identical. 
Jacksonian  epilepsy,  caused  by  a  Rolandic  lesion,  is  much  more  common  than 
Jacksonian  epilepsy  due  to  a  frontal  lesion ;  nevertheless  the  latter  form  is 
met  with  fairly  frequently,  as  the  cases  quoted  prove. 

At  present  we  have  no  sign  and  no  symptom  which  enable  us  to  differ- 
entiate between  Rolandic  and  frontal  epilepsy.  We  should  be  much  em- 
barrassed if  we  were  asked  to  point  out  precisely  the  cranial  region  to  which 
the  trephine  ought  to  be  applied.  We  should  be  liable  to  give  an  incorrect 
answer,  as  witness  my  own  case  and  the  cases  of  Faguet  and  Lowitz,  of 
Lepine,  of  Chipault,  of  Cruzon,  and  of  Lucas-Championniere.  Were  such  a 
case  to  occur,  we  should  not  dare  to  express  an  opinion. 

I  must  make  a  remark,  if  only  in  the  nature  of  a  simple  reflection. 
Amongst  the  types  of  Jacksonian  epilepsy  due  to  a  Rolandic  lesion  there  is 


DISEASES  OF  THE  BRAIN  1437 

one  wliich  I  have  not  seen  reproduced  in  Jacksonian  epilepsy  of  fn^ntal 
origin— viz.,  the  criirul  tv[)e,  where  tlie  convulsive  attack  commences  in 
the  leg. 

In  such  a  case  the  cerebral  lesion  which  causes  the  attack  of  epilepsy  is 
localized  in  the  paracentral  lobule,  or  in  the  highest  part  of  the  motor  convo- 
lutions which  unite  to  foi'm  the  paracentral  lobule.  Does  the  crural  type  of 
Jacksonian  epilei)sy  t^s<'a])e  the  similitude  which  we  have  just  pointed  out  in 
the  other  types,  and  may  it  not  be  produced  by  a  frontal  lesion  ?  I  do 
not  know, 

XIV.  TUBERCULAR  MENINGITIS. 

The  word  "  meningitis  "  includes  the  inflammation  of  the  arachnoid,  of 
the  subarachnoid  tissue,  and  of  the  pia  mater ;  but  it  does  not  apply  to 
inflammation  of  the  dura  mater,  which  will  be  described  later. 

Acute  meningitis  may  be  divided  into  two  large  classes  :  (a)  non-tuber- 
cular meningitis  ;  (6)  tubercular  meningitis.  I  shall  first  describe  tubercular 
meningitis. 

etiology. — The  designation  tubercular  rneningitis  does  not  apply 
indiscriminately  to  all  cases  of  meningeal  tuberculosis  ;  the  tubercles  may 
become  agglomerated  so  as  to  form  a  large  tumour,  which  causes  symptoms 
of  cerebral  tumour,  but  not  of  meningitis.  Tubercular  meningitis  varies  in 
its  appearance.  Sometimes  it  forms  a  part  of  the  general  invasion  of  the 
system  by  acute  tuberculosis,  and  in  this  case  it  is  of  secondary  importance  ; 
sometimes  it  appears  to  be  the  entire  disease  :  the  latter  form  is  generally 
described  under  the  name  of  tubercular  meningitis. 

Tubercular  meningitis  is  almost  always  accompanied  by  pulmonary  or 
abdominal  tuberculosis.  It  is  seen  at  aU  ages,  but  it  is  most  common  in 
children  between  the  ages  of  two  and  seven  years.  It  is  hereditary,  like  all 
the  manifestations  of  tuberculosis,  and  it  is  not  rare  for  several  children  of 
the  same  family  to  be  carried  off  at  about  the  same  age  by  meningitis.  Head 
injuries  have  an  undoubted  influence  on  the  development  of  tubercular 
meningitis,  just  as  traumatism  has  an  undoubted  influence  on  the  develop- 
ment of  pulmonary  tuberculosis. 

Martin,  Vaudremer  and  Martin,  and  Sicard  have  produced  tubercular 
meningitis  experimentally  by  injecting  bacilli  into  the  bloodvessels  or  into 
the  cerebro- spinal  fluid.  The  toxines  secreted  by  the  bacillus  play  an 
important  part  in  the  evolution  of  the  meningitic  process.  Armand  Deiille, 
by  means  of  the  caseif  ving  and  sclerosing  poisons  of  Auclair,  has  been  able 
experimentally  to  reproduce  the  lesions  of  tubercular  meningitis.  The 
lymphatic  system  does  not  seem  to  serve  as  a  means  of  transport  in  this 
experimental  infection,  except  when  the  leucocAd:.es  emigrate  from  adjacent 
cavities  (nasal,  ocular,  or  auricular  cavities).     Tubercular  meningitis  may  be 


1438  TEXT-BOOK  OF  MEDICINE 

secondary  to  more  or  less  latent  infection  of  the  naso-pliaryngeal  cavity, 
adenoid  and  tubercular  lesions,  described  under  Masked  Tuberculosis  of 
the  Three  TonsUs.  Once  in  situ,  Koch's  bacillus  and  its  toxines  seem  to 
make  use  of  the  cerebro-spinal  fluid  as  their  means  of  transport. 

Pathological  Anatomy. — Acute  tubercular  meningitis  is  generally  more 
marked  at  the  base  than  at  the  convexity  of  the  b^ain  ;  it  affects  the  fissure 
of  Sylvius.  The  exudation  is  more  or  less  abundant,  greyish,  purulent,  and 
sometimes  almost  lardaceous.  The  meningitis  is  generally  diffuse,  but  in 
some  cases  it  is  localized  (see  the  section  on  Jacksonian  Epilepsy).  The 
grey  semi-transparent  granulations  are  usually  found  on  the  lymphatic 
sheath  of  the  vessels  of  the  pia  mater  ;  they  tend  to  be  confluent  at  the  base 
of  the  brain,  and  if  the  Sylvian  artery,  with  its  branches,  is  carefully  removed 
and  floated  in  water,  it  is  easy  to  observe  the  disposition  of  these  tubercular 
granulations.  Under  the  influence  of  the  granulations,  and  of  the  obliterating 
arteritis  which  accompanies  them,  the  blood  coagulates  m  the  interior  of  the 
vessels  and  causes  arterial  thrombosis,  which  produces  superficial  or  deep 
centres  of  softening  (Rendu). 

Bacilli  are  found  in  the  tubercular  granulations  around  the  vessels,  in 
their  walls,  and  in  their  contents.  Other  pathogenic  agents — streptococci, 
pneumococci,  etc. — are  sometimes  associated  with  the  tubercle  baciUus. 

The  meninges  are  often  adherent  to  the  cortical  substance,  which  at  this 
point  presents  a  superficial  encephalitis  (Hayem).  The  pia  mater  is  thick- 
ened, and  its  small  vessels  (venules  and  arterioles)  are  often  obliterated  by 
fibrinous  coagula.  The  central  parts  of  the  brain,  commissures  and  walls 
of  the  ventricles  are  softened,  and  the  ventricular  cavities  often  contain  so 
much  effusion  that  the  disease  formerly  received  the  name  of  acute 
hydrocephalus. 

.  The  choroid  plexuses  often  show  tubercular  granulations  ;  in  some  cases 
the  trouble  in  the  choroid  plexuses  may  be  the  only  tubercular  lesion 
present,  so  that  Loeper  has  described  a  choroidal  form  of  tubercular 
meningitis. 

The  choroid  is  almost  always  the  seat  of  tubercles.  According  to  cir- 
cumstances, more  or  less  generalized  tubercular  lesions  are  met  with, 
especially  in  the  thoracic  and  abdominal  organs.  Changes  analogous  to 
those  of  the  brain  may  exist  in  the  spinal  cord  (see  the  section  on  Cerebro- 
spinal Meningitis). 

Description. — As  tubercular  meningitis  is  much  more  frequent  in  children 
than  in  adults,  I  shall  lay  most  stress  on  the  meningitis  of  childhood  in  the 
present  description.  The  disease  generally  commences  with  a  prodromal 
period,  varying  from  a  few  days  to  three  months.  This  period  is  characterized 
by  various  phenomena :  there  are  general  symptoms,  such  as  change  of 
character,  loss  of  flesh,  attacks  of  fever,  partially  attributable  to  pulmonary, 


DISE.\SES  OF  THE  BRAIN  1439 

or  abdominal  tuberculization  which  precedes  or  accompanies  the  tubercular 
meningitis ;  and  there  are  local  symptoms,  such  as  visual  troubles,  diplopia, 
headache,  and  vomiting,  depending  on  the  invasion  of  the  brain  by 
tuberculosis. 

Period  of  Excitation. — Three  symptoms  open  the  scene  :  headache,  which 
may  be  most  intense  ;  vomiting  of  greenish  bilious  matter  ;  and  constipa- 
tion. The  fever  is  of  a  remittent  character,  being  higher  at  night  and  showing 
oscillations  during  the  day.  The  temperature  rarely  exceeds  103°  F.  The 
little  patient  suffers  at  times  from  generalized  hypersesthesia  ;  he  has  con- 
vulsive jerks,  contractures  of  the  nuchal  muscles,  strabismus,  and  con- 
striction of  the  pupils.     Patients  who  are  older  at  times  suffer  from  delirium. 

At  this  period  appears  the  hydrocephalic  cry  (Coindet).  It  is  a  short 
and  plaintive  scream,  repeated  at  varying  intervals. 

Period  of  Depression. — The  period  of  excitation,  lasting  from  a  few  days 
to  two  weeks,  is  followed  by  a  period  of  depression.  The  headache  and  the 
vomiting  disappear ;  somnolence  follows  the  insomnia,  and  the  child  seems 
to  enjoy  rest,  which  might,  wrongly,  lead  us  to  believe  in  an  improvement 
which  is  fictitious.  The  little  sufferer,  indifferent  to  everything  and  plunged 
in  torpor,  replies  with  difficulty  to  questions.  Anaesthesia  replaces  hyper- 
aesthesia,  and  the  hydrocephalic  cries  become  less  frequent.  The  tempera- 
ture, though  lower,  still  remains  above  normal.  The  pulse  is  irregular,  and 
falls  to  60  per  minute.  The  belly  is  retracted,  the  face  is  red  and  pale  in 
turn,  and  the  tache  cerebrale  is  very  pronounced  (Trousseau).  The  respira- 
tion is  irregular.  Thus  the  patient,  after  a  few  deep  and  hurried  inspirations, 
stops  suddenly  for  a  few  moments,  as  though  he  had  forgotten  to  breathe. 
At  this  period  we  see  convulsions,  which  may  be  general  or  limited  to  a  leg, 
to  an  arm,  or  to  the  face  ;  transitory  contractures  may  affect  the  hands,  the 
muscles  of  the  neck  and  of  the  jaws  (trismus),  and  the  muscles  of  the  eye 
(strabismus). 

This  period  of  depression,  sometimes  complicated  by  transitorv  pheno- 
mena of  excitation,  lasts  a  few  days,  and  gives  place  to  the  paralytic  period. 
The  paralyses  of  tubercular  meningitis  have  special  characters.  They 
generally  follow  on  a  convulsive  attack  ;  they  often  assume  the  hemiplegic 
form,  involving  an  arm  and  then  a  leg,  and  are  successive  rather  than 
simultaneous.     They  rarely  attack  the  face  (Rendu). 

In  the  last  period  the  fever  reappears.  The  pulse  goes  up  to  130  to  150 
beats  a  minute,  the  belly  becomes  ballooned,  the  breathing  is  distressed,  and 
the  little  sufferer,  who  has  lost  consciousness,  dies  in  coma  or  in  convulsions, 
or  is  carried  off  by  progressive  asphyxia. 

The  ocular  troubles  of  tubercular  meningitis  are  of  divers  kinds.  At 
the  commencement  of  the  disease  the  pupil  and  the  motor  nerves  of  the  eye 
show  irritative  phenomena — myosis,  nystagmus,  and   strabismus.      Later 


1440  TEXT-BOOK  OF  MEDICINE 

the  paTal}H:ic  phenomena  predominate — mydriasis,  ptosis,  and  paralytic 
strabismus. 

The  ophthalmoscope  reveals  multiple  lesions  of  the  fundus.  The 
tubercles  of  the  choroid  generally  occupy  both  eyes  in  the  neighbourhood 
of  the  optic  nerve  and  of  the  macula ;  they  form  rounded,  greyish  protuber- 
ances, variable  in  number  ;  they  emanate  directly  from  the  spreading  of  the 
meningitis,  along  the  sheath  of  the  optic  nerve  or  the  vessels  of  the  eye. 
When  tubercles  exist  in  the  choroid,  they  are  of  value  in  the  diagnosis  of 
tubercular  meningitis,  but  they  are  often  absent.  (Edema  of  the  optic 
papiUa  is  frequently  met  with  as  a  consequence  of  the  hydrocephalus  and 
cerebral  oedema  (Parinaud).  This  oedematous  neuritis,  which  is  sometimes 
accompanied  by  hsemorrhage  into  the  retina,  often  ends  in  more  or  less 
complete  atrophy  of  the  optic  nerve. 

The  convulsions,  contractures,  and  paralyses  met  with  in  tubercular 
meningitis  deserve  notice.  The  paralyses  appear  to  be  due  to  foci  of 
softening  in  the  corpora  striata,  the  cerebral  peduncles  (Rendu),  and  the 
motor  zones  of  the  fronto-parietal  convolutions.  These  foci  of  softening 
are  caused  by  thrombi,  induced  by  the  tubercular  granulations  in  the 
vessels.  The  pathogenesis  of  the  convulsions  and  of  the  contractures 
differs,  according  as  they  are  general  or  partial.  When  they  are  general, 
remote  cerebral  excitation  may  be  invoked ;  when  they  are  partial,  they 
result  from  the  direct  excitation  of  the  fronto-parietal  motor  zones 
(Landouzy). 

Tubercular  Meningitis  in  the  Adult. — Meningitis  m  the  adult  does  not 
always  resemble  the  meningitis  of  childhood.  Its  abnormal  forms,  which  are 
fairly  frequent,  have  been  described  by  Chantemesse.  In  some  cases  the 
meningitis,  after  being  latent  for  some  time,  appears  suddenly  with  an 
apoplectiform  attack,  epileptiform  convulsions,  or  an  attack  of  acute  delirium. 
These  various  forms  rapidly  end  in  coma  and  death ;  and  the  delirious  form 
presents  this  peculiarity — that  the  disease  may  run  its  course  without  any 
rise  of  temperature. 

A  comatose  form  of  tubercular  meningitis  may  be  seen.  The  first,  and 
sometimes  the  only,  symptom  is  an  invincible  desire  to  sleep.  The  following 
case  occurred  in  the  Hotel-Dieu  : 

A  young  man  was  seized  with  rapid  coma ;  vomitiag,  headache,  and  deHrium  were 
absent.  Lumbar  puncture  showed  numerous  lymphocytes.  At  the  autopsy  the 
meninges  showed  no  tubercles  ;  the  ventricles  were  distended  by  fluid  ;  the  walls  of  the 
ventricles  had  a  characteristic  washed  appearance,  while  the  choroid  plexuses  were 
gi'anular,  swollen,  and  filled  with  tubercular  granulations — some  young,  others  m  process 
of  caseation. 

Our  knowledge  of  the  troubles  consequent  on  exaggerated  distension 
of  the  ventricles  allows  us  to  consider  the  comatose  form  of  tubercular 


DISEASES  OF  THE  BRAIN  1441 

meniii^^itis  as  <lt'|)riulent  upon  chan<^cs  in  tlic,  choroid  [dexuses  and  in  the 
ventncles,  witli  niurked  hydrops  ventriculonun  (Loeper). 

In  other  cases  the  spinal  symptoms  open  the  scene  ;  the  disease  simulates 
a  meningo-myelitis,  and  then  the  symptoms  of  cerebral  meningitis  declare 
themselves.  Tubercular  cerebro-spinal  meningitis  will  be  studied  in  one 
of  the  following  sections. 

In  some  patients  cerebral  meningitis  concentrates  its  action  on  the 
motor  convolutions  of  the  brain.  Patches  of  tubercular  meningo-ence- 
phalitis  are  found  over  the  ascending  frontal  and  parietal  convolutions  and 
the  paracentral  lobule.  These  patches  are  announced  by  contracture  or 
paralysis,  limited  to  the  arm  or  to  the  leg.  Dissociated  paralysis  of  the  third 
pair  of  nerves  (ptosis)  has  been  seen  in  cases  of  meningitis  of  the  angular 
gyrus. 

The  other  s}Tiiptoms  of  meningitis — headache  and  vomiting — are 
wanting  ;  but  restlessness,  delirium,  somnolence,  and  coma  soon  carrv  ofE  the 
patient,  if  he  does  not  succumb  to  the  rapid  progress  of  the  pulmonary 
tuberculosis. 

Diagnosis. — The  diagnosis  between  meningitis  and  typhoid  fever  is  given 
under  the  latter  disease.  A  propos  of  the  diagnosis,  apoplectiform  meningitis 
in  the  adult  must  not  be  forgotten.  Tubercular  meningitis  does  not  give 
Kernig's  sign  as  long  as  the  spinal  meninges  are  not  affected.  The  bacterio- 
logical examination  of  the  fluid  obtained  by  lumbar  puncture  gives  valuable 
information.  I  shall  give  full  details  in  the  chapter  dealing  with  cerebro- 
spinal meningitis,  when  we  shall  see  that  we  can  make  the  diagnosis  of 
tubercular  meningitis  by  laboratory  methods  (Widal,  Griffon). 

The  prognosis  is  always  grave,  and  death  is  the  natural  result  of  tubercular 
meningitis.  There  is  said  to  be  only  one  midoubted  case  of  cure,  that  of 
Freyhan.  The  treatment  is  very  limited.  It  consists  in  the  application  of 
ice  to  the  head  and  of  leeches  behind  the  ears.  Inunctions  and  intravenous 
injections  of  collargol  have  been  recommended.  The  object  of  the  palliative 
treatment  is  to  maintain  the  nourishment  of  the  child,  and  to  prevent,  as  far 
as  possible,  any  cause  of  cerebral  excitation.  With  regard  to  the  treatment, 
we  must  bear  in  mind  the  possibility  of  meningeal  complications  due  to 
hereditary  syphilis,  and  apply  specific  treatment  if  necessary. 


XY.  NON-TUBERCULAR  MENINGITIS. 

Pathogenesis. — A  few  years  ago  the  pathogenesis  of  non-tubercular 
meningiti.s  was  almost  unknown.  A  patient  died  of  meningitis,  and  the  post- 
mortem examination  revealed  more  or  less  purulent  exudate.  As  tubercu- 
losis Avas  not  found,  the  meningitis  was  called  primary  or  idiopathic.  The 
study  of  non-tubercular  meningitis  is  the  outcome  of  bacteriology.     We 


1442  TEXT-BOOK  OF  MEDICINE 

know  that  most  of  the  microbes  which  cause  pleurisy,  peritonitis,  pericar- 
ditis, etc.,  are  also  capable  of  causing  meningitis.  Meningitis  may  be 
pneumococcal,  streptococcal,  or  staphylococcal.  Some  cases  of  meningitis 
are  due  to  Eberth's  bacillus,  to  the  Bacillus  se-pticus  putridus  (Roger),  or  to 
the  BaciUus  coli,  while  other  cases  are  due  to  the  associations  of  these  various 
agents.  In  some  circumstances  the  entrance  gateway  of  these  agents 
remains  unknown,  and  we  then  speak  of  auto-infection.  In  the  greatest 
number  of  cases  these  agents  enter  the  system  or  reach  the  meninges  by 
reason  of  traumatic  causes  or  of  infectious  diseases.  Traumatism,  insolation, 
osseous  lesions,  otitis,  rhinitis,  amygdalitis,  influenza,  pneumonia,  erysipelas, 
pyaemia,  typhoid  fever,  the  eruptive  fevers,  rheumatism,  and  syphilis  are 
the  most  common  causes  of  non-tubercular  meningitis. 

Meningitis  following  on  Otitis. — Suppurative  meningitis  is  fairly  common 
in  acute  or  chronic  otitis  media.  It  may  likewise  result  from  lesions  of  the 
internal  and  of  the  external  ear,  polypi,  boils,  abscesses  (Duplay).  Netter 
found  that  in  young  children  the  middle  ear  is  almost  always  affected. 
Post-mortem  examinations  performed  between  the  ages  of  nine  months  and 
two  years  have,  in  a  large  number  of  cases,  shown  that  the  middle  ear 
contained  muco-pus,  with  streptococci,  staphylococci,  or  pneumococci. 
It  is  probable  that  these  agents  enter  through  the  Eustachian  tube. 
The  propagation  of  the  lesions  from  the  ear  to  the  meninges  is  easy,  whether 
it  occurs  by  contiguity  or  by  way  of  the  bloodvessels.  As  a  matter  of  fact, 
the  veins  of  the  tympanum  empty  themselves  into  the  middle  meningeal 
vein,  and  anastomoses  exist  between  the  veins  of  the  tympanum  and  the 
superior  petrosal  sinus  (Troeltsch).  The  infectious  diseases  which  are 
accompanied  by  otitis — namely,  syphilis,  pneumonia,  measles,  scarlatina, 
or  influenza — may  cause  meningitis  preceded  by  otitis,  or  meningitis  without 
previous  otitis. 

The  variety  of  the  pathogenic  agents  in  meningitis  consequent  on  otitis 
explains  the  equal  variety  of  the  symptoms.  These  cases  of  meningitis 
may  be  fulminant,  rapid,  acute,  subacute,  or  chronic  (Jaccoud).  The 
fulminant  form  kills  in  twenty-four  hours,  with  comnilsions,  intense  head- 
ache, and  coma.  One  form  simulates  typhoid  fever,  except  for  the  period 
of  onset,  which  commences  suddenly  with  vomiting  and  headache.  In 
another  form  we  find  the  symptoms  of  pyemia — febrile  attacks,  rigors,  and 
sweating.     Finally  there  is  the  common  form  of  classical  meningitis. 

Pneumococcdi  Meningitis. — This  is  the  most  frequent  form  of  non- 
tubercular  meningitis.  It  supervenes  in  the  decline  or  in  the  course  of 
pneumonia  ;  it  may  be  independent  of  pneumonia.  Pneumococcal  menin- 
gitis is  often  associated  with  endocarditis,  and  in  many  cases  it  becomes 
generalized  in  the  spinal  meninges,  so  that  there  is  pneumococcal  cerebro- 
spinal meningitis.     The  foetus  may  suffer  from  this  form.     Netter  found 


DISEASES  OF  THE  BRAIN  1443 

that  a  pregnant  woman  attacked  by  pneiunonia  nriay  trunHmit  both  [incu- 
monia  and  meningitis  to  the  fcctus. 

In  pneumo(()(H-iil  meningitis  the  lesions  are  most  niiirked  over  tlie  con- 
vexity of  the  bruin.  The  exudate  is  incorporated  in  the  pia  mater,  and^it 
may  be  detached  without  injuring  the  cerebral  cortex.  The  exudate  is  of 
a  soft  consistency,  and  diflcrs  from  the  greyish  lardaceous  exudate  of  tuber- 
cular meningitis,  as  well  as  from  the  creamy  pus  seen  in  meningitis  due  to 
caries  of  the  petrous  bone  (Netter).  The  spinal  meninges  are  frequently 
attacked.  Sometimes  the  lesions  are  less  extensive ;  they  are  localized  in 
various  regions  of  the  cerebro-spinal  axis  in  the  form  of  mUky  tracts  or  in 
the  shape  of  islets  of  variable  dimensions.  In  the  spinal  meninges  the  pus 
is  more  abundant  at  the  cervical  and  lumbar  swellings.  The  character  of 
the  pneumococcal  pus  is  evident  when  other  microbes  are  associated  with 
the  pneumococcus. 

Pneimiococcal  meningitis  at  times  presents  special  symptoms.  Some- 
times, in  a  patient  suffering  from  pneumonia  in  process  of  resolution,  a 
sudden  and  considerable  rise  in  the  temperature  is  the  only  s}Tiiptom 
pointing  to  the  presence  of  meningitis  (Jaccoud).  A  prominent  and  almost 
constant  symptom  is  the  rigidity  of  the  nape  of  the  neck  :  the  rigidity  often 
attacks  the  muscles  of  the  face,  and  descends,  in  the  shape  of  painful  con- 
tracture, to  the  muscles  of  the  dorsal  and  of  the  sacro-lumbar  regions. 

Our  knowledge  of  the  frequent  generalization  of  the  pneumococcus  in  the 
cerebro-spinal  meninges  explains  the  rigidity  and  the  more  or  less  general 
contractures.  In  young  children  the  abundance  of  the  purulent  effusion 
sometimes  causes  excessive  intracranial  pressure  (Vaudremer),  with  bulging 
of  the  anterior  fontaneUe.  Pneumococcal  meningitis  rmis  a  very  variable 
course.  Sometimes  the  disease  is  fulminant,  and  kills  in  twenty -four 
hours  ;  in  some  cases  the  onset  is  apoplectiform  (Netter). 

Meningitis  caused  hy  the  Bacillus  Coli. — The  Bacillus  coli  may  produce 
suppurative  meningitis,  as  well  as  pseudo-puerperal  fever  and  pseudo- 
enteric  fever,  when  it  spreads  through  the  system  by  changes  in  the  organs 
which  normally  contain  it.  Most  cases  of  suppurative  meningitis  which 
have  been  published  during  the  past  few  years,  and  in  which  a  pseudo- 
typhoid  bacillus  was  incriminated,  are  due  to  the  Bacillus  coli  (Chante- 
messe,  Widal  and  Legry). 

Conclusions. — I  have  just  reviewed  the  principal  forms  of  nob-tubercular 
meningitis  ;  this  question  is  stih  under  discussion.  In  many  cases  non- 
tubercular  meningitis  shows  all  the  symptoms  described  under  tubercular 
meningitis.  On  what,  then,  are  we  to  base  the  diagnosis  ?  Non-tubercular 
meningitis  generally  differs  from  tubercular  meningitis  in  the  absence  of  a 
prodromal  period,  which  is  especially  met  with  in  children.  Furthermore, 
in  young  children  with  tubercular  meningitis  or  with  latent  tuberculosis. 


1444  TEXT-BOOK  OF  MEDICINE 

it  is  very  rare  not  to  find  enlargement  of  the  inguinal,  axillary,  cervical,  or 
submaxillary  glands.  The  diagnosis  of  the  pathogenic  agents  is  simplified 
by  lumbar  puncture,  which  allows  bacteriological  examination  of  the  liquid. 
The  method  will  be  described  under  Cerebro- spinal  Meningitis.  We  must 
not  forget  that  early  hereditary  syphilis  may  reveal  itself  by  symptoms  of 
meningitis  which  yield  to  specific  treatment. 


XVI.  CEKEBRO-SPINAL  MENINGITIS. 

History. — I  have  devoted  two  clinical  lectures*  to  cerebro -spinal  meningitis,  and  I 
shall  make  use  of  them  in  this  section. 

In  1837  a  severe  epidemic  of  cerebro -spinal  meningitis  broke  out  at  Bayonne  and 
in  the  department  of  the  Landes.  Two  regiments  paid  a  heavy  tribute  to  the  disease. 
The  reoiments  were  removed  from  their  initial  station,  but  in  their  changes  of  quarters 
they  transported  the  disease  wth  them,  and  sowed  it  as  they  went.  Epidemics  then 
broke  out  in  Perigueux,  Auch,  Rochefort,  Versailles,  Metz,  Strasbourg,  etc.— so  much 
so  that  during  a  period  of  four  years  many  garrisons  were  afflicted  by  the  scourge. 
Furthermore,  the  26th  Regiment,  which  embarked  at  Port  Venclres,  took  meningitis 
to  Constantine.  Fi'om  this  period  originate  the  remarkable  works  of  Lalanne,  Forget, 
Tourdes,  etc.,  to  which  pubHcations  from  abroad  weie  added,  because  cerebro-spinal 
meningitis  made  its  appearance  in  several  European  countries. 

Since  then  the  clinical  and  pathological  history  of  cerebro-spinal  meningitis  has  been 
written.  We  must  notice,  in  fact,  the  scrupulous  exactness  with  which  our  predecessors 
described  cerebro-spinal  meningitis  :  fulminant  forms  which  kill  in  twelve  hours  ;  slower 
forms  which  last  four  or  five  days  ;  drawn-out  forms,  with  or  without  remission,  which 
last  for  weeks ;  and  attenuated  forms.  They  have  left  us  an  almost  complete  picture 
of  the  disease  :  its  sudden  commencement  with  rigors,  fever,  terrible  headache,  vomiting, 
pains  and  contractures  in  the  muscles  of  the  nape  of  the  neck  and  of  the  back,  trismus 
and  opisthotonos,  contractures  and  convulsive  movements  of  the  Umbs,  ocular  troubles 
(strabismus  and  photophobia),  dehrium,  torpor,  somnolence,  and  coma.  They  noticed 
facial  herpes,  morbillous,  papular,  and  peteehial  eruptions.  Their  anatomo-patho- 
lo2;ical  description  is  as  complete  as  it  could  be  at  that  period :  dissemination  of  the 
lesions  throughout  the  cerebro-spinal  axis ;  turbid  and  sero-puruelnt  fluid ;  purulent 
tracts,  thin  or  tliick,  and  discrete  or  confluent,  spread  unequally  over  the  surface  of  the 
brain  and  of  the  spinal  cord,  etc. 

Relying  on  these  descriptions,  it  seemed  that  the  morbid  entity  of  cerebro-spinal 
meningitis  was  definitely  settled.  Many  points  were,  however,  still  obscure,  and  the 
pathogenic  agent  had  to  be  discovered.  This  want  has  been  supphed.  The  researches 
of  the  past  few  years  have  completed  the  chnical  picture  of  the  disease,  and  bacteriology 
has  revealed  the  nature  of  the  micro-organisms.  The  discovery  of  the  meningococcus 
{Diplococais  intracellularis  meningitidis),  made  by  Weichselbaum  in  1887,  seemed  to 
settle  the  specific  nature  of  cerebro-spinal  meningitis,  just  as  the  discovery  of  Eberth's 
baciUus  settled  the  specific  nature  of  typhoid  fever  ;  but,  whereas  typhoid  fever  is  a 
morbid  entity,  due  solely  to  Eberth's  bacillus,  cerebro-spinal  meningitis  is  not  a  clearly- 
defined  morbid  entity.  In  other  words,  there  is  no  such  thing  as  "a  cerebro-spinal 
memngitis  "  due  to  Weichselbaum's  meningococcus ;  there  are  pneumococcal,  strepto- 
coccal,''staphylococcal  forms  of  cerebro-spinal  meningitis,  and  also  cases  due  to  Koch's 
bacillus,  to  mixed  infections,  including  Eberth's  bacillus,  etc. 


*  CUnique  Medicak  de  VEotd-Dieu,  1899,  16^  et  17^  legons. 


DI8I<:A.SK8  of  TlliO  BKAIN  1445 

Fioin  tlio  j)iilli(i;:fiiii'  piiiiit  of  viow  it  is  HJiflicicut  if  tli«j  micro  orj^.viiisiu  (ijnuingo- 
coccus  or  other  iiiicrobo),  mulowod  with  siilliciont  viruicnc(',  inviulcB  tlio  corohro-Hpiiml 
avis,  luul  by  ditTusion  produces  the  lesions  and  tho  compiicutioiis  of  corobro-Hpinul 
uieniniiilis.  The  pneumococcal,  stroptocoecal,  stapliylocoecal  forms  of  corobro-Bpinai 
monin^'itis  are  clinically  identical  \vith  tho  meningococcal  form  ;  thoy  may  have  tho  sumo 
onset,  the  same  syiuptoms,  tho  same  course,  and  tho  same  termination  by  dea^h  or  by 
recoveiy. 

From  the  setiologioal  point  of  viow  cerobro-spinal  meningitis  may  bo  primary  or 
secondary' — primary,  as  is  customary  during  an  epidemic,  when  tho  patient  iias  pre- 
viously showTi  no  pathological  defect  capable  of  being  the  starting-point  of  the  infection  ; 
secondary  when  the  patient,  by  reason  of  some  pathological  defect,  such  as  otitis, 
pneumonia.  Pott's  disease,  etc.,  presents  an  opening  for  the  inf(;ctious  agent. 

Clinical  Cases.— A  healthy  man,  thirty  years  of  age,  was  suddenly  taken  ill  on 
Wednesday  with  rigors  and  profuse  cpistaxis.  At  the  same  time  the  headache  rendered 
sleep  impossible.  Next  day  fresh  epistaxis,  fever,  and  continuous  headache.  On 
Thursday  night  diarrho-a,  persistence  of  tho  fever  and  of  the  headache.  The  onset 
thus  far  resembled  that  of  typhoid  fever.  On  Friday  morning  the  man  was  admitted 
to  my  wards,  and  whilst  he  was  being  undressed  he  was  seized  with  vomiting,  and 
brought  up,  without  any  effort,  greenish  fluid.  The  respiration  was  normal,  the  pulse 
was  100,  and  the  temperature  102°  F.  During  the  day  tho  patient  complained  of 
violent  headache,  and  frequently  carried  his  hand  to  his  forehead,  crying :  "  ^ly  head, 
my  head  !"  There  was,  however,  no  photophobia,  and  pressure  on  the  eyeballs  did  not 
cause  pain.  The  intelligence  was  intact,  and  the  patient  rephed  clearly  to  questions, 
but  he  was  so  fatigued  that  the  examination  had  to  be  stopped  repeatedly. 

The  left  tonsil  was  enlarged  and  covered  with  a  pulpy  exudate.  The  heart  and  the 
limgs  were  normal.  The  belly  was  not  painful ;  it  was  neither  tympanitic  nor  re- 
tracted. On  the  outer  and  back  part  of  the  thighs  there  was  an  erythematous  eruption, 
formed  of  non-proniinent  rosy  patches,  which  almost  disappeared  on  pressure.  During 
the  day  this  eruption  spread  over  the  whole  body,  the  head  excepted.  The  headache, 
the  epistaxis,  and  the  diarrhoea  at  the  onset  were  rather  in  favour  of  typhoid  fever. 
On  the  other  hand,  the  greenish  vomit  and  the  terrible  headache  on  his  admission  were 
in  favour  of  meningitis.  It  was  true  that  several  meningitic  symptoms — photophobia, 
pain  in  the  back  of  the  neck,  and  muscular  contractiu'es — ■n'ere  for  the  moment  absent. 

On  Saturday  morning  I  found  the  patient  lying  in  the  position  called  chicn  de 
fusil.  The  pains  in  the  head  had  lasted  all  night,  the  deUrium  had  been  violent,  the 
muscles  of  the  nape  of  the  neck  and  of  the  vertebral  column  were  contracted,  the 
photophobia  was  intense,  the  belly  was  sliglitly  retracted,  constipation  had  taken  the 
place  of  the  dian'hoea,  and  Kemig's  sign  was  present.  Although  tubercular  meningitis 
may  in  the  adult  assume  the  most  varied  forms,  as  Chantemesse  has  sho\\'n,  we 
could  hardly  admit  the  hypothesis  of  a  tubercular  lesion.  Griffon  obtained  by 
lumbar  pimcture  3  c.c.  of  turbid  cerebro -spinal  fluid,  which  became  clear  on 
standing  and  formed  a  deposit  in  the  tube.  This  puncture  caused  transient  im- 
provement. The  cyanotic  tint  disappeared,  the  respiration  improved,  and  the  paralysis 
of  the  limbs  became  less  complete.  The  coma,  nevertheless,  persisted,  and  death 
occmTed  on  the  fifth  day.  The  autoi)sy  confirmed  the  diagnosis  of  cerebro-spinal 
meningitis  and  revealed  the  following  lesions  :  the  lower  lobe  of  the  right  limg  was  much 
congested;  it  was  not  granular  on  section,  and  the  tissue  was  only  shghtly  friable  and 
did  not  sink  in  water.  The  examination  of  the  brain  showed  neither  the  granulations 
of  tubercular  meningitis  nor  the  tliick  and  purulent  exudate  of  pneumococcal  menin- 
gitis. At  the  junction  of  the  vessels  we  found  some  tracts  of  pus  so  firm  that  It  was 
difficult  to  remove  sufficient  for  examination.  The  pus  was  more  abundant  in  the 
fissures  of  Sylvius  and  over  the  superior  vermis  of  the  brain.  In  the  cerebro-spinal  fluid 
Griffon  found  Weichselbaum's  meningococcus. 

n.  92 


1446  TEXT-BOOK  OF  MEDICINE 

Another  patient  was  admitted  to  the  same  ward  for  cerebrospinal  meningitis 
— on  a  Saturday  morning.  On  admission  he  sank  down  on  a  chair,  incapable 
of  replying  to  our  questions,  which  he  did  not  seem  to  understand.  The  pohceman 
who  brought  him  to  the  Hotel-Dieu  had  no  information  to  give.  He  had  been  found 
on  the  second  story  of  a  mansion,  which  he  had  entered  without  being  known.  The 
patient's  brother-in-law  could  not  teU  us  anytliing  except  that  the  patient,  who  some- 
times drank  to  excess,  had  been  in  good  health  during  the  previous  days,  and  that 
on  Saturday  morning  he  had  left  home  early  to  go  to  his  work. 

When  the  patient  was  put  to  bed,  he  turned  on  his  side,  his  legs  bent  in  the  so-caUed 
cMen  de  fusil  position.  The  mouth  was  slightly  drawn  to  the  left,  and  the  right 
half  of  the  face  was  immovable  and  paretic.  The  eyes  were  wide  open.  The  hands 
were  constantly  moving.  Pressure  on  the  eyebaU  produced  reflex  contraction  of  the 
jaws.  The  nape  of  the  neck  and  the  vertebral  region  were  rigid  and  contracted.  This 
rigidity  made  auscultation  difficult,  on  account  of  the  difficulty  in  moving  the  patient 
and  making  him  sit  up.  Kernig's  sign  was  present.  The  heart  and  the  lungs  appeared 
to  be  healthy ;  the  respiration  was  normal.  The  urine  contained  much  albumin,  but 
not  any  sugar.     The  fever  was  high — pulse  90,  temperature  102°  F. 

The  unconscious  patient  did  not  seem  to  be  suffering ;  he  had  no  photophobia  and 
did  not  carry  his  hand  to  his  head.  He  neither  groaned  nor  complained.  Nevertheless, 
in  spite  of  the  absence  of  pain,  the  rigidity  of  the  nape  of  the  neck  and  of  the  trunk, 
the  muscular  contractures,  Kernig's  sign,  the  rapid  and  febrile  onset  of  the  disease, 
and  the  prostration  of  the  patient,  led  me  to  diagnose  cerebro-spinal  meningitis. 

The  following  night  the  patient  became  dehrious  and  very  restless  ;  his  motions  were 
passed  under  him.  On  Sunday  morning,  the  second  day  of  the  disease,  the  contrac- 
ture was  still  more  pronounced.  The  tache  cerebrale  (Trousseau's  sign)  was  clear,  and 
the  patient  uttered  a  few  groans.  I  prescribed  antispasmodic  treatment,  as  well  as 
very  hot  baths  (102°  F.),  with  cold  compresses  to  the  head.  On  Monday  the  condition 
was  the  same — contractures,  plaintive  cries,  lateral  decubitus,  and  Kernig's  sign. 
Griffon  performed  lumbar  puncture,  and  withdrew  3  c.c.  of  cerebro-spinal  fluid.  In 
the  evening  an  epileptiform  attack  appeared. 

On  Tuesday,  the  fourth  day  of  the  disease,  the  body  was  stifE  and  so  contracted  that 
the  trunk  seemed  to  form  only  one  piece.  The  respiration  was  noisy  and  hurried — 
80  respirations  to  the  minute ;  pulse  112.  During  the  morning  there  was  a  fi'esh 
epileptiform  attack,  similar  to  that  of  the  previous  evening.  The  patient  died  about 
eight  o'clock  in  the  evening. 

The  post-mortem  examination  confirmed  the  diagnosis  of  cerebro-spinal  meningitis. 
On  examining  the  brain,  tracts  of  firm  pus  were  found  at  the  confluence  of  the  principal 
sulci.  The  exudate  was  firm  and  difficult  to  remove  ;  it  occupied  the  arachnoid  space 
and  was  plastered  over  the  brain.  Many  purulent  patches  were  found  on  the  inferior 
surface  of  the  cerebellum;  they  were  less  spread  out  and  more  consistent  over  the  anterior 
perforated  space.  Throughout  the  whole  length  of  the  spinal  cord  this  same  firm  pus 
covered  the  posterior  surface  of  the  spinal  cord.  The  cerebro-spinal  fluid  was  turbid 
and  scanty.  The  lungs  were  congested  at  their  bases.  The  spleen  was  enlarged. 
Nothing  was  noticeable  in  the  other  organs. 

The  cerebro-spinal  fluid,  which  was  very  turbid  at  the  time  of  its  evacuation,  grew 
clearer  on  standing,  and  deposited  a  shghtly  rose-coloured  coagulum.  The  microscopic 
examination  of  the  turbid  hquid  showed  numerous  polynuclear  leucocytes  and  meningo- 
cocci— some  intracellular,  others  encapsuled  and  extracellular  and  unstained  by  Gram, 
a  fact  which  ehminated  any  question  of  the  pneumococcus.  The  pus,  on  various 
media  (broth,  agar,  rabbit  serum,  jeUifiedox  serum),  gave  rise  to  colonies  of  Weichsel- 
baum's  meningococcus.  Some  blood  taken  during  life  by  an  aseptic  punctm-e  from 
a  vein,  and  sown  on  agar  and  rabbit  serum,  did  not  give  a  positive  culture  of  the 
meningococcus  ;  the  tubes  remained  sterile. 


DISEASKS  OK    11  IK  HKAiiN  1447 

III  conclusiitn,  tlioso  two  patients  succurabtnl  -the  formor  in  livt;  <layB,  tho  Utt«r  in 
thrti-  (lavH — to  fiassio  meningococcal  ccrdno-Hpinal  nn-ninj^itiH.  In  thoBe  caucH  it  waH 
not  a  quostjon  of  ciTobro-spinal  menini^ntis  conseciitivo  to  pic  (jxiHting  losionH,  such  aH 
pneumonia,  otitis,  etc.  Tho  cliaeas*-  hero  certainly  had  tlie  aj)f>earanco  of  primary 
eerobro-spina!  meningitis,  witli  its  microbe,  wliirh  is  oonsiderod  as  tho  specific  agent : 
Woicheelbaum's  meningococcus. 

If  we  were  to  rely  only  on  this  type  of  cerehro-spinal  rneningitw,  we  might 
make  a  specific  disease  of  it,  having  its  own  pathogenic  agent.  But,  as  I 
have  said,  the  question  deserves  to  be  examined  from  another  aspect. 
Other  pathogenic  agents — pneumococcus,  streptococcus,  staphylococcus, 
etc.— \ntli  or  without  pre-existing  organic  lesions,  may,  in  times  of  an 
epidemic  or  not,  cause  the  complete  syndrome  of  cerebro-spinal  meningitis. 

I  shall  first  describe  cerebro-spinal  meningitis  consecutive  to  pneumonia. 
We  know  that  in  many  cases  the  pneumococcal  infection  does  not  remain 
limited  to  the  lung.  It  is  not  rare  to  find  otitis,  endocarditis,  pericarditis, 
or  meningitis  in  patients  suffering  from  pneumonia.  In  the  case  of  menin- 
geal complications  the  cerebral  meninges  are  generally  affected.  Sometimes, 
however,  the  pneumococcal  infection  spreads  to  the  spinal  meninges,  and 
gives  rise  to  cerebro-spinal  meningitis.  The  following  case  was  published 
by  Rendu : 

In  a  certain  family  three  little  girls  were  successively  attacked.  One  of  the  sisters 
was  taken  ill  with  a  rigor,  temperature  of  104*^  F.,  intense  angina,  otitis,  and  perforation 
of  the  tympanum.  A  week  later  the  elder  sister  was  taken  with  severe  apical  pneu- 
monia, which  ran  a  regular  course,  the  crisis  occurring  on  the  seventh  day.  The  third 
sister,  a  Httle  girl  of  five  years  of  age,  was  taken  ill  dm-ing  the  night  of  February  18 
with  a  violent  rigor,  high  fever,  restlessness,  and  delirium.  Rendu,  thinking  that  the 
delirium  was  pneumonic,  placed  the  child  in  a  bath  at  90°  F.,  and  prescribed  an  enema 
of  antipyrine.  On  Monday  the  situation  remained  about  the  same.  On  Tuesday, 
February  21,  the  third  day  of  the  disease,  auscultation  revealed  for  the  first  time  some 
signs  of  pneumonia.  On  Wednesday  the  signs  of  pneumonia  were  evident.  The  child 
was  restless  and  deUrious  ;  the  respiration -rate  was  60. 

On  Saturday,  the  seventh  day  of  the  pneumonia,  the  crisis  showed  itself,  but,  con- 
trary tb  expectation,  a  sudden  change  took  place.  On  Sunday  morning,  February  25, 
the  temperattu:e  rose  to  104°  F.  ;  the  pulse  was  140.  The  pupils  were  widely  dilated, 
and  the  jaws  were  fixed ;  the  head  was  retracted.  The  nuchal  muscles  were  con- 
tracted. The  upper  Umbs  were  rigid,  and  it  was  almost  impossible  to  flex  them.  The 
thighs  were  flexed  on  the  pelvis ;  Kemig's  sign  was  evident.  The  legs  were  reachly 
extended  when  the  child  was  lying  down,  but  •with  difficulty  when  she  was  seated. 
Ikloreover,  the  sitting  position  was  very  difficult  on  accoimt  of  the  opisthotonos.  It 
was  noticed  that  the  tubular  breathing  had  reappeared,  the  pneumonia  having  imder- 
gone  a  recrudescence  when  the  cerebro-spinal  meningitis  declared  itself.  In  three  days 
the  signs  of  cerebro-spinal  meningitis  reached  their  maximiim,  and  the  prognosis  was 
most  grave.  The  child,  who  was  unconscious,  could  neither  see  nor  hear.  The  rigidity 
of  the  nape  of  the  neck  became  more  marked  ;  the  contracture  of  the  Umbs  was  per- 
manent ;  the  passage  ot  urine  was  involuntar\' ;  the  fever  was  high,  and  the  pulse  was 
140.  Boils  covered  the  occipital  region,  and  a  fairly  large  bedsore  appeared  over  the 
buttocks. 

On  Thursday,  the  fifth  day  of  the  meningitis,  the  meningeal  symptoms  improved. 
On  Friday  the  pneumonia  entered  the  defervescent  stage.     On  Simday,  the  fifteenth 

92—2 


1448  TEXT-BOOK  OF  MEDICINE 

day  of  the  disease,  the  rigidity  of  the  najie  of  the  neck  had  disappeared.  The  contracture 
was  no  longer  present  in  the  right  arm,  but  it  persisted  in  the  left  arm  aud  in  the  lower 
limbs.     These  symptoms  gradually  disappeared,  and  recovery  followed. 

I  quote  two  fatal  cases  of  the  same  kind,  also  from  Rendu  : 

A  man  was  admitted  into  hospital  with  symptoms  of  adynamic  pneumonia.  After 
an  incomplete  crisis,  he  was  taken  ill  on  the  twelfth  day  with  dehrium  and  con- 
tracture of  the  nape  of  the  neck.  He  succumbed  in  forty-eight  hours,  and  the  post- 
mortem examination  revealed  suppurative  cerebro-spinal  meningitis.  The  pneumo- 
coccus  was  the  cause.  The  second  case  refers  to  a  man  admitted  into  hospital 
with  severe  pneumonia.  Contrary  to  aU  expectation,  the  pulmonary  comphcations 
improved,  and  the  crisis  was  normal.  After  the  temperature  had  been  normal  for 
six  days,  the  fever  reappeared,  and  lasted  for  a  week  without  definite  local  symptoms. 
The  patient  then  had  an  apoplectiform  attack,  with  rigidity  of  the  nape  of  the  neck, 
contraction  of  the  pupils,  and  coma.  Death  supervened  in  thirty-six  hours.  The 
autopsy  showed  cerebro-spinal  meningitis.  The  brain,  the  balb,  and  the  spinal  cord  were 
covered  with  purulent  exudate.  The  bacteriological  examination  showed  a  pneumo- 
coccal infection. 

These  cases  prove  beyond  a  doubt  that  cerebro-spinal  meningitis  may 
supervene  with  aU  the  classic  symptoms  during  the  course  of  pneumonia,  or 
after  the  crisis,  when  the  patient  is  on  the  high-road  to  convalescence.  The 
pneumococcus  is  the,  pathogenic  agent.  Up  to  what  point  can  epidemic 
influence  be  invoked  here  ?  I  do  not  Imow.  One  thing  is  certain — viz., 
that,  in  the  cases  just  quoted,  the  cerebro-spinal  meningitis  was  consecu- 
tive to  pneumonia,  and  it  is  probable  that  it  would  not  have  appeared  if 
pneumonia  had  not  been  present. 

Let  us  now  study  the  relations  which  may  exist  between  suppurative 
otitis  media  and  cerebro-spinal  meningitis.  Abscesses  of  the  cerebrum 
and  of  the  cerebellum,  phlebitis  of  the  sinuses  and  cerebral  meningitis,  may 
follow  on  otitis,  whether  it  is  in  active  progress  or  apparently  cured.  This 
question  is  discussed  in  detail  under  Abscesses  of  the  Cerebellum.  Besides 
these  complications,  however,  otitis  may  be  the  starting-point  of  cerebro- 
spinal meningitis, 

A  youth,  nineteen  years  of  age,  was  admitted  into  Rendu's  ward  on  the  fourth 
day  of  an  acute  infectious  disease  of  an  ataxo -adynamic  nature.  The  patient,  whilst 
in  a  state  of  good  health,  had  been  taken  Ol  with  lassitude  and  heaviness  in  the  head. 
On  the  third  day  he  had  epistaxis,  pains  in  the  nape  of  the  neck,  and  headache,  followed 
by  insomnia  and  delirium.  On  his  admission,  the  patient  seemed  to  be  suffering 
from  severe  ataxo-adynamic  typhoid  fever.  The  tongue  was  dry,  the  nostrils  were 
caked,  the  hps  were  covered  with  sordes,  and  the  breath  was  fcstid.  The  motions 
were  serous,  abundant,  and  passed  imder  him.  The  belly  was  shghtly  distended, 
and  the  ileo-csecal  gurgling  very  clear.  No  rose  spots  were  noticed,  which  is  not  sur- 
prising on  the  fifth  day  of  the  disease.  The  spleen  was  enlarged,  and  showed  a  dullness 
of  5  inches.  The  urine  was  scanty,  turbid,  and  albuminous.  The  limgs  were  abso- 
lutely normal.  The  thermometer  registered  105°  F.,  and  the  pulse-rate  varied  between 
120  and  130. 

The  chief  symptoms  were  cerebral.  The  patient  was  in  a  condition  of  stupor, 
having  restless  dreams  and  uttering  incoherent  words.     It  was  hardly  possible  to  rouse 


DISEASES  OF  THE  BRAIN  1449 

hiiM  finin  his  cnnflition  of  somnoliiicd  \>y  (juostioning  liiiii.  Id-  siimcd,  hcsidcs,  to  ho 
rather  (k-af.  This  (loafiu'sa,  as  wo  foiirul  out,  aroso  from  a  forinor  otilis  of  tho  right 
ear,  an  otitis  wliich  socinucl  to  bo  cxLiiict,  bocauso  there  was  no  a<;tual  running  fn^m  tho 
oar.  Tho  pationt  coinphiincd  chiefly  of  licadatlu!.  Tho  niovfniontM  of  llie  licid  and 
of  (he  nerk  wcn>  very  painful.  Tho  act  of  sitting  him  up  for  ausfultation  cauH«»d  hini 
to  complain,  anil  he  instinctively  kept  his  head  fixed,  without  daring  to  touch  or 
move  it. 

These  symptoms  led  Rendu  to  think  of  typhoid  fever  of  the  cerebral  form.  Some 
blood  was  romovod  to  examine  for  Widal's  reaction.  Before  the  result  was 
knowTi  the  disorder  suddenly  entered  on  a  new  phase,  which  proved  tho  diagnosis 
of  cerehro-spinal  meningitis.  The  patient  took  on  a  marked  cerebral  look  ;  his  physiog- 
nomy was  expressionless  ;  the  right  pupil  was  contracted,  tho  left  one  was  dilated  ;  the 
belly  was  retracted.  Large  cyanotic  patches  appeared  on  tho  skin  of  tho  Umbs  and  of 
the  abdomen.  The  patient,  instead  of  being  stretched  on  his  bed,  lay  bent  in  the 
chien  de  fusil  position,  the  knees  and  the  thighs  flexed  on  the  abdomen.  The  nape  of 
the  neck  was  more  rigid  than  during  the  previous  days,  and  opisthotonos  was  present. 
Straightening  of  the  legs  was  painful.  Kemig's  sign  was  manifest.  The  patient 
remained  dehrious,  and  mumbled  incoherent  words.  No  convulsions,  no  paraly.si3, 
no  Jacksonian  epilepsy.  The  urine  was  passed  involimtarily.  Tho  respiration 
assumed  the  bulbar  type.     The  patient  died  on  the  ninth  day  of  the  disease 

At  the  post-mortem  examination  the  lesions  confirmed  the  diagnosis  of  cerebro- 
spinal meningitis.  Under  the  pia  mater,  over  the  surface  of  the  hemispheres,  there 
was  thick  purulent  exudate,  which  occupied  the  frontal  region,  the  interhemispherical 
fissure,  and  the  Sylvian  fissures,  follo^ving  the  anatomical  distribution  of  the  middle 
and  anterior  cerebral  arteries  on  each  side.  Similar  but  less  confluent  exudate  was 
seen  on  the  upper  surface  of  the  cerebellum,  in  the  anterior  subarachnoidal  space,  on 
the  optic  chiasma,  and  on  the  anterior  surface  of  the  bulb  and  of  the  pons.  These 
exudates  were  of  a  yellowish  colour,  and  not  as  green  as  the  pus  of  pneumococcal 
meningitis.  They  resembled  butter  or  cooked  albumin ;  in  some  places  thev 
were  ^  centimetre  in  thickness.  Their  consistency  was  elastic,  and  they  did  not 
tear  to  pieces.  The  cerebro-spinal  fluid  was  turbid  and  moderate  in  amount.  The 
convolutions  were  fairly  difficult  to  decorticate,  adhering  to  the  pia  mater,  from  which 
they  could  not  be  separated  without  leaving  behind  some  brain  tissue.  They  were 
injected,  and  manifestly  hypersemic,  but  not  softened. 

In  the  spinal  cord  the  lesions  were  less  confluent.  A  fibrino-purulent  exudate  formed 
a  continuous  layer  under  the  pia  mater  of  the  posterior  spinal  region  from  the  bulb  to 
the  Cauda  equina.  The  arachnoid  was  distended,  and  at  the  lumbar  sweUing  it  was 
easy  to  collect,  before  the  removal  of  the  meninges,  a  considerable  amount  of  pus  in 
sterihzed  pipettes  for  subsequent  bacteriological  examination.  The  other  organs 
presented  some  accessory  lesions,  pointing  to  the  presence  of  an  infectious  agent. 
The  liver  was  enlarged,  soft,  and  yellowish-brown  ;  the  kidneys  were  fatty  ;  the  spleen 
was  enlarged  and  soft.  The  aUmentary  canal  showed  no  ulcerations  and  no  folhculitis — 
in  a  word,  not  one  of  the  lesions  of  typhoid  fever. 

The  right  ear  contained  some  muco-purulent  exudate.  Therefore,  it  is  probable  that 
the  otitis  was  the  starting-point  of  the  cerebro-spinal  infection.  Bacteriological  examina- 
tion of  the  pus  showed  the  presence  of  the  streptococcus. 

This  case  is  a  type  of  streptococcal  cerebro-spinal  meniagitis,  consequent  on  a 
partially  extinct,  but  still  virulent,  focus  of  otitis  media.  The  signs  and  symptoms 
observed  in  the  course  of  this  case  are  quite  comparable  with  those  of  epidemic  or  non- 
epidemic  meningococcal  cerebro-spinal  meningitis. 

Netter,  at  the  Societe  Medicale  des  Hopitaux,  showed  the  anatomical 
specimens  from  a  child  in  Josias's  ward,  which  proved  that,  in  this  child, 


1450  TEXT-BOOK  OF  MEDICINE 

suppurating  otitis  had  been  the  entrance  gateway  of  the  cerebro-spinal 
infection. 

Traumatism  may  cause  cerebro-spinal  meningitis,  having  the  classical 
signs  and  symptoms  of  epidemic  cerebro-spinal  meningitis.     As  an  example  : 

Stadelmann  saw  a  man  who,  several  weeks  after  a  severe  injiiry  to  the  skull,  was 
seized  with  symptoms  of  cerebro-spinal  meningitis  :  rigors,  headache,  vomiting,  rigidity 
of  the  nape  of  the  neck,  convulsions,  and  obnubilation.  laimbar  puncture  gave  issue 
to  50  grammes  of  a  purulent  liquid.  A  second  puncture,  a  few  days  later,  gave  issue 
to  15  grammes  of  similar  hquid.  In  spite  of  the  punctures  the  muscular  spasms  became 
general.  A  third  puncture  was  made,  and  15  grammes  of  less  turbid  hquid  were  with- 
drawn. After  various  ups  and  downs  improvement  supervened.  A  fourth  puncture 
yielded  only  5  grammes  of  hmpid  fluid.  The  bacteriological  examination  of  the  spinal 
fluid  revealed  the  presence  of  large  and  very  mobile  bacteria. 

With  regard  to  Stadelmann's  case,  Frankel  states  that  he  has  seen  a  boy 
of  six  years  of  age  in  whom  meningococcal  cerebro-spinal  meningitis  imme- 
diately followed  on  an  injury.  In  order  to  explain  the  pathogenesis,  Frankel 
admits  that  the  meningococcus,  which  was  present  in  the  upper  air  passages, 
had  emigrated  after  the  injury  into  the  cranial  cavities.  Whatever  may  be 
the  explanation  of  these  facts,  and  whatever  opinion  may  be  adopted  with 
regard  to  the  migration  and  the  exaltation  of  virulence  of  the  pathogenic 
microbes,  it  is  none  the  less  true  that,  clinically,  we  may  see  cerebro-spinal 
meningitis  following  on  traumatism. 

Guibal  has  published  a  case  of  streptococcal  and  staphylococcal  cerebro- 
spinal meningitis  following  on  Pott's  Disease  : 

A  httie  girl  had  dorsal  curvature,  with  spasmodic  paraplegia  and  paralysis  of  the 
sphincters.  One  day  the  child  was  taken  ill  with  high  fever,  vomiting,  headache,  and 
general  hypersesthesia.  The  belly  was  hard  and  retracted.  During  the  next  few  days, 
rigidity  of  the  nape  of  the  neck,  paralysis  of  the  left  half  of  the  face  and  of  the  left  arm, 
somnolence  and  coma,  terminating  in  death.  At  the  autopsy  pm-ulent  cerebro-spinal 
meningitis  was  discovered.  The  bacteriological  investigations  revealed  the  presence 
of  the  streptococcus  and  of  the  staphylococcus.  It  is  probable  that  the  infection  was 
due  to  a  fistulous  abscess  in  contact  with  the  spinal  dura  mater. 

Pneumococcal,  streptococcal,  and  staphylococcal  cerebro-spinal  menin- 
gitis are  not  only  secondary  to  pre-existing  lesions  (pneumonia,  otitis,  osseous 
suppurations,  etc.) ;  they  may  be  primary,  like  meningococcal  meningitis. 
As  an  example  : 

A  child  of  eleven  years  of  age  was  admitted  into  Josias's  ward  with  pains  in  the 
head ;  fever,  and  constipation.  During  the  following  days  fresh  symptoms  appeared  : 
vomiting,  pains  in  the  nape  of  the  neck,  paralysis  of  the  limbs  on  the  right  side,  and 
inferior  facial  paralysis.  These  symptoms  were  followed  by  rigidity  of  the  nape  of  the 
neck  and  of  the  trunk  (opisthotonos),  by  convergent  strabismus,  and  by  retention  of 
urine.  An  erui)tion  of  herpes  was  noticed  around  the  hps.  The  patient  grew  emaciated, 
and  the  eyes  became  hollow.  Netter  made  a  lumbar  puncture,  and  obtained  some 
purulent  hquid.  The  child  died  in  coma.  At  the  post-mortem  examination  the  case 
was  foimd  to  be  one  of  cerebro-spinal  meningitis.     The   bacteriological  examination 


DISEASES  OF  THE  BRAIN  1451 

was  carried  out  by  Netter.  "Tho  culture,  on  various  media  (broth,  agar,  soriira,  and 
gelatine),  ruvoaled  tho  Sta'phylococcus  pyogenes  mire  us  in  a  furuJidon  of  jmrity,  witli  itH 
normal  chiinu-torH. 

At  the  siime  meeting  of  the  Societe  Medicale  des  Hopitaux  Antony 
reported  two  cases  of  cerebro-spinal  meningitis,  caused  by  the  Staphylococcits 
aureus,  "  tlioiigh  it  was  impossible  to  find  on  the  patient  a  suppurating  spot 
which  might  have  been  considered  the  origin  of  the  infection."  It  was, 
then,  a  case,  like  the  cases  of  Netter  and  Josias,  of  primary  staphylococcal 
c«'.rel)r(>-s]unal  meningitis. 

iflEtiology — Pathogenesis. — In  its  epidemic  form  cerebro-spinal  menin- 
gitis affects  the  military  more  than  the  civil  population.  It  may  be  imported, 
and  it  is  contagious.  The  history  of  former  epidemics  shows  that  it  changed 
its  quarters  with  our  regiments  in  Rome,  in  Algeria,  etc.  The  epidemics 
develop  gradually,  attacking,  first,  a  certain  barracks,  a  few  houses,  or  a 
certain  quarter,  "  the  third  storey  of  the  North  building  and  the  second 
storey  of  the  South  Block  "  (Lemoine),  and  radiating  thence  in  the  shape  of 
secondary  foci. 

It  is  an  important  fact  that  epidemic  cerebro-spinal  meningitis  is 
often  associated  with  some  other  epidemic  disease.  Thus,  in  1848,  Michel 
Levy  noticed  the  coexistence  of  meningitis  and  influenza  ;  in  the  Rastadt 
epidemic  of  1864  meningitis  coexisted  with  typhoid  fever  ;  its  coexistence 
has  been  noted  with  typhus  (Boudin),  with  mumps  (Massonaud),  with 
measles  (Vallin),  and  with  scarlatina  (Laveran).  Lemoine's  monograph 
dealing  with  the  subject  is  most  interesting.  In  the  epidemic  which  he  ob- 
served at  Orleans,  in  1886,  ceret)ro-spinal  meningitis  appeared  at  the  same 
time  as  a  double  epidemic  of  scarlatina  and  pneumonia.  The  patients 
suffering  from  meningitis  suffered  from  throat  troubles,  recaUmg  scarlatina, 
and  at  the  post-mortem  examination  of  the  patients  in  whom  the  meningitis 
proved  fatal  (in  the  proportion  of  50  per  cent.)  the  pneumococcus  was 
found. 

During  a  slight  epidemic  in  Paris,  in  twenty-one  cases  of  cerebro-spinal 
meningitis  observed  in  1899,  Netter's  figures  are  as  follows  :  Seven  cases,  the 
pneumococcus ;  six  cases,  Weichselbaum's  diplococcus  (meningococcus)  ; 
four  cases,  a  streptococcus  ;  three  cases,  the  streptococcus  pyogenes  ;  one 
case,  a  staphylococcus.  If  we  also  add  cases  of  cerebro-spinal  meningitis, 
due  to  Koch's  bacillus,  to  Eberth's  bacillus,  and  to  associated  infections,  it 
is  clear  that  the  question  is  singularly  broadened. 

This  proves,  then,  as  I  remarked  at  the  commencement  of  this  section, 
that  cerebro-spinal  meningitis  does  not  form  a  definite  morbid  entity.  It 
must  be  divided  into  several  varieties.  In  one  of  its  varieties,  the  most 
important  one,  especially  in  time  of  an  epidemic,  Weichselbaum's  meningo- 
coccus appears  to  be  the  specific  agent,  as  was  the  case  in  two  of  my  patients. 


1452  TEXT-BOOK  OF  MEDICINE 

In  the  other  varieties,  leaving  epidemics  out  of  the  question,  the  lesions  and 
symptoms  are  dependent  on  various  micro-organisms — pneumococcus, 
streptococcus,  staphylococcus,  Koch's  bacillus,  Eberth's  bacillus,  etc. 
Several  varieties  of  cerebro-spinal  meningitis  may  be  primary,  like  the 
meningococcal  type.  They  may  be  secondary — that  is  to  say,  dependent 
on  pre-existing  lesions.  Whatever  the  entrance-point  of  the  infective  agent, 
its  diffusion  to  the  cerebro-spinal  axis  causes  cerebro-spinal  meningitis.  A 
single  pathogenic  agent  may,  according  to  circumstances,  limit  its  action 
to  the  brain,  or  invade  the  entire  cerebro-spinal  axis.  A  single  pre-existing 
lesion  may  b(fe  the  origin  of  an  infection  which  limits  itself  to  the  brain,  or 
which  becomes  diffused  through  the  entire  cerebro-spinal  axis.  Thus,  side 
by  side  with  cases  in  which  suppurative  otitis  produces  only  cerebral  com- 
plications, there  are  others  in  which  it  causes  general  cerebro-spinal  infection. 
Side  by  side  with  cases  in  which  Pott's  disease  causes  only  spinal  complica- 
tions, there  are  others  in  which  it  is  the  origin  of  an  infection  of  the  entire 
cerebro-spinal  axis,  just  as  a  tubercular  lesion,  visible  or  latent,  sometimes 
causes  cerebral  meningitis.  At  other  times  tubercular  infection  of  the 
entire  cerebro-spinal  axis.  If,  however,  the  varieties  of  cerebro-spinal 
meningitis  are  distinct  as  to  their  pathogenesis,  it  may  be  said  that,  clinically, 
they  resemble  one  another — similar  symptoms,  similar  course,  fulminant, 
ambulatory,  rapid,  or  slow ;  similar  anomalies ;  similar  masked  or  attenuated 
forms. 

Description. — The  onset  of  cerebro-spinal  meningitis  is  generally  sudden 
and  febrile,  with  or  without  rigors.  There  are  few  or  no  prodromata. 
Patients  are  sometimes  attacked  in  the  midst  of  good  health.  An  individual 
who  was  in  excellent  health  on  the  previous  day  is  suddenly  struck  by  the 
disease,  especially  during  an  epidemic.  In  a  few  hours  the  temperature 
rises  to  104°  F.  Headache  is  almost  always  the  first  signal ;  it  may  be  either 
frontal  or  occipito-frontal,  and  dull  or  lancinating.  The  headache  becomes 
so  severe  as  to  provoke  the  hydrocephalic  cry.  The  patient  complains  of 
pains  in  the  nape  of  the  neck,  in  the  back,  in  the  limbs,  and  in  the  joints.  In 
some  cases  the  articular  pains  somewhat  resemble  those  of  acute  rheumatism. 

Vomiting  of  food  and  of  bile  generally  appears  during  the  first  stage  of 
meningitis  ;  the  attacks  follow  one  after  the  other,  and  the  fluid  is  brought 
up  without  effort.  Diarrhoea  is  exceptional,  constipation  being  the  rule  ; 
the  beUy  is  hard  and  retracted.  On  the  first  day  painful  contracture  of  the 
muscles  of  the  nape  of  the  neck,  with  retraction  of  the  head,  supervenes. 
"  This  cramp  in  the  nape  of  the  neck  "  is  rarely  absent.  It  was,  however, 
absent  in  some  of  Netter's  cases.  The  painful  contracture  likewise  attacks 
the  muscles  of  the  back,  and  the  trunk  is  bent  backwards  in  the  position  of 
opisthotonos.  The  painful  contractures  may  extend  to  the  muscles  of  the 
arms  and  of  the  legs. 


DISEASES  OF  TlfE  BRAIN  145.1 

From  the  commencement  of  the  disease,  or  during  the  first  few  days, 
paralysis  soinetiinos  supervenes  ;  hemiplej^ia  of  tli*^  face,  or  of  the  limbs, 
paralysis  af  the  muscles  of  the  eye  (strabisnms),  of  the  sphincters  (inconti- 
nence of  urine) ;  photophobia,  and  hyperesthesia  have  been  noted  in  several 
cases.  The  tache  cerebrale  (Trousseau's  sign)  is  easily  obtained.  Kernig's 
sign  is  almost  always  present. 

Sometimes,  in  the  first  phase  of  cerebro-spinal  meningitis,  the  patient, 
who  is  prostrated,  replies  with  difi&culty  to  the  questions  put  to  him.  He 
looks  like  a  patient  suffering  from  enteric  fever.  The  respiration  is  often 
panting,  irregular,  and  of  the  Cheyne-Stokes  type,  and  auscultation  is 
made  very  difficult,  because  the  rigidity  produced  by  the  contractures 
prevents  easy  movement  of  the  patient.  The  heart-beats  are  often  irregular. 
Erythematous  eruptions,  accompanied  at  times  by  purpura  and  by 
petechige,  are  seen  fairly  frequently.  Herpes  is  present  in  a  fair  number  of 
cases.     It  may  be  seen  on  the  lips,  on  the  tonsils,  and  on  the  trunk. 

The  symptoms  of  excitation  (deliriimi,  restlessness,  cries,  and  groans)  are 
often  followed  by  depression,  the  patient  remaining  in  the  dorsal  or  lateral 
decubitus  in  a  state  of  prostration  bordering  on  coma.  Cerebro-spinal 
meningitis,  though  very  grave,  sometimes  ends  in  recovery.  We  had  such 
a  case  at  the  Hotel-Dieu.  When  death  occurs  it  supervenes  on  coma,  as 
in  my  first  patient,  or  after  epileptiform  convulsions,  as  in  my  second  one. 

I  must  now  refer  to  "  Kernig's  sign,"  a  diagnostic  sign  of  the  first  im- 
portance, discovered  in  1882  by  Kernig,  and  studied  in  France  by  Netter. 
Kernig's  sign  is  as  follows  :  As  long  as  the  patient  is  in  the  dorsal  decubitus, 
his  legs  can  be  extended  and  can  be  kept  so,  without  meeting  any  muscular 
resistance.  If  the  patient  is  seated  (which  is  sometimes  difficult  on  account 
of  the  painful  rigidity  of  the  muscles  of  the  nape  of  the  neck  and  of  the  back), 
the  legs  are  at  once  flexed  on  the  thighs  and  the  thighs  on  the  trunk  ;  it 
is  a  contracture  of  flexion.  In  other  words,  the  patient,  whilst  seated,  by 
an  involuntary  movement,  draws  the  legs  and  the  thighs  towards  himself, 
and  the  knees  are  raised.  Firm  pressure  on  the  knees  is  required  to  over- 
come this  movement  and  to  keep  the  limbs  extended.  If  the  patient  is 
replaced  in  dorsal  decubitus,  the  contracture  of  flexion  ceases  immediately, 
and  the  legs  are  extended.  Although  we  are  unable  to  explain  the  mechan- 
ism of  this  sign,  it  certainly  indicates  the  participation  of  the  spinal 
meninges. 

Kernig's  sign  is  rarely  absent  in  cerebro-spinal  meningitis.  It  has  been 
verified  by  Bull  of  Christiania,  Henoch  of  Berlin,  Friis  of  Copenhagen, 
Widal,  and  Merklen.  Netter,  who  has  collected  their  papers,  met  with  it 
in  twenty-three  cases — epidemic  cerebro-spinal  meningitis  in  twelve  cases 
(six  in  the  stationary  stage),  four  defaced  forms  (two  on  the  road  to  conva- 
lescence), eight  cases  of  tubercular  meningitis,  three  cases  of  mixed  menin- 


1454  TEXT-BOOK  OF  MEDICINE 

gitis  (association  of  the  meningococcus  and  of  the  tubercle  bacillus). 
"  Kernig's  sign  persists  in  convalescents  for  a  longer  or  shorter  time.  Kemig 
and  Henoch  have  seen  it  after  two  months  and  a  half.  We  have  also  seen  it 
in  convalescent  or  cured  patients.  It,  therefore,  enables  a  retrospective 
diagnosis  to  be  made,  and  has  no  less  a  value  in  revealing  the  defaced  forms 
of  the  disease  "  (Netter). 

A  method  of  investigation  very  useful  in  the  diagnosis  of  cerebro-spinal 
meningitis  is  lumbar  puncture,  first  advised  by  Quincke,  and  employed  in 
France  by  Netter.  In  1890  Quincke  proposed  to  puncture  the  subarachnoid 
space  in  the  lower  portion  of  the  lumbar  column.  His  idea  was  to  diminish 
the  excess  of  tension  of  the  cerebro-spinal  fluid  by  giving  an  issue  to  the 
liquid  contained  in  the  large  subarachnoid  space  of  the  cauda  equina.  The 
therapeutic  value  of  lumbar  puncture  has  declined  to-day ;  not  so,  however, 
its  diagnostic  value. 

The  method  is  as  foUows  :  The  patient  is  placed  on  his  right  or  left  side. 
The  thighs  are  flexed  on  the  pelvis,  and  the  legs  are  flexed  on  the  thighs,  so 
as  to  separate  the  vertebral  laminae  to  theic  utmost.  The  landmarks  are 
as  foUows  :  First  the  base  of  the  sacrum,  then  the  space  between  the  fifth 
lumbar  and  the  first  sacral  vertebra  (the  selected  point  for  lumbo-sacral 
puncture  (Chipault),  which  is  preferable  to  Quincke's  true  lumbar  puncture), 
and,  finally,  the  spinous  process  of  the  fifth  lumbar  vertebra.  The  trocar,  or 
the  needle,  is  then  inserted  about  half  a  centimetre  external  to  the  median 
line  (Sicard).  The  depth  should  be  from  4  to  6  centimetres  in  the  adult,  and 
from  1  to  3  centimetres  in  a  child.  The  instrument  is  directed  forwards, 
slightly  upwards  and  inwards,  towards  the  median  line.  The  cerebro- 
spinal fluid  then  flows  out,  but  it  should  be  evacuated  slowly,  drop  by  drop. 
It  is  collected  in  sterilized  tubes,  centrifugalized,  and  examined  bacterio- 
logically.  The  amount  of  fluid  withdrawn  should  not  exceed  15  to 
20  grammes,  since  paralysis  and  death  may  result  from  the  removal  of  too 
much  fluid. 

The  liquid  may  be  limpid  or  turbid.  It  may  be  limpid  and  yet  contain 
micro-organisms.  When  the  liquid  is  turbid, -it  suffices  to  leave  it  standing 
in  the  tube,  and  it  becomes  clear,  whilst  a  small  clot  forms  at  the  bottom 
of  the  tube.  Cultures  made  with  the  fluid  obtained  by  puncture  enable  us 
to  ascertain  the  nature  of  the  pathogenic  microbes. 

In  short),  the  recent  study  of  cerebro-spinal  meningitis  has  been  enriched 
by  two  new  signs  :  Kernig's  sign,  and  lumbar  puncture  (Quincke),  which 
aUows  histological  and  bacteriological  examination  of  the  liquid.  These 
two  signs  are  of  supreme  importance  when  the  diagnosis  is  uncertain. 

Diagnosis. — The  diagnosis  of  cerebro-spinal  meningitis  is  at  times  very 
difficult.  In  fact,  this  disease  presents  many  points  of  analogy  with  influenza 
and  with  typhoid  fever  of  an  ataxo-adynamic  type.     In  other  cases,  rare 


DlSRASr:S  OF  TilK  BRAIN  1455 

it    is    trup,    till'    jniiit     tnMil)l»\s   are   of    unusual    iiii[)(»rtauc«?.      'I'i»    (juotf 
examples : 

A  nmn.  forly-fwo  yi^ars  of  ago,  who  had  previously  had  two  altat-kH  of  a<'ul<'  aiticiilar 
rhouinatiain,  was  admitted  under  (iailiard  for  very  sharp  pains  in  tho  luft  Racro-lumbar 
muscles  and  in  the  aacro-ihae  joint.  The  leiiiperaturo  was  close  on  104**  P.  The  case 
was  diagnosed  as  rhcnmatism  of  the  left  sacro-iliae  articulation.  There  was  no 
blenon-hagia.  SaUcylato  of  soda  was  prescribed.  Eight  days  later  symptoms  of 
meningitis  appeared  :  headache,  delirium,  strabismus,  and  rigidity  of  the  muscles  of 
the  nape  of  the  neck.  The  course  was  rapid,  and  the  patient  succumbed.  The 
post-mortem  examination  showed  tlio  case  to  bo  pneumococcal  meningitis.  Netter 
saw  a  patient  wlio,  during  the  course  of  c(!rebro-spiiial  meningitis,  had  pains  in  the 
right  elbow.  At  the  post-mortem  examination  a  turbid  hqiiid,  containing  the  meningo- 
coccus, was  witlldI•a^vn  from  the  joint.  In  one  of  Frentz's  patients  meningococci  were 
found  in  the  purulent  fluid  from  an  inflamed  ankle-joint.  In  the  recent  Bayonne 
epidemic  "  articular  complications  were  frequently  noted  "  (Oamiado). 

The  diagnosis  must  be  made  between  cerebro-spinal  meningitis  and 
certain  forms  of  influenza  of  an  ataxo-adynamic  type.  In  such  cases,  it  must 
be  admitted,  we  think  of  influenza  rather  than  of  meningitis.  Kernig's  sign 
and  lumbar  puncture  will  clear  up  the  diagnosis. 

Cerebro-spinal  meningitis  often  resembles  ataxo-adynamic  typhoid 
fever — headache,  photophobia,  restlessness,  delirium,  depression,  somno- 
lence, torpor,  coma,  are  all  symptoms  common  to  both  conditions — and  we 
have  to  decide  whether  the  patient  is  suffering  from  cerebro-spinal  menin- 
gitis of  a  typhoid  form  or  from  typhoid  fever  of  a  meningeal  type.  The 
duration  of  the  disease  is  of  value  in  diagnosis,  because  the  ataxo-adynamic 
symptoms  appear  much  earlier  in  meningitis  ;  furthermore,  they  are  accom- 
panied by  Kernig's  sign,  which  is  not  present  in  typhoid  fever.  Finally, 
Widal's  reaction  is  in  favour  of  typhoid  fever.  These  means,  to  which 
the  lumbar  puncture  may  be  added,  will  give  the  diagnosis.  We  must, 
however,  reckon  with  cases  in  which  the  sero- diagnosis  is  delayed  in  its 
appearance.  Account  must  also  be  taken  of  the  cases  in  which  meningitis 
supervenes  in  an  individual  who  has  had  t}^hoid  fever  and  whose  serum 
has  preserved  the  agglutinative  power.  Finally,  it  must  not  be  forgotten 
that  typhoid  fever  and  cerebro-spinal  meningitis  may  coexist  in  the  same 
patient. 

In  this  connection  the  foUowing  cases  are  instructive  : 

One  of  my  colleagues  was  taken  ill  with  symptoms  which  might  have  been  due  to 
influenza,  to  typhoid  fever,  or  to  meningitis.  After  an  indefinite  phase,  the  late  appear- 
ance of  rose-spots  and  sero-diagnosis  proved  the  presence  of  typhoid  fever,  but  the 
patient  also  had  symptoms  of  cerebro-spinal  meningitis,  including  Kernig's  sign.  I 
had  the  happiness  of  seeing  him  recover.  In  Ibis  case,  however,  must  we  admit  that 
Kernig's  sign  was  due  to  typhoid  fever  alone,  or  must  we  suppose  that  the  typhoid  fever 
was  comphcated  with  cerebro-spinal  meningitis  ?  This  latter  hypothesis  is  not 
admissible,  because  this  association  has  been  verified,  as  the  following  case  will 
prove. 


1456  TEXT-BOOK  OF  MEDICINE 

A  boy  was  admitted  under  Natter  with  the  symptoms  of  typhoid  fever  in  the  second 
week :  typhoid  look,  dry  tongue,  tympanitic  abdomen,  diarrhoea,  enlarged  spleen,  rose- 
spots,  sibilant  rales  in  both  lungs,  urine  albuminous  and  rich  in  indican,  and  temperature 
104°  F.  Widal's  reaction  gave  a  positive  result.  The  patient  showed  no  meningeal 
symptoms  (delirium,  painful  contractures,  paralysis,  and  convulsions  being  absent), 
and  yet  Kemig's  sign  was  present.  It  was  thought  that  Kemig's  sign  might  be  due  to 
the  typhoid  fever.  The  patient,  who  was  treated  with  cold  baths,  died  suddenly  after 
a  week's  treatment. 

The  post-mortem  examination  showed  the  lesions  of  tj^phoid  fever  :  intestinal  per- 
foration, ulcerations  of  Peyer's  patches,  softening  of,  the  mesenteric  glands,  swelHng 
of  the  spleen.  Cultures  revealed  the  presence  of  Eberth's  bacillus  in  the  spleen  and  in 
the  glands.  The  patient,  therefore,  had  had  typhoid  fever,  but  he  had  also  had  typhoid 
cerebro-spinal  meningitis.  Purident  tracts  were,  in  fact,  discovered  in  the  brain  and 
in  the  spinal  cord,  with  accumulation  of  serous  fluid  at  the  cauda  equina.  The  cultures 
showed  the  presence  of  Staphylococcus  pyogenes  aureus  at  these  points,  together  with 
Eberth's  bacillus.  The  presence  of  Kemig's  sign  was  thus  explained,  the  typhoid  fever 
having  caused  cerebro-spinal  meningitis. 

It  is  not  sufficient  to  diagnose  cerebro-spinal  meningitis  ;  we  must  also 
decide  whether  it  is,  or  is  not,  tubercular.  The  diagnosis  is  sometimes  beset 
with  difficulties,  but  it  is  of  great  importance,  because  tubercular  meningitis 
is  fatal,  whilst  the  non-tubercular  infections  are  fairly  often  curable.  If  we 
conffiie  ourselves  to  the  classical  descriptions,  the  difference  is  great  between 
tubercular  and  non-tubercular  meningitis.  The  former,  it  is  said,  is  generally 
preceded  by  prodromata,  whilst  the  other  forms  have  a  sudden  commence- 
ment. This  statement  is  generally  true.  There  are,  nevertheless,  cases 
(I  have  had  some  in  my  wards)  in  which  tubercular  meningitis  breaks  out 
suddenly,  and,  on  the  other  hand,  cases  have  been  cited  (Netter)  in  which 
non-tubercular  cerebro-spinal  meningitis  is  preceded  by  prodromata,  and  is 
characterized  by  several  outbursts,  with  periods  of  calm,  which  lead  to  the 
hope  of  recovery.  Non-tubercular  meningitis,  it  is  asserted,  is  often  limited 
to  the  convexity  of  the  brain,  and  causes  contractures,  paralyses,  and 
localized  convulsions,  which  show  the  nature  of  the  disease.  This  is  true, 
but  similar  localizations  (hemiplegia  of  the  face  or  of  a  limb — partial  epilepsy) 
exist  likewise  in  the  case  of  tubercular  meningitis. 

Kemig's  sign,  it  is  said,  does  not  occur  in  tubercular  meningitis  ;  this  is 
true  when  the  meningitis  is  purely  cerebral.  Marfan  told  me  that  in  two 
years  he  had  not  once  met  with  Kernig's  sign  in  young  children  with  cerebral 
tubercular  meningitis.  If,  however,  tubercular  meningitis  spreads  to  the 
spinal  meninges,  the  medullary  symptoms  are  added  to  the  cerebral  symp- 
toms, and  Kernig's  sign  appears  (Netter).  The  presence,  or  the  absence,  of 
Kernig's  sign  cannot,  therefore,  settle  the  question  as  to  whether  a  case  ol 
cerebro-spinal  meningitis  is,  or  is  not,  tubercular. 

It  has  been  thought  that  the  bacteriological  examination  of  the  nasal 
muco-pus  might  throw  Hght  on  the  diagnosis  in  difficult  cases.  Scherer, 
who  has  found  Weichselbaum's  diplococcus  in  eighteen  cases  of  epidemic 


DISEASES  OF  THE  BKAIN  U57 

cerebro-spinal  meningitis,  attributes  great  diagnostic  value  to  this  examina- 
tion. Tlu'  iiuj)ortance  of  this  fact  must  not  1)0  exa(i;j,'i'ruted,  first,  because 
cerebro-spinal  moningitis  may  be  produced  by  organisms  other  than  the 
meningococcus,  and,  secondly,  because  the  meningococcus  is  often  absent 
from  the  nasal  fossa^  in  meningococcal  meningitis.  It  is,  therefore,  not  the 
presence  or  the  absence  of  the  meningococcus  in  the  nasal  muco-pus  which 
will  prove  that  meningitis  is,  or  is  not,  tubercular. 

The  bacteriological  examination  of  the  blood  may  be  of  help  in  making 
a  diagnosis.  Netter  found  the  meningococcus  three  times  in  the  broth 
sown  with  blood  from  patients  with  cerebro-spinal  meningitis  ;  but  the 
absence  of  the  meningococcus  is  not  sufficient  to  prove  that  the  meningitis 
is  tubercular. 

These  methods  of  diagnosis  have  their  importance,  but  they  are  insuffi- 
cient, because  they  often  leave  us  undecided  as  to  the  tubercular  or  non- 
tubercular  nature  of  the  meningitis.  There  remains  lumbar  puncture.  The 
cerebro-spinal  fluid  obtained  by  lumbar  puncture  can  be  analysed  for  the 
pathogenic  agent,  either  by  direct  examination  or  by  culture.  \VTien  the 
presence  of  the  meningococcus,  of  the  pneumococcus,  or  of  the  streiDtococcus 
has  been  observed,  we  are  almost  certain  as  to  the  nature  of  the  disease — 
I  say  "  almost  "  certain  as  to  the  nature  of  the  disease,  but  not  quite,  because 
cerebro-spinal  meningitis  may  be  tubercular,  although  the  culture  remains 
sterile.  These  two  hypotheses  have  been  verified  by  Netter,  who,  in  ten 
cases  of  tubercular  meningitis  which  were  punctured  during  life,  found  that 
six  times  the  sown  liquid  remained  sterile,  and  that  three  times  staphylococci 
developed.  "  The  presence  of  these  latter  microbes,"  adds  Netter,  "  does 
not  exclude  the  diagnosis  of  tubercular  meningitis." 

The  presence  of  Koch's  bacillus  in  the  liquid  withdrawn  by  lumbar 
puncture  proves  the  tubercular  nature  of  the  meningitis.  In  seventy-ning 
cases  of  tubercular  meningitis  lumbar  puncture  showed  Koch's  bacilli  in  the 
cerebro-spinal  fluid  on  fifty-two  occasions  (Fiiibringer).  That  is  an  impor- 
tant result,  but  it  is  inconstant,  and,  consequently,  insufficient,  because, 
in  a  third  of  the  cases,  the  diagnosis  remained  doubtful. 

In  conclusion,  the  above  means  of  control  render  much  service,  but  they 
are  insufficient,  because  they  often  leave  a  doubt  as  to  the  tubercular,  or 
non-tubercular,  nature  of  the  meningitis.     Can  this  doubt  be  removed  ? 

Bezan9on  and  Griffon  have  obtained  cultures  of  Koch's  bacillus  on  blood 
agar.  The  first  application  of  this  method  in  the  diagnosis  of  tubercular 
meningitis  was  made  on  a  patient  in  my  ward  by  my  house-physician, 
Griffon.     The^ubjoined  accomit  was  made  to  the  Societe  de  Biologic  : 

The  results  obtained  by  cultivating  the  tubercle  bacillus  on  blood  agar,  a  medium 
of  which  we  have  given  the  mode  of  preparation,  have  led  us  to  cultivate  on  this 
favourable  medium  various  pathological  Mquids,  which  appear  clinically  to  be  tubercular 


1458  TEXT-BOOK  OF  MEDICINE 

in  nature.  By  cultivating  the  sero-tibrinous  effusion  of  acute  pleurisy  with  success, 
we  have  been  able  to  reaUze  this  desideratum.  It  was  interesting  to  apply  the  same 
method  of  bacteriological  examination  to  other  serous  fluids,  and  in  particular  to  the 
cerebro-spinal  fluid  of  patients  with  meningitis.  We  were  able  to  put  this  project  into 
practice  in  a  case  of  tubercular  meningitis  in  an  adult  under  Dieulafoy's  care.  By 
lumbar  pimcture  we  collected  transparent  Uquid,  the  last  drops  of  which  were  slightly 
yellow.  The  sown  tubes,  which  were  put  into  the  oven  at  39°  C,  showed,  at  the  end 
of  four  weeks,  colonies  smaller  than  pin's  heads,  and  contaiuing  Koch's  bacillus.  They 
were  much  more  numerous  than  in  hquid  cultivated  under  similar  conditions  from  a 
case  of  pleurisy.  Each  colony  was  well  developed,  and  the  spherical  form,  the  mulberry- 
like aspect,  and  the  chocolate  colour  were  characteristic.  A  guinea-pig,  weighing 
260  grammes,  which  had  received  an  intraperitoneal  injection  of  5  c.c.  of  this  same 
hquid,  was  ahve  two  months  later.  We  killed  it.  The  post-mortem  examination 
revealed  the  lesions  of  experimental  tuberclosis  predominating  in  the  lymphatic 
organs. 

These  interesting  researches  have  been  continued,  but  when  we  have 
to  deal  with  cerebro-spinal  meningitis — a  disease  of  rapid  course — we 
cannot  wait  a  month  in  order  to  confirm  the  diagnosis.  Widal,  Sicard,  and 
Ravaut  have  proposed  more  expeditious  methods  (cryoscopy  of  the  cerebro- 
spinal fluid).  The  freezing-point  of  the  cerebro-spinal  fluid  is,  in  the  normal 
condition,  lower  than  that  of  blood  serum  ;  it  varies  between  0'56°  and 
0'75°  C,  being  generally  above  0-60°  C.  It  is,  therefore,  hypertonic  with 
regard  to  blood  serum,  the  freezing-point  of  which  is  0*56°  C.  Widal,  Sicard, 
and  Ravaut  have  shown  that  in  four  out  of  five  cases  of  tubercular  menin- 
gitis the  cerebro-spinal  fluid  is,  on  the  contrary,  hypotonic  with  regard  to 
blood  serum,  the  freezing-point  varying,  then,  between  0"48°  and  0'55°  C. 
We  have  here  a  new  method,  of  easy  clinical  application.  Hypertonia  of 
the  cerebro-spinal  fluid  is  in  favour  of  tubercular  meningitis. 

Some  information  may  also  be  gathered  from  the  meningeal  permeability. 
The  ingestion  of  3  to  5  grammes  of  iodide  of  potassium  is,  in  the  normal 
condition,  not  followed  by  the  passage  of  the  iodide  into  the  cerebro-spinal 
fluid.  In  tubercular  meningitis,  on  the  contrary,  the  iodide  may  be  found 
in  the  liquid  by  ordinary  reagents.  Meningeal  permeability,  however,  exists 
only  in  54" 7  per  cent,  of  the  cases  (Widal,  Sicard,  and  Lutier). 

The  method  of  cyto-diagnosis  proposed  by  Widal  and  Ravaut  in  sero- 
fibrinous pleurisy  is  applicable  to  tubercular  meningitis.  Widal,  Sicard,  and 
Ravaut  have  shown  that  in  tubercular  meningitis  the  liquid  withdrawn  by 
lumbar  puncture,  even  when  it  is  limpid,  contains  lymphocytes,  which  are 
readily  brought  into  evidence  by  centrifugalization  and  by  staining.  If, 
in  certain  cases,  some  polynuclears  are  found,  a  simple  count  shows  that 
they  are  always  much  fewer  in  number  than  the  lymphocytes.  In  non- 
tubercular  cerebro-spinal  meningitis,  on  the  contrary,  the  cerebro-spinal 
fluid  contains  almost  solely  polynuclears,  and  the  number  of  the  lymphocjiies 
is  always  restricted.  The  diagnosis  of  the  tubercular  form  may  be  made 
by  Nattan-Larrier's  method  of  injecting  1  c.c.  of  the  cerebro-spinal  fluid  into 


DISEASKS  OK  TIIK   liKALN  1459 

the  breast  of  a  nursing  guinea-pig  ;  ii  few  days  later  tlio  niilk  containH  Koch's 
bacilli. 

Acute  syphilitic  tnciiiii«.,Mtis  is  also  characterized  by  the  presence  of 
lymphocytes  (Widal  and  Le  Sourd,  Brissaud  and  Brecy),  but  this  variety  of 
meningitis  is  exce])tional.  From  the  ])oiiit  of  view  of  the  lymphocytic; 
formula  of  meningitis  in  general,  it  must  be  remembered,  in  order  to  avoid 
a  mistake,  that  the  cytological  examination,  made  at  a  period  remote  from 
the  commencement  of  bacterial  meningitis,  will  show  only  the  lymphocytes. 
The  pol>Tiuclears  have  disappeared.  The  observations  of  Labbe  and 
Castaigue,  Sicard,  Widal,  Griffon,  and  Apert  show  clearly  the  pathogenic 
interpretation  of  such  cases.  When  the  disease  tends  towards  recovery, 
the  pol}Tiuclear,  the  element  of  severe  infection  en  masse,  gives  place  to  the 
lymphocyte,  the  element  of  organization. 

The  diagnosis  of  cerebro-spinal  meningitis,  therefore,  comprises  two 
stages.  It  is  not  sufficient  to  distinguish  cerebro-spinal  meningitis  from 
influenza  or  from  t}^hoid  fever  ;  we  must  also  make  a  pathogenic  diagnosis, 
and  ascertain  whether  the  lesion  is,  or  is  not,  tubercular.  It  is  not  always 
easy  to  avoid  a  mistake.  Clinical  observation  must  be  supplemented  by 
laboratory  methods. 

Prognosis. — Every  variety  of  cerebro-spinal  meningitis,  except  the  tuber- 
cular, may  end  in  recovery  ;  the  cures  vary  from  15  to  40  per  cent.  In 
Netter's  statistics  "  the  proportion  of  cures  is  about  two  in  three — a  very 
encouraging  number — which  shows  how  important  it  is  to  distinguish  non- 
tubercular  from  tubercular  meningitis  by  accurate  diagnosis." 

Incomplete  recovery  may  also  occur,  the  cerebro-spinal  meningitis 
leaving  sequelae  behind.  Military  physicians  (Vincent,  Simonin)  have  noted 
persistent  disturbance  of  sight  and  of  hearing,  intellectual  troubles,  and 
hydrocephalus.  Raymond  and  Sicard  have  described  a  special  t}^e — 
cerebro-spinal  meningitis  of  the  infantile  paraljrtic  type.  They  have  shown 
the  relations  which  may  exist  between  cerebro-spinal  meningitis  and  infantile 
paralysis.  During  the  course  of  certain  epidemics  (the  Vermont  epidemic 
of  1894)  some  children  were  stricken  with  cerebro-spinal  meningitis,  others 
with  infantile  paralysis.  Certain  cases  of  poliomyelitis  may  be  considered  as 
the  ineffaceable  relics  of  cerebro-spinal  meningitis. 

Bacteriology. — In  1887  Weichselbaum  described  a  microbe  which  he 
called  the  Diplococcus  intraceUularis  meningitidis,  and  which  has  been  con- 
sidered the  specific  agent  of  cerebro-spinal  meningitis.  This  microbe  is  an 
immobile  coccus,  occurring  in  pairs,  never  in  chains,  but  sometimes  in 
masses.  Each  element  of  the  diplococcus  possesses  a  plane  surface,  which 
faces  an  analogous  surface  of  the  opposite  element.  This  form,  which  is 
that  of  the  coffee-bean,  recalls  the  aspect  of  the  gonococcus.  The  meningo- 
coccus is  often  enclosed  in  the  protoplasm  of  a  leucocyte.     It  deserves, 


1460     -  TEXT-BOOK  OF  MEDICINE 

tlierefore,  tke  name  of  intracellular,  but  it  "would  be  wrong  to  suppose  that 
it  is  always  enclosed  in  a  cell.  It  is  sometimes  extracellular  and  encap- 
suled.     These  two  varieties  existed  in  the  spinal  fluid  of  our  two  patients. 

The  meningococcus  on  rabbit  serum  shows  a  perfect  capsule.  Some 
elements  may  show  but  a  single  coccus,  and,  in  the  common  two-grained 
form  we  often  meet  with  a  small  grain  opposite  to  a  grain  two  or  three  times 
as  large. 

The  meningococcus  is  decolourised  by  Gram's  reaction,  and  therefore 
differs  from  the  pneumoccoctis.  "  It  differs  radically  from  the  common 
pnemnococcus  by  its  cidtuje  characters  on  sertmis  and  on  gelatine."  Griffon 
made  the  following  communication  to  the  Societe  de  Biologie  concerning 
Weichselbaum"s  meningococcus,  found  in  a  state  of  purity  in  the  cerebro- 
spinal fluid  of  my  first  patient : 

The  meningococcus  grows  with  difficulty  on  the  usual  media ;  it  does  not  develop 
on  gelatine.  Even  on  favourable  media  it  grows  slowly,  and  the  colonies  are  not  well 
formed  until  after  an  incubation  of  forty-eight  hours  in  the  oven  at  37°  C.  The  broth 
is  slightly  turbid,  or  remains  sterile.  On  agar,  no  apparent  colonies  are  at  first  developed 
on  the  stuface  of  the  sohd  medium ;  nevertheless,  the  condensed  liquid  in  the  lower  part 
of  the  tube  is  turbid  and  rich  in  diplocoeci.  At  the  end  of  three  or  four  days  an  isolated 
colony  may  appear  on  the  surface  of  the  agar  where  it  reaches  matuiity — a  large,  fiat 
colony,  opaque  in  the  centre,  with  translucent  and  somewhat  irregular  edges,  remarkably 
viscous.  In  proportion  to  the  number  of  stabs,  the  microbe  becomes  accHmatized 
to  the  artificial  media,  and  the  growth  on  agar  is  then  more  rapid,  more  certain,  and 
more  abundant.  To  the  naked  eye  it  may  present  the  look  of  a  culture  of  Eberth's 
bacillus. 

The  microbe  doe5  not  grow  abundantly  in  milk.  Only  a  few  diplocoeci  are  seen 
in  the  preparations.  The  culture  medium  does  not  coagulate,  even  at  the  end  of  ten 
days.  Xon-coagulated  rabbit  serum  gives  a  culture  which,  at  the  end  of  forty-eight 
hours,  is  fairly  abundant,  though  less  rich  than  in  the  case  of  the  pneumococcus.  Blood 
agar,  so  valuable  for  growing  Koch's  bacillus,  is  also  a  good  medium  for  the  meningo- 
coccus. The  colonies  are  abundant,  close  to  the  stabs,  and  early  in  their  appearance. 
They  are  flat,  macular,  of  a  brownish-yellow,  translucent,  and,  if  several  colonies  coalesce, 
they  look  Hke  a  plaque  with  polycychcal  edges. 

Experimentally,  the  action  of  the  microbe  on  the  mouse  was  such  as  Weichselbaum 
described  it.  Subcutaneous  inoculations  gave  no  result,  whether  the  pus  was  injected  or 
whether  a  culture  was  employed.  On  the  other  hand,  intrapleural  injection  caused  the 
death  of  the  animal  in  three  days,  and  the  post-mortem  examination  revealed  double 
pleurisy  with  sero-hsemorrhagic  effusion,  more  abxmdant  on  the  side  of  the  puncture, 
and  generaHzation  of  the  microbe  in  the  blood  and  in  the  organs.  A  rabbit  was  taken, 
and  a  small  dose  of  the  culture  was  injected  into  a  vein.  It  clid  not  die,  even  at  the 
end  of  twelve  days ;  but  it  became  cachectic,  and  exa-rnination  of  the  blood  showed 
intense  leucocytosis  and  the  presence  of  free  meningococci  between  the  white  and  red 
corpuscles.  It  was  interesting  to  examine  the  agglutinating  property  in  the  blood 
of  the  patient.  The  serum  did  not  agglutinate  the  meningococcus,  whether  we  employed 
a  broth  culture,  as  in  Widal's  method,  for  Eberth's  bacillus,  or  whether  we  tried  to  culti- 
vate the  microbe  in  pure  serum.     The  meningococcus  did  not  develop  in  undiluted  serum. 

At  the  same  meeting  of  the  Societe  de  Biologie  Netter  gave  a  description 
of   Weichselbaum's  meningococcus,   which  he   had  previously  considered 


DISEASES  OF  THE  BRAIN  1461 

"  as  a  variety  of  the  pneumococcus."  Chantemesse,  speaking  on  these 
conunuiiications,  summed  up  the  c[uestioa  by  remarking :  "  Everybody 
knows  that  cases  of  cerebro-spinal  meningitis  are  produced  by  WeicLsel- 
baum's  meningococcus,  which  has  no  connection  with  Talamon's  pneumo- 
coccus." 

Treatment. — The  treatment  of  cerebro-spinal  meningitis  is  the  more  im- 
portant, in  that  we  are  dealing  with  a  disease  which  is  often  curable.  It  was 
hoped  that  a  therapeutic  means  had  been  found  in  lumbar  puncture.  Quincke 
expected  to  obtain  favourable  decompression  of  the  nerve  centres  by  mean? 
of  the  puncture,  but  experience  proves  that  the  withdrawal  of  too  large  a 
quantity  of  the  cerebro-spinal  fluid  may  cause  grave  complications.  The 
puncture  is  an  excellent  means  of  diagnosis,  but  it  is  not  a  means  of  treat- 
ment. In  some  subjects,  as  in  the  case  of  my  first  patient,  the  pimcture 
caused  a  slight  and  transient  improvement  in  the  disease,  but  that  was  all. 
Therefore,  lumbar  puncture  cannot  be  called  a  therapeutic  measure. 

Hot  baths  have  been  rightly  ad\'ised.  Baths  at  102^  F.,  lasting  from 
five  to  ten  minutes,  and  repeated  several  times  in  twenty-four  hours,  produce 
a  certain  remission,  and  give  a  good  result.  During  the  bath  it  is  necessar}- 
to  apply  cold  compresses  to  the  patient's  head.  The  painful  contractures 
of  the  limbs,  of  the  nape  of  the  neck,  and  of  the  loins  makes  the  administra- 
tion of  these  baths  difficidt.  It  is  difficult  enough  to  sit  the  patient  up  in 
his  bed  to  auscultate  him,  and  a  fortiori  it  is  more  difficult  to  keep  bim  in  a 
bath. 

The  headache  and  the  delirium  must  be  treated  by  bleeding,  leeches 
behind  the  ears  and  on  the  nape  of  the  neck,  and  wet  cupping  to  the  spine. 
The  bleeding  may  be  repeated  daily,  some  5  ounces  of  blood  being  with- 
drawn. The  bleeding  may  be  followed  by  the  injection  of  artificial  serum. 
Intravenous  injections  of  coUargol  have  been  advised.  Antispasmodic 
remedies  find  here  a  perfect  application — bromides,  in  doses  of  40  to  60  grains 
a  day  ;  musk,  antipyrine,  chloral,  hvpnal,  sulphonal,  syrup  of  ether,  and 
small  injections  of  morphia. 

The  treatment  of  cerebro-spinal  meningitis  has  made  definite  progress 
since  the  systematic  employment  of  serotherapy.  The  antimeningococcic 
serum  is  obtained  by  immunizing  horses,  first  with  dead  bacilli,  and  then 
with  cultures  of  increasing  virulence. 

The  serum  should  be  used  as  soon  as  the  bacteriological  diagnosis 
is  made ;  its  action  is  the  more  certain  the  earlier  it  is  given.  The  serum 
must  always  be  injected  into  the  spinal  canal. 

Lumbar  puncture  is  first  performed,  withdrawing  an  amount  of  fluid  at 

least  equal  to  the  amount  of  serum  to  be  injected.     The  first  dose  should 

be  30  c.c,  even  in  very   young   children,  and  the  injections  should  be 

deliberately   repeated   on  three  or  four   consecutive   days,   ignoring  the 

IL  93 


1462  TEXT-BOOK  OF  MEDICINE 

clinical  signs,  because  calms  are  deceptive,  and  the  temperature  as  well  as 
the  rigidity  of  the  nape  of  the  neck  vary  from  day  to  day.  The  cerebro- 
spinal fluid  furnishes  the  only  information  of  value ;  it  gradually  clears 
up,  the  polynuclears  diminish  in  number,  the  lymphocytes  multiply  and 
the  meningococci  tend  to  disappear.  After  the  first  four  injections,  the 
examination  of  the  cerebrospinal  fluid  must  guide  us  in  giving  or  in  with- 
holding the  serum.  By  these  measures  Netter  has  obtained  rapid  and 
definite  results  ;  65  cases  out  of  85  were  cured  by  four  injections  of  30  c.c. 
At  times,  however,  the  results  are  not  so  rapid,  relapses  occur,  and  some 
cases  require  large  doses  of  serum. 

The  following  statistics  (Netter)  are  peculiarly  suggestive.  Cerebro- 
spinal meningitis,  which  in  the  nurseling  is  often  defaced,  the  only 
symptom  being  convulsions,  and  in  which  we  must  rely  on  lumbar 
puncture  to  make  our  diagnosis,  is,  as  we  know,  a  most  deadly  malady. 
Before  the  use  of  serum  the  death-rate  was  85'7  per  cent. ;  it  has  now 
fallen  to  46  per  cent.  The  aggregate  mortality  per  100  cases  has  been 
28  per  cent.,  while  it  was  40  per  cent,  in  the  most  favourable  figures 
previous  to  the  introduction  of  the  serum.  From  this  total  of  28  per 
cent,  we  must  deduct  17  cases  brought  to  the  hospital  in  a  moribund  con- 
dition, thereby  leaving  a  mortality  of  11  per  cent. 

Injections  of  antimeningococcic  serum  may  be  followed  by  various 
disturbances.  Some  are  benign :  urticarial  eruptions  appearing  several 
days  after  the  inoculation,  and  transient  arthropathies,  which  must  be 
distinguished  from  true  meningococcal  arthritis.  The  injection  of  the 
serum  may  increase  the  pain  and  the  rigidity ;  in  this  case,  examination  of 
the  cerebro-spinal  fluid  will  remove  any  doubt  as  to  the  possibility  of  a 
relapse.  More  rare,  fortunately,  but  also  more  grave,  are  other  disturb- 
ances that  appear  immediately  after  the  injection,  and  are  especially 
characterized  by  orfchopncea,  followed  by  apncea.  These  disturbances  may 
be  fatal;  they  would  seem  to  be  due  to  the  noxious  principles  which 
form  an  integral  part  of  the  normal  serum  of  the  horse,  Nevertheless, 
they  must  not  not  prevent  us  from  employment  of  the  serum. 

The  physician's  duty  does  not  end  here;  he  must  remember  that 
meningococcia,  with  or  without  meningitis,  may  be  transmitted  by  the 
convalescent,  or  by  the  apparently  healthy,  in  whose  nasal  fossae  Wechsel- 
baum's  diplococcus  still  lurks.  Accordingly,  it  is  necessary  to  examine 
them  for  the  meningococcus,  and  to  impose  quarantine  as  long  as  the 
coccus  is  present  in  the  nasopharynx. 

Inhalations  of  iodine  are  said  to  hasten  the  destruction  of  the  germs. 
The  formula  commonly  employed  by  Vincent  and  Bellot  is :  Iodine, 
20  grams;  guaiacol,  2  grams;  thymic  acid,  0"15  gram;  alcohol  (60  per 
cent.),  200  grams. 


DISEASES  OF  THE  VAIM^  U63 


XVII.  CHRONIC  MENINGITIS-PACHYMENINGITIS— 
HiEMATOMA  OF  THE  DURA  MATER. 

Of  the  different  varieties  of  chronic  meningitis  two  deserve  special 
attention  :  the  one  comprises  cases  of  partial  meningitis  at  the  base  of  the 
brain,  the  other  refers  to  meningitis,  which  is  often  huemorrhagic ;  it  is  known 
under  the  name  of  "  pachymeningitis,"  and  usually  affects  the  convexity  of 
the  hemispheres. 

1.  Basal  Meningitis. — This  form  is  usually  secondary  ;  it  often  accom- 
panies tumours  at  the  base  of  the  brain,  and  is  frequently  of  syphilitic 
origin  (Fournier).     Circumscribed  sclero-gummatous  meningitis  has  a  well 
marked  predilection  for  the  base  of  the  brain.     I  have  described  it  under 
Cerebral  Syphilis. 

2.  Pachymeningitis— Haematoma.— Pachymeningitis  means  chronic  in- 
flammation of  the  dura  mater,  the  inflammation  being  especially  limited  to 
the  parietal  surface  when  it  follows  on  changes  in  the  bones  of  the  skull. 
Inflammation  of  the  visceral  layer  of  the  dura  mater  forms  a  part  of  the 
history  of  haematoma.  Pachymeningitis  is  frequent  at  the  two  extremes 
of  life.  Its  causes  may  be  grouped  thus  :  mania,  diffuse  periencephalitis, 
injury,  alcoholism,  rheumatism,  and  fevers  (Jaccoud). 

Pathological  Anatomy. — In  pachymeningitis  we  find  thin  superposed 
neomembranes,  which  arise  on  the  inner  surface  of  the  dura  mater  ;  as  many 
as  twenty  stratified  layers  may  be  counted  (Viichow).  These  false  mem- 
branes, which  are  often  symmetrical,  are  usually  situated  on  the  cranial 
vault,  on  both  sides  of  the  falciform  process  of  the  dura  mater ;  the  most 
recently-formed  membranes  are  next  to  the  dura  mater.  As  they  grow 
older  they  become  thick  and  vascular.  The  vessels  in  these  membranes  are 
friable,  and  their  rupture  causes  a  hsematoma  of  the  dura  mater. 

The  pathogenesis  of  the  clot  and  of  its  encystment  has  given  rise  to  muoli 
discussion.  The  membrane  around  the  clot  is  not  formed  at  the  expense 
of  the  clot.  The  haematoma  is  formed  as  the  result  of  the  pachymeningitis 
and  the  haemorrhage  arises,  not  between  the  dura  mater  and  the  false  layer 
of  the  arachnoid,  but  in  the  thickness  of  the  neomembrane  itself.  This 
theory,  however,  does  not  apply  to  all  cases.  Most  often  the  haemorrhage 
is  consequent  on  the  pachymeningitis,  just  as,  in  other  regions,  haemorrhage 
is  consequent  on  neomembranes  of  the  pleura  and  of  the  tunica  vaginalis  ; 
but  this  mode  of  formation  of  the  meningeal  haematoma  must  not  be  looked 
upon  as  exclusive.  In  1837  Baillarger  asserted  that  the  meningeal  haemor- 
rhage is  primary,  and  that  its  enveloping  membrane  is  secondary.  Recent 
experiments  (Vulpian,  Laborde)  prove  the  correctness  of  this  view,  and  are 
in  favour  of  the  existence  of  primary  supra-arachnoid  haemorrhages,  which 

93-2 


1464  TEXT-BOOK  OF  MEDICINE 

later  become  encysted ;  but  their  envelope  is  not  formed  of  organized  fibrin 
as  Baillarger  had  supposed,  it  is  formed  of  a  membrane  due  to  the  irritation 
of  the  neighbouring  tissue. 

The  hsematoma  of  pachymeningitis  is  not  always  encysted  ;  the  blood 
may  tear  the  membranes  and  inundate  the  arachnoid  cavity,  but,  most 
frequently,  the  haemorrhage  collects  in  the  shape  of  a  cyst,  the  clot  retracts, 
a  part  is  absorbed,  and  the  remainder  assumes  the  yellow  aspect  of  old 
haemorrhagic  foci  in  the  brain.  The  cerebral  matter  is  generally  depressed 
and-  softened  at  the  site  of  the  heematoma. 

Description. — Pachymeningitis  may  at  first  pass  unnoticed,  or  may 
reveal  itself  by  headache,  vertigo,  and  contraction  of  the  pupils.  This 
first  period,  which,  in  the  adult,  lasts  for  several  months,  is  followed  by  a 
phase  of  depression,  generally  provoked  by  the  formation  of  the  hsematoma. 
If  the  haemorrhage  is  shght,  acute  symptoms  are  absent ;  if  it  is  sudden 
and  abundant,  it  causes  apoplexy  and  coma.  It  usually  induces  incom- 
plete hemiplegia,  and  in  some  cases  contractures  and  convulsions.  In 
grave  cases  the  pulse  is  slow  and  irregular,  the  pupil  is  contracted  on  the 
side  of  the  lesion,  the  sphincters  are  paralyzed,  and  death  is  the  usual 
termination. 

The  paralytic  phenomena  may  exist  alone,  without  any  previous 
apoplexy ;  they  differ  materially  from  hemiplegia  due  to  cerebral  haemor- 
rhage. Facial  paralysis  is  rare,  and  the  hemiplegia  is  generally  incomplete 
or  dissociated.  The  diagnosis  of  haematoma  in  certain  cerebral  lesions 
(softening,  tumour)  is  sometimes  impossible, 

XVIII.  SYPHILITIC  PACHYMENINGITIS  OF  THE  BASE  OF 

THE  BEAIN.* 

Clinical  Case. — On  September  18, 1908, 1  was  examining  a  woman,  tMrty-nine  years 
of  age,  in  the  Sainte-Jeanne  ward.  She  was  answering  my  questions  when  she 
suddenly  fell  back  on  her  pillow  and  lost  consciousness  in  a  major  attack  of  epilepsy. 
She  had  had  two  similar  seizures  a  week  before  her  admission.  We  had  to  find  their 
cause,  in  order  to  prescribe  appropriate  treatment. 

Dr.  Mazet  kindly  supplied  the  following  details : — Five  years  before,  she  had  been 
seized,  when  four  months  pregnant,  with  symptoms  like  those  of  acute  meningitis : 
headache,  romiting,  trismus,  nuchal  rigidity,  and  inequaKty  of  the  pupils.  For  some 
days  the  temperature  stood  at  104°  F.,  with  a  slight  remission  in  the  morning.  The 
coma  lasted  a  week,  the  symptoms  then  improved  and  three  weeks  later  the  meningitis 
appeared  to  be  cured,  except  that  the  headache  remained. 

Later,  when  Dr.  Mazet  saw  the  patient,  she  had  developed  ejDilepsy — loss  of 
consciousness,  biting  of  the  tongue,  and  involuntary  passage  of  urine  and  fasces. 
From  this  time  on  headache  and  epilepsy  were  her  two  troubles.  The  attacks  came  on 
by  day  or  by  night,  and  the  headache  was  practically  continuous,  affecting  chiefly  the 

*  Dieulaf oy,  CUnique  Medicate  de  V Hotel-Dieu,  1909, 6®  volume.  "  Pachymeningite 
syphilitique  basilaire,  premiere  et  deuxieme  legons." 


DISEASES  OF  THE  BRAIN  1465 

occipifiil  vppion  ;  at  iimos  tlio  paroxysms  were  terrible.     Moan  while  kIio  was  ddliverod 
of  a  wi'll  t'oriiu'il  jrirl,  who  is  to-day  a  lino  rhild,  five  yours  of  a^f((. 

In  19((7  Dr.  Mazet  nolieod  that  her  jrait  was  ct.rol)(*llur.  Slio  c-omplainod  of  severe 
vertig-o,  and  staggorod  liki>  a  drunkon  jx'rson  when  slie  took  a  few  sti'ps.  To  keep  her 
balaui-e  she  held  on  to  llic  furniture  ;  but  in  spite  of  everyihin)/  sIk!  liad  a  t<mdenoy  to 
fall  to  the  right  side.  Hrr  hrari'iKj  was  nut  affected.  For  8om«t  timo  her  sight  had 
been  atVecU'd  ;  at  first  merely  a  fog  before  her  eyes,  lator  aiich  marked  disturbance  that 
she  could  not  see  <o  walk.  Tlui  oplithaliiioscoije  .showed  papillary  stasis  with  much 
OMlema  of  the  papilln>  and  enormous  dilatation  of  the  retinal  veins.  These  .symptoms 
are  so  im])ort!int  in  the  diagnosis  of  encei)halic  lesions  as  to  demand  further  mention. 

Under  normal  conditions,  the  papilla  or  expansion  of  the  optic  nerve  appears  with 
the  ophthalmoscope  as  an  oval  white  disc,  clearly  defined  against  the  red  of  the 
choroid.  The  disc  is  transparent,  with  well  marked  edges,  and  is  furrowed  by  vessels, 
the  veins  being  larger  than  the  arteries. 

Papillary  stasis,  also  called  ])apillitis  or  oedema  of  the  papilla,  may  be  unilateral  or 
bilateral.  If  it  is  bilateral,  it  almost  always  indicates  an  encephalic  lesion.  With  the 
ophthalmoscope  the  abnormal  prominence  and  the  hypertemic  reddish  tint  of  the 
pa^iilla  are  at  once  noticeable.  Its  transparency  is  lost,  its  outlines  are  blurred  and 
shaded  off  into  the  surrounding  retina.  The  veins  are  sinuous  and  distended,  while  the 
arteries  are  in  part  effaced  and  are  often  indistinguishable  save  at  a  certain  distance  from 
the  papilla  which  hides  them.  The  lesions  of  papillary  stasis  are,  in  a  great  measure, 
cedematous  in  natiire.  Mechanical  obstruction  to  the  circulation  is  not,  however,  the 
sole  cause ;  in  addition  there  is  some  infection  of  the  cerebro- spinal  fluid,  thus  making 
the  oedema  of  the  disc  an  inflammatory  oedema.  When  the  stasis  affects  both  eyes,  we 
may  diagnose,  says  Terrien,  the  existence  of  a  cerebral  tumour  or  of  basal  meningitis. 

The  usual  result  of  papillary  stasis  is  narrowing  of  the  visual  field  and  impairment 
of  vision.  As  long  as  the  lesion  is  limited  to  inflammatoiy  oedema,  complete  recovery 
is  easy,  especially  if  the  brain  lesions  are  syphilitic  and  accessible  to  treatment.  If,  on 
the  other  hand,  the  impillitis  is  of  some  duration,  the  termination  is  far  less  favoiu-able. 
'•  The  papillary  swelling*  gradually  disappears,  losing  its  reddish  look  and  taking  on  a 
dirty  greyish  tint.  The  dilatation  of  the  veins  disappears,  the  change  in  the  arteries 
grows  marked  and  the  atro])hy  of  the  pupil  becomes  more  and  more  evident.  At  the 
same  time  vision  gradually  disappears  "  (Terrien). 

In  the  present  case  the  stasis  was  marked  and  bilateral.  The  ophthalmoscope 
showed  that  the  papilla  was  swollen  and  reddish.,  with  ill-defined  edges,  while  the 
arteries  were  indistinct  and  the  veins  were  three  times  as  large  as  normal.  Fortunately 
the  papillitis  had  not  as  yet  ended  in  definite  atrophy. 

In  five  years,  then,  the  landmarks  in  the  course  of  the  disease  were  :  meningitis, 
headache,  attacks  of  ej)ilepsy ;  vomiting",  vertigo,  reeling  gait,  and  visual  ti-oubles  due 
to  oedema  of  the  optic  disc.  In  August,  1908,  complete  paralysis  of  the  perii)heral 
type  affected  the  left  side  of  the  face. 

On  examining  the  patient,  the  left  half  of  the  face  was  quite  paralyzed ;  the  reaction 
of  degeneration  was  j^resent.  About  this  time  the  next  feature  was  i)aresis  of  the  left 
sixth  nerve  and  partial  paralysis  of  the  right  third  nerve,  the  levator  palpebrje.  the 
ciliary  muscle  and  the  internal  rectus  being  involved.  The  pupils  were  ujiequai ;  the 
right  pujnl  reacted  to  light,  the  left  did  not.  The  dipleg-ia  caused  by  the  ocular  palsy 
was  difiicult  to  recognize,  because  vision  was  partly  abolished  by  .the  papillitis. 

The  senses  of  liearing  and  of  taste  were  normal,  the  arterial  tension  was  nearly 
normal.  The  heart  and  the  lungs  were  unaffected;  no  sign  of  tuberculosis.  The 
urine  was  siifficient;  no  sugar,  no  albumin.  The  mental  faculties  were  perfect;  no 
somnolence,  no  delirium.  No  stigmata  of  hysteria  were  j^resent.  There  was  no 
evidence  of  hemiplegia ;  the  reflexes  were  normal ;  the  pj'ramidal  ti'act  was  free. 
These  data  will  be  of  interest  in  the  discussion  as  to  the  seat  of  the  brain  lesion. 


14G6  TEXT-BOOK  OF  MEDICINE 

The  patient,  who  was  very  weak  and  wasted,  complained  of  the  headache,  which  at 
times  redoubled  in  its  severity ;  the  attacks  of  epUepsy  were  hecoming  more  frequent ; 
she  slept  badly,  her  sight  was  almost  gone,  her  appetite  was  lost,  and  eating  and  drinking 
caused  her  great  suffering .  She  sneered  from  giddiness  even  when  lying  down ;  she 
could  not  walk  without  reeling- ;  her  distress  and  her  mental  depression  were  pitiable. 

Topographical  Diagnosis. — We  had  obviously  to  deal  with  a  cerebral  lesion  which 
had  spared  the  pyramidal  tract.  In  what  part  of  the  brain  was  this  lesion  ?  What  was 
its  nature  ?    A  correct  answer  was  essential  in  order  to  institute  apx)ropriate  treatment. 

The  illness  had  commenced  with  all  the  symptoms  of  meningitis.  Next,  for  several 
years,  the  only  symptoms  were  headache  and  attacks  of  epUepsy.  There  was  no 
question  of  essential  epilepsy,  because  the  first  attack  did  not  appear  until  the 
age  of  thirty-four  ;  so-called  essential  epilepsy  does  not  begin  so  late  in  Hfe.  There 
was  no  question  of  Jacksonian  epilej)sy ;  it  was  a  case  of  grand  mal,  and  it  is 
weU -known  that  any  lesion  of  the  brain  (whatever  its  situation  may  be,  but  especially 
one  in  the  cortex)  can  cause  epUepsy.  It  matters  little  whether  we  invoke  as  the  cause 
of  the  attacks  some  excitation  of  the  nerve  tissue  or  some  neighbouring  compression, 
hydrops  ventriculortim  or  cerebral  oedema ;  syphiloma,  tuberculoma,  neoplasms,  hydatids, 
exostoses,  splinters  of  bone,  etc.,  may  aU  be  material  in  causing  epilepsy  without  the 
need  of  assigning  a  special  situation  to  the  provoking  lesion.  In  this  case  neither  the 
headache  nor  the  attacks  of  epilepsy  could  give  data  as  to  the  site  of  the  brain  lesion. 

Was  it  possible  to  fix  the  site  from  the  symptoms  which  had  appeared  some  years 
later?  The  vomiting,  the  disordered  gait  and  the  loss  of  equilibrium  with  latero- 
pulsion  to  the  right  side  (the  hearing  being  intact)  directed  attention  to  the 
cerebellum.  Papillary  stasis  with  dilatation  of  the  retinal  veins  and  oedema  of  the 
papiUa  is  of  value  in  that  it  means  in  eighty  out  of  a  hundred  cases  either  a  cerebral 
tumour  or  a  basal  meningitis.  This  sign,  however,  gave  no  clue  as  to  the  seat  of  the 
tumour  ;  any  cerebral  tumour  may  cause  papillary  stasis  ;  and  yet  this  stasis  is  most 
common  when  the  lesion  is  at  the  base  of  the  brain. 

These  considerations  were  in  favour  of  a  basal  lesion,  but  the  sitiiation  was  not 
made  certain  thereby.  This  certainty  was  fixed,  however,  by  the  paralysis  of  the  three 
cranial  nerves  :  left  facial,  left  sixth  nerve,  and  right  third  nerve.  Accordingly  there 
was  no  room  to  doubt  that  the  lesion  was  situated  at  the  base  of  the  brain. 

Pathogenic  Diagnosis. — What  was  the  nature  of  the  lesion?  Passing  over  the 
rare  lesions  met  with  at  the  base  of  the  brain,  the  question  was  simplified  to  deciding 
between  the  three  most  common  lesions :  syphilis,  tuberculosis  or  neoplasm.  Although 
tumours  are  most  likely  to  cause  papillary  stasis  (De  Lapersonne's  figures  are  :  tumour, 
60  to  70  per  cent. ;  syphilis,  13  per  cent. ;  and  tuberculosis,  10  per  cent.),  yet  there  were 
several  reasons  against  the  diagnosis  of  a  new  growth.  Lumbar  punctui-e,  repeated 
several  times,  showed  no  cancer  cells  in  the  spinal  fluid.  A  peremptory  reason  against 
a  new  growth  was  that  the  disease  had  existed  for  five  and  a  haK  years.  Was  the 
condition  due  to  a  tuberculoma  or  to  tiibercular  meningitis  ?  Tubercles  of  the  brain 
sometimes  reach  the  size  of  a  small  tumour,  and  cii-cumscribed  patches  of  tubercular 
pachymeningitis  may  exist  for  a  long  wliile  without  compromising-  life. 

In  reference  to  the  question  of  chronic  tiibercular  pachymeningitis  we  must  not  forget 
that  the  disease  began  with  symptoms  of  an  acute  meningitis,  which  might  have  passed 
into  the  chronic  state.  Moreover,  the  patient  said  that  several  of  her  brothers  and 
sisters  had  died  at  an  early  age  from  meningitis.  These  arguments,  however,  were  not 
sufficient  to  prove  a  tubercular  lesion.  Although  lesions  of  this  nature  are  of  long  diu-a- 
tion,  the  diagnosis  of  tubercular  pachymeningitis  did  not  fit  in  with  the  remarkably 
long  dui-ation  of  the  disease.     Lastly,  the  cutaneous  reaction  gave  a  negative  result. 

Syphilis  remained.  Was  there  any  good  reason  to  show  that  the  woman  was 
syphilitic  ?  She  denied  it,  and  the  most  careful  examination  showed  no  ti-ace  either  of 
hereditary  or  acquired  syphilis.     Her  daughter,  a  well- developed  and  intelligent  child. 


DISEASES  OF  TllK  F.llAIN  14G7 

fivo  years  of  ape,  was  1)orn  at  full  iovm,  and  Hliowod  no  Ki^^'iiw  of  Jioro'liiuvy  syi»liili8, 
iiKlioiiyli  it  was  in  Uui  fourth  nionlli  of  i>n>j,'-nancy  that  her  niotlnM-  had  shown  the  iirst 
syuipfonis  (h('adach(>  and  opilnp.sy),  wliii-h  had  never  disappeared,  and  to  whiidi  <ho  other 
irouhlcs,  already  cinuuerated,  ha<l  been  added. 

lu  spite  of  all  these  facts  I  made  a  diapnosis  of  syjihilitic  paeliymoninffitis  of  the 
base  of  the  brain  ;  the  eourse  of  the  lesion  and  the  app(;arance  of  tho  symjjtoms  may 
be  thus  explained  :  the  pachymening-itis  liad  been  slow  in  its  prof,'"resH  ;  it  was  locali/,<!d 
to  the  base  of  the  brain,  like  certain  regional  and  inveterate  8yi)hilitic  lesions  which 
limit  themselves  for  years  to  their  chosen  territory.  It  had  remained  juxta-cortical, 
and  the  nerve-tissue  of  the  mesencephalon,  buUi,  pons  and  cerebral  peduncles  had  not 
been  touched ;  hemiplegia  wius  ab.sent  botuiuse  the  pyramidal  tract  was  not  involved. 
The  pachjnneningitis,  spreading  over  the  surface,  had  sown  in  its  wide  march  foci 
which  explain  the  symi)tonis  idready  enumerated.  These  symptoms  may  be  classed  as 
follows: — (1)  Symptoms  of  ii-ritation  :  headache,  epilepsy,  vertigo,  vomiting  and  latero- 
pulsion.  (2)  Symptoms  of  compression  :  oedema  of  the  papilla  with  dilatation  of  th(! 
retinal  veins  and  paralysis  of  the  third,  sixth,  and  seventh  nerves. 

It  remained  to  prove  the  truth  of  the  imthogenic  diagnosis.  The  old  aphorism  : 
naturam  viorhonrm  curationes  ostendant  received  a  striking  confirmation. 

Treatment. — Having  made  a  diagnosis  of  s}i)liilitic  pachymeningitis,  I  commenced 
merciu-ial  treatment  on  Sex)tember  17,  giving-  an  injection  of  biniodide  of  mercuiy 
daily  in  increasing  doses,  so  that  at  the  end  of  nine  days  she  had  taken  21  centigrams. 
As  there  was  no  improvement,  the  daily  dose  was  increased  to  4  centigrams.  Still  no 
im23rovemeut  oeciu'red,  and  on  October  1  a  dose  of  5  centigrams  was  given. 

In  spite  of  this  intensive  treatment  the  symptoms  remained  in  statu  quo,  and  I  felt 
somewhat  nneasy.  The  injections  were  well  borne,  and  stomatitis,  owing  to  the  mo.st 
careful  attention  to  the  mouth,  idid  not  appear.  I  was  about  to  increase  the  dose  when 
suddenly,  on  October  5,  the  patient  told  me  that  her  pains  had  gone  and  that  she  had 
slept  for  several  hours  dui'ing  the  previous  night.  The  injections  were  continued  and 
rapid  imin-ovement  followed.  The  headache  and  the  attacks  of  epilepsy,  which  had 
lasted  for  five  years,  did  not  come  back.  In  two  and  a  half  months  she  had  taken  two 
and  a  half  grammes  of  biniodide. 

At  the  end  of  December  she  felt  another  woman  ;  she  was  fat,  ate  well,  slept  well, 
remained  up  all  day,  and  could  read  easily.  The  oi)hthalmoscope  showed  that  the 
papillary  oedema  had  disappeared.  The  facial  paralysis  gradually  improved ;  the  speech 
became  less  defective  ;  mastication  was  easy  ;  liquids  and  saliva  no  long'er  di'ooledfrom 
the  mouth. 

When  she  left  the  hospital  on  February  22,  1909,  she  had  gained  20  lbs.  in  weight, 
and  was  able  to  resume  her  work.  If  we  had  not  persevered  in  oiu-  treatment,  and  if 
we  had  rejected  our  diagnosis,  the  patient  would  have  gone  on  the  road  to  death. 

I  do  not  know  what  the  f  atiu'e  holds  for  Ehrlich's  notable  discovery.  We  may, 
to-day,  believe  in  the  value  of  606,  but  we  must  not  forget  that  the  mercurial  treatment 
has  given  wonderful  results.  Other  cases  (Sai'bo,  de  Lung-,  de  Popoff )  exist,  and  so 
closely  resemble  the  case  here  described  that  they  may  be  placed  in  the  same  categ-ory. 


XIX.  MEisrmGEAL  h^:moeehage. 

Pathological  Anatomy. — As  I  have  already  described  li£emorrliage  of 
the  dura  mater  (hteinorrliagic  pachymeningitis),  the  question  of  meningeal 
haemorrhage  remains  limited  to  the  supra-  and  subarachnoid  h£emor- 
rhages.  In  the  new-born  child  the  hasniorrhage  is  almost  always  supra- 
arachnoid,  whilst  it  is  subarachnoid  in   the   adult.      In  supra-arachnoid 


1468  TEXT-BOOK  OF  MEDICIXE 

effusion,  the  more  or  less  coagulated  blood  accumulates  at  the  base  of  the 
skuU,  and,  in  the  p^e^^ous  section,  we  saw  that  it  may  become  encysted 
by  the  formation  of  an  enveloping  membrane.  T\Tien  the  effusion  is  sub- 
arachnoid, the  pia-mater  is  infiltrated,  the  choroid  plexuses  are  injected, 
the  ventricles  may  be  inundated,  and  clots  are  frequently  found,  but  the 
blood  is  not  encysted.  Below  the  coagulum  the  cerebral  convolutions  are 
flattened,  and  i£  the  hsemorrhage  has  been  considerable  the  brain  is  ansemic. 
etiology — -Description. — The  differences  of  the  symptoms  caused  by 
meningeal  haemorrhage  in  adults  and  in  children  leads  me  to  di^ade  this 
question. 

1.  In  the  adult  the  hsemorrhage  is  almost  always  subarachnoid.  It  is 
due  to  the  rupture  of  a  vessel,  to  degeneration  of  the  arterioles,  to  peri- 
arteritis with  or  without  miliary  aneurysms  (heredity,  alcohoKsm),  to  inter- 
stitial nephritis,  and  to  the  arterio-sclerosis  (Sutton),  which  accompanies  it. 
It  is  caused  by  diseases  of  the  liver  and  by  the  hsemorrhagic  diathesis.  As 
regards  syphilis,  fuU  details  are  given  in  the  chapter  on  Cerebral  Syphilis. 

Meningeal  haemorrhage  is  sometimes  ushered  in  by  prodromata,  such  as 
Keadache,  vomiting,  and  pain  limited  to  the  area  of  the  trifacial  nerve.  The 
onset  is  sometimes  sudden,  and  the  comatose  phenomena  appear  first. 

The  prodromata  are  almost  constant  in  the  case  of  svplulitic  lesions. 
For  several  weeks,  or  several  months,  the  patients  suffer  from  more  or  less 
violent  headache  (which  may  be  worse  at  night),  dimness  of  sight,  giddiness, 
vertigo,  intellectual  torpor,  nausea  and  vomiting,  speech  troubles,  unsteady 
gait,  tendency  to  torpor,  contractures,  and  convulsions. 

When  the  hsemorrhage  comes  on,  the  apoplexy  may  be  fatal  in  a  few 
minutes.  Sometimes  it  is  slower  in  establishing  itself ;  the  patient  is  seized 
with  somnolence,  from  which  he  can  be  roused  with  difliculty.  He  scarcely 
understands  what  is  said  to  him,  his  movements  are  slow  and  difficult,  and 
in  a  few  hours,  or  in  a  few  days,  according  to  the  progress  of  the  hEemorrhage, 
he  passes  into  a  state  of  coma. 

The  compression  of  the  brain  by  the  effused  blood  is  the  cause  of  these 
complications.  Apoplexy  and  coma  are  slower  to  appear  than  in  certain 
cases  of  cerebral  haemorrhage,  and,  except  in  rare  instances  (Lepine),  we  do 
not  find  hemiplegia. 

The  course  of  the  temperature  is  the  same  as  in  cerebral  haemorrhage. 
Rapidly  spreading  bed-sores  have  been  found  on  the  buttocks.  The  disease, 
rarely  lasts  longer  than  a  week. 

2.  In  the  child,  especially  in  the  new-bom,  the  hsemorrhage  is  generally 
supra-arachnoid.  It  is  met  with  in  children  who  are  stiU-bom,  or  bom 
apparently  dead ;  in  the  new-born  ;  and  during  the  first  year  of  life.  The 
haemorrhage  is  due  to  difficult  labour,  to  compression  of  the  cord,  and  to 
diffuse  steatosis  (Parrot).     In  the  new-born  the  symptoms  show  themselves 


PTS^EASES  OF  THE  J'.RAIN  1409 

iinint'diatcly  after  Itirtli,  or  ii  lew  days  later.  The  eliiM  is  seized  with  cou- 
vulsions,  and  dies  in  coma. 

Diagnosis. — Meningeal  haemorrhage  was,  imtil  a  few  years  ago,  one  of 
the  most  diiEcult  diseases  to  recognize  ;  its  existence,  though  often  suspected, 
could  never  be  affirmed  with  certainty. 

The  diagnosis  can  now  be  established  with  certainty  by  means  of  Kernig's 
sign  and  lumbar  puncture.  I  have  already  described  Kernig's  sign  under 
Cerebro-spinal  Meningitis.  I  have  also  discussed  lumbar  puncture  (.see 
Meningitis),  but  only  from  the  cytological  point  of  view.  Here  lumbar 
puncture  will  give  us  information  as  to  the  colour  of  the  cerebro-spinal  fluid. 
The  amber-yellow  tint  (Bard,  Sicard),  or  bloody  tint,  when  we  know  how  to 
interpret  it,  has  almost  an  element  of  certainty. 


XX.  HYDROCEPHALUS. 

Division — ^^tiology. — Hydrocephalus  is  dropsy  of  the  brain.  The  fluid 
may  be  ventricular  or  extraventricular,  a  matter  of  great  difference  as  re- 
gards the  pathology  and  the  symptoms.  Extraventricular  hydrocephalus 
includes  subarachnoidal  dropsy,  oedema  of  the  pia  mater,  and  of  the  brain. 
"  According  as  the  effusion  is  subsequent  to  the  definite  occlusion  of 
the  cranial  ca\4ty,  hydrocephalus  is  called  acquired  or  congenital " 
(Jaccoud). 

Acquired  hydrocephalus  is  due  to  mechanical  causes  and  to  diathetic 
conditions.  The  mechanical  causes  are  those  which  interfere  with  the 
venous  circulation  in  the  brain — cerebral  tumours,  meningeal  exudates, 
tumours  of  the  neck  and  of  the  mediastinum,  and  lesions  of  the  right  side  of 
the  heart. 

The  diathetic  causes  include  Bright's  disease  and  cachexia,  especially 
tubercular  and  cancerous  cachexia.  Congenital  hydrocephalus  is  due  to 
arrested  development  of  the  brain,  to  a  slow  inflammation  of  the  ependyma, 
and  to  obliteration  of  the  sinuses.  It  may  be  a  manifestation  of  hereditary 
syphilis,  which  is,  indeed,  the  most  common  cause  of  hydrocephalus,  as 
appears  from  the  interesting  publications  of  Foumier.  I  have  had  the 
opportunity  of  seeing  two  cases  of  hydrocephalus  which  were  certainly  the 
result  of  hereditary  syphilis. 

Pathological  Anatomy. — (Edema  of  the  brain  and  of  the  pia  mater  is 
easily  recognized.  On  making  a  section  of  the  organ,  we  notice  the  oozing 
of  a  few  drops  of  liquid,  and  the  oedematous  brain  retains  the  imprint  of  the 
finger.  Ventricular  hydrocephalus  is  not  very  abundant  when  it  is  acute 
(2  to  3  ounces).  It  may  amount  to  12  ounces  when  it  is  chronic,  and  may 
exceed  several  pints  in  congenital  cases.     The  cerebral  tissue  is  softened. 


1470  TEXT-BOOK  OF  MEDICIKE 

the  ventricles  are  dilated,  the  choroid  plexuses  are  oedematous  and  hyper- 
trophied  (Claisse  and  Levi),  and,  in  the  case  of  congenital  hydrocephalus, 
the  cerebral  convolutions  are  flattened  and,  as  it  were,  unrolled.  Congenital 
hydrocephalus  is  sometimes  limited  to  a  portion  of  the  ventricle,  ,to  the 
anterior  or  posterior  cornu,  which  gives  a  peculiar  shape  to  the  chUd's 
head. 

Symptoms. — Acquired  hydrocephalus  may  cause  no  deformity  of  the 
skuU.  If  the  accumulation  of  the  fluid  is  rapid,  serous  apoplexy  results,  and 
if  the  cerebral  liquid  is  of  slow  formation,  the  patient  often  passes  through 
a  phase  of  excitation  (delirium,  convulsions,  and  contractures),  followed 
by  a  phase  of  depression  (coma,  resolution,  asphyxia).  As  fever  and  limited 
paralyses  are  not  seen,  we  can  from  the  first  elimiaate  inflammation  of  the 
brain  and  focal  tumours.  Hydrocephalus  also  affects  a  slow  form,  in  which 
the  symptoms  of  depression  show  themselves  from  the  first,  and  become 
gradually  worse. 

Congenital  hydrocephalus  deforms  the  skull :  the  head  becomes  enor- 
mous, the  orbits  are  sunken  under  the  protuberance  of  the  frontal  bones, 
the  vertical  diameter  of  the  face  is  diminished,  whilst  the  transverse  diameter 
of  the  forehead  is  considerably  increased  by  the  separation  of  the  frontal 
bones.  The  bones  of  the  skuU,  which  are  united  at  their  bases,  separate 
like  the  petals  of  a  flower  (Trousseau).  Convulsions  are  frequent,  the 
appetite  is  voracious,  the  power  of  movement  is  deficient,  and  the  intelli- 
gence is  lacking. 

Acquired  hydrocephalus,  though  very  serious,  is  not  absolutely  fatal. 
It  should  be  treated  with  drastic  purgatives  and  local  and  general  bleeding. 
Congenital  hydrocephalus  may  be  compatible  with  life  for  ten  or  fifteen 
years,  and  even  more.  Operations  for  the  removal  of  the  fluid  do  not  give 
definite  results.  I  have  several  times  performed  aspiration  of  the  cerebral 
fluid  with  a  No.  1  needle.  I  have  been  surprised  at  the  harmlessness  of  the 
operation.  Although  I  have  often  obtained  a  transient  improvement,  I 
have  never  seen  a  case  of  cure. 


CHAPTER   V 
NEURITIS 

POLYNEURITIS. 

Since  the  researches  of  Dumexiil,  wliich  date  from  the  year  18G4,  a  share,  formerly  given 
to  lesions  of  the  nerve  centres,  has  been  given  to  the  peripheral  lesions  of  the  nerves. 
Diimenil  endowed  the  peripheral  nervous  system  with  a  morbid  entity  which  it  did  not 
previously  possess.  Since  that  time  numberless  anatomical,  clinical,  and  experimental 
researches  have  been  pubhshed,  pruning  the  pathology  of  the  central  nervous  system  to 
the  advantage  of  the  peripheral  nervous  system. 

If  a  patient  is  attacked  by  rapid  and  progressive  paralysis,  invading  the  lower  and 
the  upper  Umbs,  and  speedily  followed  by  muscular  atrophy,  we  are  very  careful  before 
makins;  a  priori  a  diagnosis  of  poUomyelitis.  On  closer  scrutiny  we  often  make  the 
more  correct  diagnosis  of  peripheral  polyneuritis. 

If  a  patient  is  attacked  by  lancinating  pains  of  the  lower  limbs,  with  ocular  troubles, 
and  imjierfect  co-ordination  of  movements,  we  are  very  careful  about  making  a  priori 
a  diagnosis  of  tabes.  We  examine  more  carefully,  and  we  often  make  the  more  exact 
diagnosis  of  alcoholic  peripheral  polyneuritis  or  pseudo-tabes. 

If  a  patient  is  attacked  with  bulbar  symptoms,  oculo-motor  troubles,  ophthalmo- 
plegia, etc.,  we  are  very  careful  about  making  a  priori  a  diagnosis  of  disease  in  the 
medulla  and  the  pons.  We  look  closer,  and  we  often  make  a  diagnosis  of  peripheral 
polyneuritis,  which  is  less  serious. 

There  are,  then,  two  morbid  conditions,  which  at  first  sight  present  great 
analogies — in  the  one  case,  grave  troubles,  depending  on  lesions  of  the  nerve- 
centres  ;  in  the  other  case,  benign  troubles,  depending  on  peripheral  lesions 
of  the  nerves.  Paralyses,  amyotrophies,  trophic  troubles,  pain,  and  sensory 
troubles,  angesthesia,  secretory  and  vasomotor  troubles  are  common  to  both 
morbid  conditions. 

In  what,  then,  does  the  lesion  of  peripheral  neuritis  consist,  which  may 
up  to  a  certain  point  simulate  a  lesion  of  the  nerve-centres  ?  As  Ettlinger 
in  his  excellent  work  says,  the  lesion  of  polyneuritis  may  be  summed  up  as 
follows  :  The  small  muscular  and  cutaneous  nerve-trunks  are  degenerated 
in  the  regions  where  the  paralysis,  the  atrophy,  and  the  sensory  troubles 
are  observed.  This  degeneration  consists  in  destructive  changes  of  the  axis- 
cylinder  and  of  their  myeline  sheath.  Its  peculiarity  consists  in  the  fact 
that  it  attains  its  maximum  in  the  smallest  nerves.  The  number  of  the 
fibres  remaining  healthy  becomes  greater  and  greater  as  we  reach  the  large 

1471 


1472  TEXT-BOOK  OF  MEDICINE 

nerve  branclies  ;  for  instance,  whilst  the  nerve  branches  to  the  muscles  of 
the  antero- external  region  of  the  leg  have  hardly  any  healthy  fibres,  the 
external  popliteal  and  the  sciatic  nerve  show  hardly  any  diseased  fibres — or, 
at  least,  they  diminish  in  number  as  we  reach  a  higher  point  of  the  nerve 
trunk.  The  same  feature  holds  good  in  the  cutaneous  branches  ;  their 
lesions  diminish  from  the  periphery  towards  the  centre. 

Pathogenesis. — The  causes  of  polyneuritis  are  the  same  as  those  of 
myelitis.  On  referring  to  the  section  on  Myelitis  in  general,  the  reader  will 
find  in  part  the  pathogenesis  which  governs  the  development  of  neuritis. 
It  may  be  said  that  polyneuritis  is  due  to  two  great  causes  :  (1)  to  infective 
or  toxi-infective  agents  ;  (2)  to  toxic  substances.  Amongst  infective  agents, 
I  would  mention  almost  all  the  infective  diseases  which  act  directly  by 
means  of  their  microbes,  or  indirectly  by  means  of  the  toxines  :  tuberculosis, 
typhoid  fever,  influenza,  diphtheria,  smaU-pox,  syphilis,  malaria,  leprosy, 
streptococcia,  coli  bacillosis,  etc.  Amongst  the  toxic  substances,  I  would 
mention  lead,  alcohol,  arsenic,  and  carbonic  oxide.  To  these  must  be  added 
the  autointoxications  of  diabetes,  uremia,  gout,  and  cancer.  Finally,  there 
is  an  essential  factor  which  must  not  be  neglected — cold  (polyneuritis 
a  frigore) — which  plays  an  undoubted,  though  obscure,  part  in  the  causation 
of  neuritis. 

Is  it,  however,  really  true  that  the  infective,  toxic  or  toxi-infective  agents 
can  limit  their  noxious  action  to  the  periphery  of  the  nerves,  just  as  they 
limit  it  to  a  certain  part  of  the  nerve-centres  ?  It  is  undeniable  that  there 
are  more  or  less  isolated  peripheral  nervous  lesions  which  seem  to  be  indepen- 
dent of  any  central  lesion,  but  can  we  say  that  the  lesion  of  general  poly- 
neuritis, seeing  that  it  is  wholly  peripheral,  is  not  governed  by  some  visible 
or  invisible  change  of  the  cells  of  the  nerve-centres  ?  For  example,  do  we 
not  find  diphtheria  and  influenza  (toxi-infectious  diseases),  causing  peripheral 
lesions  (neuritis)  and  central  lesions  (myelitis)  ?  And,  again,  diabetes  may 
cause  peripheral  and  central  lesions.  The  same  pathogenic  agent,  therefore, 
may  separately  or  simultaneously  cause  peripheral  lesions  (neuritis)  and 
central  lesions  (poliomyelitis)  in  the  same  individual.  It  is  easy,  I  repeat, 
to  admit  the  autonomy  of  certain  isolated  cases  of  neuritis,  but  it  is  more 
difficult  to  admit  the  autonomy  of  polyneuritis  of  a  systematically  ascending 
and  progressive  form.  These  cases  of  polyneuritis  may  be  due  to  central 
lesions  (Marie,  Babinski),  but  little  appreciable  by  our  present  means  of  in- 
vestigation (Raymond),  though  Renaut  has  pleaded  the  cause  of  the  nutritive 
independence  of  the  cylinder  as  regards  the  ganglion  cell. 

In  any  case,  it  is  certain  that  we  can  clinically  describe  neuritis  and 
polyneuritis,  which  in  the  course  of  their  symptoms  and  in  their  mode  of 
termination  behave  differently  from  spinal  lesions  ;  and,  supposing  that 
the  morbid  condition  of  the  bulbo-spinal  cells  escape  our  observations,  the 


NEURITIS  1473 

evolution  of  the  symptomatology  of  what  we  are  agreed  to  call  "  peripheral 
luuirites  "  allows  us  to  describe  them  as  a  distinct  morbid  group,  whilst 
making  a  few  restrictions. 

I  have  remarked  that  it  is  necessary  to  make  some  restrictions,  because 
it  is  evident  that  some  authors  have  gone  too  far  in  trying  to  cut  out  certain 
morbid  conditions  of  spinal  origin  in  order  to  swell  the  list  of  poly- 
neuritis. I  understand  the  warning  given  by  Grasset,  and  no  more  than 
he  have  I  ever  doubted  the  autonomy  of  certain  definite  spinal  types  : 
acute  s})iiial  paralysis  in  the  adult,  and  subacute  anterior  spinal  general 
paralysis. 

Description. — The  troubles  caused  by  peripheral  neuritis  vary  according 
as  the  lesion  chiefly  affects  the  motor,  sensory,  or  trophic  nerves  ;  according 
as  the  lesion  attacks  an  isolated  nerve  or  a  group  of  nerves  ;  and  according 
as  the  nerves  attacked  are  spinal,  cranial,  or  sympathetic. 

The  causes  of  peripheral  neuritis  sometimes  undertake  of  themselves  to 
make  a  selection  ;  thus,  lead-poisoning  selects  the  motor  and  the  muscular 
trophic  nerves,  producing  only  paralysis  and  amyotrophy  ;  it  passes  over  the 
sensory  nerves.  On  the  other  hand,  alcohol  especially  affects  the  peripheral 
sensory  nerves,  but  it  also  produces  paralytic  and  amyotrophic  troubles  ; 
it  is  generally  confined  to  the  lower  limbs.  Peripheral  neuritis  sometimes 
attacks  special  nerves,  the  optic  nerves  (alcoholism),  the  nerves  of  the 
external  musculature  of  the  eye,  strabismus,  diplopia,  external  ophthalmo- 
plegia (diabetes) ;  the  nerves  wliich  preside  over  accommodation  (diph- 
theria) ;  the  nerves  of  the  larynx  (tuberculosis,  plumbism) ;  the  pneumogas- 
tric  nerve,  with  dyspnoea  and  tachycardia,  etc. 

These  varieties  of  polyneuritis  may  exist  alone,  or  may  be  associated 
with  more  general  forms.  Amongst  these  general  forms,  that  generally 
described  imder  the  name  of  polyneuritis,  without  other  qualification,  must 
detain  us  longer. 

Polyneuritis  is  a  fairly  frequent  type,  which  may  sometimes  supervene 
without  apparent  cause,  or  may  follow  on  some  infectious  disease  (influenza), 
though  it  more  often  results  from  cold.  Its  course  is  as  follows  :  An  indi- 
vidual, otherwise  well,  experiences  twtchings,  shooting  pains,  cramps,  and 
heaviness  in  the  feet  or  the  legs.  Movement  and  walking  become  difficult 
(paresis) ;  the  steppage  gait  is  seen,  and  in  a  few  days,  if  the  evolution  of  the 
disease  is  rapid,  the  paraplegia  is  complete.  The  paralysis  is  symmetrical ; 
it  is  generally  more  pronounced  in  the  extensor  muscles,  and  an  important 
feature  is  that  it  commences  in  the  muscles  of  the  extremities  of  the  limbs, 
diminishing  in  severity  as  it  ascends  upwards.  Thus,  in  the  legs  the  muscles 
most  affected  are  the  small  muscles  of  the  foot,  the  extensor  muscles  of  the 
toes,  and  the  peroneal  muscles.  The  attitude  of  the  foot  is  also  character- 
istic ;  the  foot  drops,  and  the  toes  are  flexed,  as  if  the  flexor  muscles  were 


1474  TEXT-BOOK  OF  MEDICINE 

contracted  ;  but  tliere  is  no  real  contraction,  because  the  foot  sbows  neither 
rigidity  nor  resistance  ;  it  is  flaccid  and  swinging. 

The  paralysis  rarely  remains  limited  to  the  leg ;  in  a  few  days  the  arms 
are  attacked  in  their  turn.  The  disease  announces  itself  by  tingling,  shooting 
pains  and  numbness,  and  the  paresis,  or  the  paralysis,  spreads  from  the 
hands  to  the  shoulder,  selecting  the  extensors,  and  diminishing  in  intensity 
as  it  ascends.  The  wrist-drop  recalls  the  attitude  seen  in  lead  palsy ;  the 
patient  can  neither  raise  the  arm  nor  execute  any  movement,  and  in  certain 
cases,  as  in  a  patient  whom  I  saw  with  Eaymond,  the  paralysis  of  the  four 
limbs  is  absolute,  or  nearly  so.     The  sphincters,  however,  are  normal. 

Sensory  troubles  precede  and  accompany  the  paralysis.  I  have  already 
spoken  of  tingling  and  painful  twitchings  m  the  limbs  ;  in  this  variety  of  poly- 
neuritis the  pains  are  not,  as  a  rule,  as  acute  as  they  are  in  alcoholic  neuritis. 
On  the  other  hand,  pain  is  rarely  absent,  as  in  saturnine  neuritis.  Areas  of 
hypersesthesia  or  of  anaesthesia  may  be  observed,  and  we  may  find  dissocia- 
tion of  sensibility  to  pain,  to  touch,  and  to  temperature,  but  the  usual  fact 
in  the  variety  of  polyneuritis  under  discussion  is  that  the  spontaneous  pain 
is  not  acute  ;  whilst  the  pains  caused  by  pressure  on  the  muscles  or  on  the 
nerves,  at  their  points  of  exit,  and  in  the  sciatic  nerve  by  forcible  extension 
and  abduction  of  the  leg  show  clearly  that  the  disease  is  situated  in  the 
branches  and  in  the  nerve-trunks. 

The  tendon  reflexes  are  abolished ;  this  abolition  of  the  reflexes  is  one 
of  the  chief  symptoms  of  polyneuritis. 

The  electrical  changes  follow  the  motor  and  the  reflex  changes.  Elec- 
trical examination  has  the  twofold  advantage  of  assisting  in  the  diagnosis 
of  polyneuritis  and  of  gauging  its  importance  and  its  severity.  In  a  general 
manner,  the  electrical  contractility  is  much  affected  in  the  paralyzed  regions  ; 
the  reaction  to  the  faradic  current  is  weak  or  absent ;  the  action  of  the 
galvanic  current  is  inverted  in  the  regions  which  are  severely  affected.  The 
reaction  of  degeneration  is  observed.  Between  the  extremes  we  find  inter- 
mediate stages,  which  enable  us  to  form  an  idea  of  the  severity  and  of  the 
probable  duration  of  the  lesions. 

Muscular  atrophy  is  a  constant  symptom  of  pohoieuritis.  The  atrophy 
appears  at  the  same  time  as  the  paralysis  ;  but  it  runs  a  much  slower  course 
than  the  paralysis.  The  coexistence  of  paralysis  and  amyotrophy  in 
polyneuritis  is  explained  by  the  fact  that  the  branches  of  the  nerves  which 
supply  the  muscles  govern  both  the  motor  and  the  trophic  functions. 

The  muscular  atrophy  causes  deformity  of  the  paralyzed  regions.  The 
bones  stand  out,  and  the  masses  of  muscle  are  replaced  by  flattening.  The 
muscular  pads  in  the  feet  are  flattened,  whilst  the  interosseous  spaces 
become  hollowed ;  in  the  leg,  the  bulging  of  the  muscles  of  the  calf  is  replaced 
by  flaccid  skin,  and  the  antero-external  surface  is  excavated  like  a  furrow. 


NEUR1TI8  1475 

In  the  thigh  there  is  a  similar  disappearance  of  the  muscles.  In  the  upper 
limbs  the  hand  somewhat  resemljles  the  hiind  of  progressive  muscular 
atrophy ;  the  thenar  and  hypothenar  eminences  disapp(nir.  The  back  of 
the  hand  becomes  hollowed  out  in  the  interosseous  spaces,  and  the  forearm 
is  flat. 

In  spite  of  the  extensive  decay,  which  gives  to  the  limbs  the  appear- 
ance of  a  skeleton,  the  general  condition  remains  excellent,  the  appetite 
does  not  diminish,  all  the  functions  are  performed  regularly,  and  it  is  only 
after  weeks  and  months  that  reparation  commences.  The  muscular  atroj)hy 
and  the  paralysis  disappear,  and  in  the  majority  of  cases  recovery  is 
complete. 

Some  cases  of  pohmeuritis  are  subject  to  relapses  or  to  recurrences. 
Fatal  cases  of  polyneuritis  are  quite  exceptional ;  the  danger,  then,  arises 
from  neuritis  of  the  bulbar  nerves,  or  from  bulbo-medullary  lesions  which 
complicate  the  peripheral  lesions.  In  a  few  rare  cases  multiple  neuritis  is 
accompanied  by  mental  troubles — polyneuritic  pyschosis  (Korsakoff).  The 
condition,  then,  is  most  frequently  one  of  mental  confusion,  associated  with 
lesions  of  the  cerebral  cortex,  changes  being  seen  in  the  p}Tamidal  cells  and 
in  Betz's  giant  cells — sweUing  and  chroma toly sis  (Ballet  and  Faure). 

As  pol}Tieuritis  is  relatively  benign,  it  is  very  important,  from  the  point 
of  view  of  prognosis,  not  to  confound  polyneuritis  vtith  other  grave  diseases 
which  may  simulate  it.  In  its  painful  form,  which  is  generally  of  alcoholic 
origin,  polyneuritis  simulates  tabes.  This  pseudo-tabetic  form  is  far  from 
being  rare. 

The  most  remarkable  case  wiiich  I  have  met  with  refers  to  a  young  man  of  twenty- 
five  years  of  age,  who  for  several  months  drank  a  bottle  of  cognac  a  day  without  getting 
drunk.  He  came  from  America,  where  he  had  been  considered  to  be  suflFering  from 
tabes.  The  diagnosis  of  polyneuritis,  however,  seemed  to  me  to  be  obvious.  Lacaille 
gave  him  electrical  treatment,  and  in  sis  months  he  was  completely  cured. 

In  its  parahi;ic,  amyotrophic,  and  rapidly  progressive  form  poly- 
neuritis simulates  acute  poliomyelitis.  I  saw  a  most  remarkable  case  with 
Raymond : 

A  young  officer,  who  had  taken  a  dull  during  the  manoeuvres,  was  seized  in  a 
few  days  with  parah'sis,  commencing  in  the  lower  limb,  and  then  spreading  to  the  upper 
limbs.  The  paralysis  was  soon  followed  by  rapid  amyotrophy.  I  have  described  this 
case  in  detail  under  Acute  Spinal  Paralysis  in  the  Adult. 

Treatment. — I  shall  not  discuss  here  the  prophylactic  treatment  peculiar 
to  each  variety  of  polyneuritis  (removal  of  the  cause,  alcohol,  lead,  etc.), 
but  I  shall  merely  say  a  few  words  concerning  the  indications  for  electro- 
therapy. Babinski  expresses  the  following  opinion,  which  I  quote  ver- 
batim :  "  Electricity  is  one  of  the  agents  most  commonly  used  in  the  treat- 
ment of  peripheral  neuritis.     It  must,  however,  be  used  with  circumspection, 


1476  TEXT-BOOK  OF  MEDICINE 

and  under  certain  determined  circumstances.  It  may  be  said,  in  a  general 
manner,  that  electrotherapy  must  not  be  prescribed  at  the  commencement 
of  the  disease,  when  the  case  is  one  of  sensory  or  of  mixed  neuritis,  but  that 
its  use  is  clearly  indicated  when  the  morbid  process  seems  to  have  spent 
its  action,  and  when  we  are  only  dealing  with  the  sequelae  of  the  lesions  which 
it  has  provoked.  In  the  former  case,  the  electrical  stimulation  of  the  muscles 
would  have  no  other  result  than  to  exaggerate  the  pains,  and  it  might  even 
increase  the  lesions  ;  whilst  in  the  second  case  this  mode  of  treatment  is 
effective,  and  favours,  at  least,  the  restoration  of  the  atrophied  muscles." 


CHAPTER  VI 
NEUROSES 

I.  ESSENTIAL  EPILEPSY— SECONDARY  EPILEPSY. 

Formerly,  only  one  kind  of  epilepsy  was  admitted — primary  or  idiopathic  epilepsy. 
Secondary  epilepsy,  symptomatic  epilepsy,  and  partial  or  Jacksonian  epilepsy  formed 
a  group  of  epileptiform  conditions.  The  more  we  study,  the  more  extensive  becomes 
this  group  of  epileptiform  conditions.  The  result  is  that  true  idiopathic  epilepsy  is 
less  common  than  was  formerly  believed  to  be  the  case.  Moreover,  this  true  epilepsy 
might  not  absolutely  be  a  case  of  neurosis.  It  might  be  associated  with  cerebral  lesions 
which  had  previously  been  latent.  But  then,  if  it  is  no  longer  the  disease  sine  materia, 
it  enters  into  the  group  of  secondary  epilepsies,  and  there  is  no  longer  such  a  thing  as 
idiopathic  epilepsy.  I  shall  refer  to  this  question  again  under  the  pathogenesis  of 
epilepsy,  but  I  am  of  the  opinion  in  any  case  that  the  time  has  not  come  to  include 
everything  in  a  single  description,  and  in  the  present  section  I  shall  first  describe 
essential  or  idiopathic  epilepsy,  and  I  shall  then  review  the  various  forms  of  secondary 
epilepsy. 

Description. — In  true  epilepsy  two  chief  forms  occur — the  one  con- 
vulsive, grand  mat  ;  the  other  non-convulsive,  petit  mal. 

1.  Grand  Med — the  Attack  of  Epilepsy. — The  attack  is  sometimes  pre- 
ceded some  hours  or  some  days  m  advance  by  prodromata,  such  as  psychical 
troubles,  genital  excitation,  insomnia,  palpitations,  or  heaviness  in  the  head, 
and  at  the  moment  of  the  outburst  it  is  frequently  preceded  by  a  sudden 
and  rapid  "waming  which  is  caUed  the  aura  {aura,  vapour).  The  aura 
epUeptica  assumes  various  forms  ;  sometimes  it  is  a  strange  sensation  of  cold 
or.  hot  vapour,  or  of  sharp  pain,  starting  in  the  hand,  the  foot,  or  some  other 
part  of  the  body,  and  ascending  to  the  head  ;  sometimes  there  is  flushing  of 
these  same  parts,  sudden  functional  trouble  may  occur,  such  as  a  fit  of 
vomiting,  palpitation,  pain  in  the  chest,  constriction  of  the  throat,  an  irre- 
sistible impulse  to  run  or  to  turn  round,  hallucinations  of  sight  and  of 
hearing  (flashes  of  lightning,  whistling  noises,  and  streaks  of  light),  or  some 
psychical  perversion  (fear  of  a  mad  dog  or  of  a  terrifying  object).  The  aura, 
then,  is  sensory,  motor,  vasomotor,  and  psychic  ;  in  all  cases  it  is  a  pheno- 
menon of  central  origin.  The  aura  lasts  a  few  seconds  or  a  few  minutes ; 
in  some  cases  it  constitutes  in  itself  an  outline  of  the  epileptic  attack. 

Whether  there  is  or  is  not  an  aura,  the  attack  is  as  follows  :  The  patient 
IL  1477  9^ 


1478  TEXT-BOOK  OF  MEDICINE 

utters  a  cry,  loses  consciousness,  and  falls  down,  as  if  struck  by  lightning. 
The  suddenness  of  the  fall  explains  the  bruises  which  are  often  seen  on  the 
face  ;  and  the  loss  of  consciousness  accounts  for  the  terrible  burns  in  epUeptic 
patients  who,  at  the  time  of  the  attack,  fall  into  the  fire.  At  the  com- 
mencement of  the  attack  the  face  is  deathly  pale,  all  sensibility  is  abolished, 
the  coma  is  complete,  and  the  con\Tilsive  period  commences.  At  first  the 
conTulsions  are  tonic,  and  aU  the  muscles  participate  in  the  tetanic  rigidity. 
The  muscles  of  the  eyes,  of  the  face,  of  the  neck,  of  the  thorax,  of  the  abdo- 
men, and  of  the  limbs  are  in  a  state  of  tetanus ;  the  eyeball  is  convulsed  under 
the  eyelid  ;  the  face  is  drawn  ;  the  teeth  are  firmly  clenched  ;  the  head  is 
drawn  backwards  and  to  one  side ;  the  limbs  are  contracted  ;  the  hand  is 
turned  backwards  ;  the  thumb  is  in  the  position  of  forced  adduction,  and 
flexed  under  the  fingers,  and  momentary  arrest  of  the  respiratory  movements 
occurs.  The  face,  which  was  pale  at  the  commencement  of  the  attack, 
becomes  congested.  The  arterial  tension  is  raised,  and  the  pulse-rate  reaches 
120  or  150. 

The  tonic  stage  lasts  twenty  or  thirty  seconds,  and  then  the  clonic  stage 
commences.  The  convulsions  at  first  recur  every  second  ;  they  soon  become 
much  more  rapid,  and  their  amplitude  gradually  increases.  The  limbs  are 
jerked  about ;  the  face  grimaces  ;  the  eyeballs  roll  in  their  sockets  ;  bloody 
froth  bathes  the  lips  ;  the  respiration  is  noisy,  jerky,  and  sometimes  ster- 
torous ;  involuntary  emission  of  urine  and  of  faeces  is  common. 

The  convulsive  stage  lasts  for  a  minute  or  two  ;  the  patient  utters  a  deep 
sigh,  and  the  third  stage  of  the  attack  then  commences  :  this  is  an  apoplecti- 
form condition,  which  lasts  for  a  variable  period,  and  which  is  often  followed 
by  sleep.  The  attack  being  over,  the  patient,  unconscious  of  what  has  hap- 
pened, gradually  comes  round ;  but  for  some  time  he  suffers  from  confusion 
of  ideas,  profound  lassitude,  pains  in  the  head,  and  transitory  aphasia  or 
hemiplegia. 

Such  is  the  grand  mal,  and  it  must  be  remembered  that  attacks  of  epilepsy, 
especially  at  first,  take  place  during  the  night,  and  unknown  to  the  patient, 
who  falls  out  of  bed,  and  is  quite  surprised  to  wake  up  on  the  floor.  The 
physician  must  bear  these  nocturnal  attacks  in  mind.  "  An  individual 
will  tell  you  that  he  awoke  in  the  morning  with  a  headache.  He  will  tell 
you  that,  during  the  night,  he  passed  his  urine  in  the  bed.  He  has  a  certain 
embarrassment  in  his  speech,  due  to  painful  swelling  of  the  tongue,  which 
he  has  bitten.  You  notice  on  the  skin  of  the  forehead  and  of  the  neck 
ecchymotic  patches  (purpura).  You  may  then  state  positively  that  the 
patient  has  had  a  nocturnal  attack  of  epilepsy  "  (Trousseau). 

In  some  cases  the  nocturnal  attack  comprises  convulsive  movements, 
preceded  or  accompanied  by  snoring  and  by  vomiting,  put  down  to  indiges- 
tion. 


NEUROSES  1479 

Tlie  attacks  of  epilepsy  have  no  fixed  time  for  their  appearance.  Days, 
weeks,  and  months  pass  witliout  an  attack,  or  else  tlie  attacks  recur  fre- 
quently— in  some  cases,  so  fre([uently  as  to  constitute  the  sUUus  epUepticus. 
This  name  is  given  to  the  incessant  repetition  of  the  fits,  which  may,  indeed, 
become  subintrant,  a  new  fit  {ip])earing  Ijcfore  the  preceding  one  is  finished. 
The  status  ej)ilc])ticus  is  characterized  by  colla])se  and  by  coma,  which  are 
prolonged  indefinitely  ;  the  respiration  is  embarrassed,  the  temperature 
may  exceed  104°  F.,  and  remain  high  in  the  intervals  of  the  attacks.  The 
sphincters  are  paralyzed,  and  the  situation  becomes  so  grave  that  Delasiauve 
reported  six  cases  where  death  supervened  during  the  status  epilepticus. 
The  condition  may  last  for  several  days. 

In  some  epileptic  patients  their  sleep  is  disturbed  by  dreams,  which  are 
the  picture  of  the  attacks.  These  reves  d'acces  have  an  important  semeio- 
logical  value  ;  they  may  constitute  a  precursory  symptom  of  a  subsequent 
attack  (Fere). 

2.  Petit  Mai. — Petit  mal  is  non-convulsive  epilepsy,  characterized  by 
attacks  of  vertigo,  by  mental  aberration,  and  by  delirium  of  various  kinds. 
The  individual,  attacked  by  epileptic  vertigo,  suddenly  experiences  a  kind 
of  stupor  ;  he  loses  consciousness,  and  falls  down  stunned,  but  gets  up 
immediately,  without  any  other  manifestation.  The  patient  attacked  by 
mental  aberration  experiences,  unknown  to  himself,  a  sudden  suspension 
of  thought.  He  stops  in  his  reading  or  his  conversation,  grows  pale,  and 
makes  some  mumbling  movements.  His  look  is  fixed  and  empty ;  two 
or  three  seconds  afterwards  he  resumes  his  conversation,  quite  unconscious 
of  what  has  happened.  The  seizures  may  occur  several  times  during  the 
same  day.  The  attacks  of  vertigo  and  mental  aberration  are  sometimes 
followed  by  fits  of  somnambulism  (Voisin). 

In  other  individuals  the  petit  mal  consists  in  a  more  or  less  violent 
delirium  ;  one  patient  will  utter  incoherent  words  in  a  loud  voice,  another 
wiU  indulge  in  fits  of  laughter,  or  in  strange  or  obscene  gesticulations. 
Some  patients  only  experience  the  various  sensations  of  the  aura  epileptica, 
not  followed  by  convulsions.  The  petit  mal  is  the  most  frequent  form  of 
epilepsy.  It  often  changes  to  the  grand  mal,  whilst  the  converse  is  very 
rare.  In  some  cases  the  epilepsy  assumes  the  so-called  "  procursive  "  form  : 
the  patient  commences  to  run,  sometimes  in  a  straight  direction,  sometimes 
in  circles,  jumping  over  obstacles,  and  unconscious  of  his  condition.  This 
unconscious  procursion  may  constitute  the  whole  attack  ;  in  other  cases  the 
procursion  is  a  sort  of  aura,  and  the  epileptic  attack  appears  subsequently. 
Finally,  in  other  patients,  the  epileptic  attack  opens  the  scene,  and  the  pro- 
cursion is  postepileptic 

The  relation  of  epilepsy  to  mental  alienation  is  most  important  from 
a  medico-legal  point  of  view.     Intellectual  troubles  may  manifest  them- 

94-2 


1480  TEXT-BOOK  OF  MEDICINE 

selves  either  during  the  attack  of  epilepsy,  as  an  epiphenomenon,  or  apart 
from  the  attacks,  and  in  an  independent  manner.  The  patient  is  generally 
irritable  and  morose  ;  he  is  often  inclined  to  vicious  habits,  and  sometimes 
subject  to  true  delirium.  The  character  of  epileptic  delirium  is  essentially 
impulsive  and  instantaneous  (Falret).  Its  invasion  is  much  more  rapid 
than  that  of  the  other  varieties  of  mania,  and  it  ceases  as  suddenly  as  it 
appears.  Under  the  influence  of  irresistible  impulses  the  patient  with 
epileptic  delirium  leaves  his  home  and  wanders  about ;  he  fancies  himself 
persecuted,  suffers  from  terrifying  hallucinations,  and  in  the  most  un- 
expected and  sudden  manner  gives  himself  up  to  suicide,  manslaughter, 
theft,  or  incendiarism,  having  hardly  any  recollection  of  what  has  happened 
when  he  comes  round.  These  attacks  of  mania  may  last  for  some  hours  or 
for  some  da5^s  ;  they  vary  in  severity,  from  passing  dimness  of  the  intelli- 
gence to  the  most  acute  mania.  In  such  cases  the  responsibility  of  the 
individual  is  absolutely  lost,  and  it  is  the  duty  of  medical  jurist  to  solve 
this  often  difficult  problem.  The  petit  mal,  as  weU  as  the  grand  mal,  may 
lead  to  epileptic  mania. 

^Etiology. — True  idiopathic  epilepsy  is  often  hereditary,  the  parents 
saffering  from  epilepsy  or  from  general  paralysis,  alienation,  hysteria,  or 
tabes.  Epilepsy  appears  most  frequently  about  the  age  of  puberty ;  it 
rarely  declares  itself  after  twenty  years  of  age.  Fright,  moral  impressions, 
alcoholic  excesses,  and  onanism  are,  according  to  certain  authors,  the 
usual  determining  causes.  Congenital  malformation  of  the  skull  has  been 
given  as  a  cause.  Lasegue  has  upheld  an  analogous  theory,  by  pointing  out 
the  relation  between  epilepsy  and  facial  asymmetry.  This  facial  asymmetry 
is  said  to  result  from  a  defect  in  the  conformation,  or  from  a  vicious 
consolidation  of  the  bones  at  the  base  of  the  skull. 

The  determining  cause  of  the  attack  of  epilepsy  seems  to  be  due  to  abnor- 
mal excitation  of  the  bulb  (Schroder,  van  der  Kolk).  This  excitation, 
whether  primary  or  reflex,  and  the  cerebral  radiations  which  accompany  it  in 
part  explain  the  convulsions,  the  loss  of  consciousness,  and  the  initial  pallor  of 
the  face  (spasmodic  contraction  of  the  vessels  of  the  pia  mater  and  of  the  face). 

According  to  Chaslin,  epilepsy  is  said  to  depend  on  more  or  less  appreci- 
able changes  in  the  brain.  His  description  of  the  lesions  in  the  brains  of 
several  epileptic  patients  is  as  follows  :  "  In  the  first  three  brains  the  lesions 
were  visible  to  the  naked  eye.  The  meninges  were  not  adherent,  nor  were 
they  appreciably  changed.  The  convolutions,  which  in  certain  places 
appeared  completely  normal,  were  in  other  places  reduced  in  size,  hard  to 
the  touch  like  cartilage — some  being  shagreened,  others  smooth.  The  comua 
of  Ammon  and  the  bulb  were  also  aflected  to  a  more  .or  less  marked  extent." 
The  microscopic  examination  showed  sclerosis  of  the  neuroglia,  which  he 
considers  is  the  result  of  an  hereditary  process. 


NEUROSKS  1481 

Diagnosis.  Tn  a  subsequent  section  I  shall  give  the  distinctions  between 
epilepsy  and  hysteria.  True  epilepsy  must  not  be  mistaken  for  the  epilepti- 
form conditions  which  I  sliall  describe  in  a  moment.  Given  an  attack  of 
epilepsy,  it  is  not  sufficient  to  differentiate  it  from  the  other  convulsive 
neuroses  (hysteria) ;  we  must  also  ascertain  whether  we  are  dealing  with  a 
case  of  true  epilepsy  or  with  convulsions  symptomatic  of  intoxication 
(plumbism,  uraemia),  of  cerebral  tumour  (syphilis,  cancer),  of  cerebro- 
bulbar  sclerosis  or  with  epilepsy  of  reflex  origin  (foreign  bodies  in  the 
intestine,  taenia,  worms). 

The  diagnosis  must  also  be  made  in  the  case  of  the  petit  mal,  which 
must  not  be  confounded  with  vertigo  ab  aure  IcBsa  or  with  lar}'ngeal 
vertigo.  Furthermore,  we  must  not  forget  that  epilepsy  may  assume  a 
defaced  form  limited  to  the  aura,  and  that  many  cases  of  so-called  apoplecti- 
form cerebral  congestion,  and  of  angina  pectoris,  are  simply  cases  of  disguised 
epilepsy  (Trousseau). 

The  prognosis  of  epilepsy  is  extremely  grave,  because  it  often  induces 
weakening  of  the  faculties  and  different  forms  of  mental  alienation. 

Treatment. — The  treatment  of  the  fits  of  epilepsy  is  almost  nil.  Certain 
patients,  in  whom  the  aura  commences  in  the  hand  or  the  foot,  can  arrest 
the  attack  by  compression  of  the  parts  above  the  seat  of  the  aura.  The 
most  efficacious  measure  in  epilepsy  appears  to  me  to  be  the  association  of 
bromide  of  potassium  and  belladonna,  continued  for  a  long  time.  The 
bromide  of  potassium  must  be  taken  in  doses  of  30  to  120  grains  daily 
during  the  first  and  third  weeks  of  each  month,  while  the  belladonna  is 
administered  in  doses  of  |  to  1  grain  daily  during  the  second  and  fourth 
weeks.  The  bromide  of  potassium  may  be  replaced  by  bromide  of  camphor 
or  of  sodium,  and  by  Yvon's  polybromide.  The  elimination  of  salt  from  the 
diet  renders  the  patient  more  susceptible  to  the  action  of  the  bromide 
(Richet  and  Toulouse). 

This  treatment  must  be  continued  for  years,  with  periods  of  inter- 
mission. The  bromides  may  be  administered  in  large  doses  as  enemata. 
Physical  and  mental  depression,  dilatation  of  the  pupils,  and  paresis  of 
accommodation  indicate  that  the  bromide  must  not  be  pushed. 

In  a  recent  work  De  Fleury  has  shown  that  most  epileptic  patients  suffer 
from  physiological  distress  ;  tonics  should  then  be  given  with  the  bromide. 
Nerve  stimulants  are  unsuitable  (alcohol,  coffee).  On  the  other  hand, 
they  benefit  from  douches,  massage,  static  electricity,  and  especially  saline 
injections,  which  lessen  the  mental  dullness,  whilst  increasing  the  absorption 
and  the  elimination  of  the  bromide.  In  this  manner  most  of  the  patients 
may  be  kept  free  from  attacks,  on  the  limits  of  bromide  saturation,  with 
much  smaller  doses  than  are  usually  given.  The  same  writer  has  pointed  out 
the  importance  of  diet  in  the  treatment  of  the  haut  mal.    It  suffices,  in  fact, 


1482  TEXT-BOOK  OF  I\IEDICINE 

to  put  a  fair  number  of  epileptics  on  an  easily  digested  diet,  and  to  give  them 
water  or  milk  to  drink  ia  order  to  render  tlie  attacks  less  frequent  and  less 
severe,  tlie  doses  of  bromide  being  unchanged.  Surgery  has  a  place  in 
the  treatment  of  epilepsy,  diampionniere  has  obtained  encouraging  results 
from  trepliuiing,  not  only  in  s}Tn.ptomatic  (exostoses,  tumours),  but  also  in 
true  epHepsy. 

Secondary  Epilepsy — Epileptiform  Conditions. 

We  may  place  in  one  class  cases  of  secondary  epilepsy  witb  more  or  less 
coarse  lesions  of  the  brain.  In  tlie  first  place,  I  would  mention  epUepsy 
associated  with,  infantile  ceTebral  hemiplegia,  consequent  on  porencephalia, 
cerebral  lacunse,  and  lobar  sclerosis.  In  such  a  case  the  course  of  events  is  : 
Some  months  after  birth  a  child  is  taken  ill  with  fever,  convulsions,  and 
hemiplegia.  The  storm  then  disappears,  the  hemiplegia  gradually  improves, 
and  the  intelligence  remains  practically  normal,  but  a  few  years  later,  or  at  the 
onset  of  puberty,  the  attacks  of  epilepsy  appear.  Perhaps  the  epilepsy 
develops  as  the  result  of  a  secondary  infection.  Epilepsy,  consequent  on 
cerebral  tumours  (glioma,  sarcoma,  cysts,  tuberculosis,  syphilis),  on  general 
paralysis,  or  on  descending  sclerosis  of  the  mesencephalon,  belongs  to  the 
same  category. 

To  a  second  class  belongs  secondary  epilepsy  of  toxic  origin  (satur- 
nine encephalopathy,  urgemia).  Under  convulsive  ursemia  we  saw  that 
the  epileptic  attacks  of  Bright' s  disease  very  closely  simulated  true 
epilepsy. 

To  a  third  class  belongs  secondary  epilepsy  of  reflex  origin  (foreign  bodies 
in  the  intestine,  worms,  taenia).  I  have,  with  Krishaber,  published  the  case 
of  a  voung  boy  who  had  swallowed  prune-stones.  He  was  seized  with 
epileptiform  convulsions,  and  died.  At  the  post-mortem  examination  we 
found  the  stones  in  the  lower  portion  of  the  ileum. 

The  varieties  of  secondary  epilepsy  just  enumerated  differ  somewhat 
from  true  epilepsy.  The  initial  cry  is  often  absent,  the  pallor  of  the  face 
is  less  pronounced,  the  con\'Tdsions  are  not  so  markedly  unilateral,  and  the 
comatose  condition  which  follows  the  attack  is  less  prolonged,  but  the 
clinical  resemblance  between  secondary  epilepsy  and  true  epilepsy  is  absolute 
(Trousseau). 

Acquired  or  hereditary  s}^hilis  claims  the  largest  share  in  symptomatic 
epilepsy  ;  according  to  circumstances,  it  produces  partial  or  true  epilepsy. 
The  crises  which  at  first  occur  far  apart  appear  closer  together,  and  are  often 
accompanied  by  paralyses.  "  If  a  healthy  adult,  over  thirty  years  of  age, 
is  attacked  for  the  first  time  with  epilepsy,  the  chances  are  that  the  epilepsy 
is  of  syphilitic  origin  "  (Fournier),  and  the  reason  is  that  essential  epilepsy 
always  shows  itself  in  childhood  or  youth.     There  is,  however,  a  form  of 


NEimOSES  1483 

syphilitic  epilepsy  which  may  show  itself  in  childhood  or  in  youth — viz., 
epilepsy  consequent  on  hereditary  syphilis.  TJiis  question  is  discus.scd 
under  (V^rehral  Syi)]iilis. 

II.  PAETIAL  EPILEPSY— JACKSONIAN  EPILEPSY. 

Partial  epilepsy  was  named  by  Charcot  Jacksonian  epilepsy,  because 
Jackson  gave  an  excellent  description  of  it.  To  give  an  idea  of  it,  I  shall 
quote  a  case  from  one  of  my  clinical  lectures  :* 

A  man  was  send  into  my  ward  at  the  Hotel-Dieu.  On  the  evening  of  his  admission, 
and  during  the  next  morning,  he  had  two  attacks,  which  I  saw.  At  the  moment  of  the 
attack  the  patient  uttered  a  cry,  witliout  losing  consciousness,  the  head  and  the  eye.s 
were  turned  to  the  right,  the  right  arm  became  contracted,  the  fingers  were  flexed  on 
the  forearm,  the  forearm  was  flexed  on  the  arm,  and  the  arm  was  abducted  over  the 
chest.  Immediately  after  this  phase  of  contraction,  which  lasted  but  a  few  seconds, 
the  upper  limb  showed  jerky  movements,  as  in  the  clonic  convulsions  of  epilepsy.  Two 
minutes  later  the  convulsions  became  less  severe,  and  were  replaced  by  fibrillary  con- 
tractions, followed  by  convulsive  movements  of  the  right  side  of  the  face  and  of  the 
neck.  The  face  had  a  grimacing  look,  the  angle  of  the  mouth  twitched,  the  alse  nasi 
were  raised,  but  the  tongue  was  neither  bitten  nor  pushed  forward  between  the  teeth, 
and  we  noticed  no  foaming  at  the  mouth. 

The  whole  attack  lasted  from  three  to  four  miuutes,  during  which  time  the  head 
and  the  eyes  remained  in  a  condition  of  conjugate  deviation.  The  patient,  who  remained 
conscious,  was  an  alarmed  vitness  of  the  seizure,  but  was  incapable  of  uttering  a  word. 
The  attack  was  not  followed  by  incontinence  of  urine,  intellectual  torpor,  or  stertorous 
breathing ;  in  short,  none  of  the  symptoms  which  follow  the  major  attack  of  epilepsy 
(but  which  may,  nevertheless,  exist  after  Jacksonian  epilepsy)  were  present.  In  my 
patient  this  partial  epilepsy  invariably  commenced  in  the  right  arm,  and  remained 
limited  to  the  ann  and  to  the  right  side  of  the  face.  There  was,  therefore,  no  possible 
doubt  as  to  the  diagnosis  of  Jacksonian  epilepsy  of  the  brachio-facial  type. 

The  affected  region  was  paretic,  the  face  was  shghtly  deviated  to  the  left,  the  arm 
had  lost  some  of  its  power,  as  was  shown  by  the  dynamometer,  and  the  patient  could 
only  write  with  difficulty.  This  paresis  was  not  simply  a  sequela  of  the  epileptic 
attack,  since  it  preceded  the  attacks.  Speech  was  embarrassed,  and  a  certain  degree 
of  paraphasia  was  present.  Sensation  was  quite  normal.  The  reflexes  were  shghtly 
exaggerated  on  the  right  side. 

The  patient,  about  a  fortnight  prior  to  his  admission  into  the  hospital,  had  suffered 
from  vertigo  and  heaviness  in  the  head ;  he  was  less  able  to  carry  out  his  duties  as  an 
accountant.  His  arm  grew  heavy,  and  writing  became  more  difficult  every  day.  In 
the  meantime,  a  couple  of  days  prior  to  his  admission,  the  patient  happened  to  be  in 
a  shop,  when  he  felt  a  painful  twitching  in  the  index-finger  of  his  right  hand.  This  aura 
was  followed  by  the  first  attack  of  brachio-facial  epilepsy.  During  this  attack,  although 
he  did  not  lose  consciousness,  there  was  slight  mental  confusion,  because,  after  having 
witnessed  the  first  period  of  the  attack,  he  did  not  perceive  that  he  had  been  taken 
from  the  shop  to  a  neighbouring  chemist. 

What  was  the  precise  seat  of  the  lesion,  and  what  was  its  nature  ?  The  precise 
seat  of  the  lesion  must  be  in  the  middle  portion  of  the  frontal  and  ascending  parietal 
convolutions,  without  encroachment  on  the  paracentral  region.  As  to  the  nature  of 
the  lesion — the  man  was  not  syphilitic — I  diagnosed  a  patch  of  chronic  tubercular 

*  "  Epilepsie  Jacksonienne  "  {Clinique  Medicate  de  V Hotel-Dieu,  1897,  9""^  le^on). 


1484  TEXT-BOOK  OF  MEDICINE 

meningitis.  As  a  matter  of  fact,  our  patient  had  an  abscess  of  the  ribs,  and  a  cold 
abscess  in  the  neck,  the  pus  of  which  was  tubercular.  It  was,  therefore,  reasonable  to 
admit  three  tubercular  lesions  in  his  case,  two  abscesses,  and  a  patch  of  meningo- 
encephalitis. 

Description. — Jacksonian  or  partial  epilepsy  is  characterized  by  con- 
vulsive attacks',  commencing  in  a  definite  group  of  muscles.  The  attack 
may  be  limited  to  the  region  attacked,  or  may  extend  to  other  regions. 
Following  Bravais's  example,  we  may  describe  three  principal  varieties  of 
partial  epilepsy  :  epilepsy  commencing  in  the  arm  (brachial),  in  the  face 
(facial),  and  in  the  leg  (crural). 

The  brachial  type  is  the  most  common.  In  this  variety  the  various  parts 
of  the  upper  limb  are  flexed  on  one  another  by  contraction  of  the  flexor 
muscles,  and  the  convulsive  attack  limited  to  the  arm  at  once  follows.  In 
the  facial  or  cervico-facial  type  the  head  and  the  eyes  are  deviated  (conjugate 
deviation) ;  the  convulsions  are  limited  to  the  face  and  to  the  neck,  affecting 
the  angle  of  the  mouth,  the  orbicularis  palpebrarum,  the  motor  muscles  of 
the  eye  and  of  the  tongue,  and  the  sterno-mastoid  muscle.  In  the  crural 
type  the  lower  limb  is  extended  ;  the  attack  commences  in  the  big  toe,  and 
extends  to  the  entire  limb. 

In  some  cases  Jacksonian  epilepsy  is  partial,  m  the  true  sense  of  the 
^ord — that  is  to  say,  that  it  does  not  go  beyond  its  original  limits  ;  it  remains 
confined  to  the  arm,  the-  face,  or  the  leg,  without  extending  to  other  regions. 
Most  frequently,  however,  it  commences,  for  example,  in  the  arm,  and 
extends  to  the  face,  thus  realizing  the  mixed  brachio-facial  type.  Or,  again, 
after  commencing  in  the  arm  and  in  the  face  it  invades  the  leg,  thus  realizing 
the  brachio-cervico-crural  type  ;  it  may  commence  in  the  face,  and  then 
invade  the  upper  limb  and  the  lower  limb,  thus  realizing  the  mixed 
facio-brachio-crural  type ;  or,  finally,  it  may  commence  in  the  lower  limb, 
subsequently  attacking  the  arm  and  the  face,  thus  realizing  the  mixed 
cruro-brachio-facial  type.  Jacksonian  epUepsy  may  not  remain  confined 
to  one  side  of  the  body,  but  may  cross  to  the  opposite  side. 

The  onset  of  the  attack  is  not  always  identical ;  the  aura,  the  initial  cry, 
and  the  loss  of  consciousness  may  be  present  or  absent.  My  patient  had  an 
aura  which  commenced  in  his  right  index-finger  in  his  first  attack.  In  the 
two  attacks  which  I  saw  he  uttered  the  initial  cry,  but  did  not  lose  conscious- 
ness. The  duration  of  the  attack  varies  from  a  few  moments  to  an  hour ; 
on  an  average  it  lasts  for  a  few  minutes.  The  attack  is  sometimes  followed 
by  stertorous  breathing,  delirium,  amnesia,  vertigo,  vomiting,  and  headache. 

The  regions  which  have  been  convulsed  during  the  fit  are  generally 
paretic  after  the  attack ;  the  condition  may  go  as  far  as  complete  paralysis. 
These  paralyses  are  of  the  same  type  as  the  convulsive  attack,  being  facial, 
brachial,  or  crural ;  they  may  be  slight  and  transito7:y,  or  severe  and  perma- 


NEUROSES  148.-, 

nent ;  they  may  follow  or  precede  the  convulsive  symptoms.  In  my  j)atiwit 
the  paralysis  had  preceded  the  convulsions,  since  the  arm  and  tlio  face 
remained  paretic. 

It  is  to  be  noti(!ed  that  the  limbs  which  are  contracted  and  convulsed 
during  the  attack  are,  apart  from  the  attack,  in  a  condition  of  flaccid 
hemiplegia.  This  proves  that  a  muscle  may  be  alternately  paralyzed  and 
convulsed  by  the  same  nervous  lesion  ;  it  is  paralyzed  as  long  as  it  is  deprived 
of  normal  stimulus,  l)ut  it  may  nevertheless  become  convulsed  or  contracted 
when  the  stimulus  is  very  much  increased.  This  condition  must  be  com- 
pared with  that  of  the  glottis  in  lesions  of  the  recurrent  nerve.  I  have  given 
details  under  Aneurysm  of  the  Aorta :  A  lesion  of  the  left  recurrent  nerve 
causes  paralysis  of  the  left  vocal  cord,  which  does  not  pre\*ent  severe  spasms 
of  the  glottis  from  supervening — that  is  to  say,  contracture  of  the  two  vocal 
cords. 

The  frequency  with  which  the  Jacksonian  attacks  may  be  repeated  is 
most  variable  ;  they  are  sometimes  separated  by  intervals  of  several  weeks 
or  months ;  at  other  times  they  recur  at  close  intervals.  In  some  cases, 
which  are  fortunately  very  rare,  they  become  subintrant,  cause  a  consider- 
able rise  in  temperature,  and  the  subject  dies  in  a  condition  of  status 
epilepticus. 

Some  years  ago  I  had  in  my  ward  at  the  Necker  Hospital  a  patient  with  Jacksonian 
epilepsy  on  the  right  side,  of  the  brachio -facial  type.  The  attacks  increased  in  number 
and  in  severity.  We  counted  as  many  as  380  attacks  ia  the  same  day,  and  the  patient 
succumbed  in  a  condition  of  status  epilepticus,  with  general  epileptiform  convulsions, 
the  temperature  reaching  104° F.  At  the  autopsy,  I  found  a  glioma  in  the  left  ascending 
frontal  and  parietal  region.  Last  year,  at  the  Hotel-Dieu,  I  had  a  patient  suffering 
from  Jacksonian  epilepsy  operated  on  by  Marion.  This  patient  had  as  many  as  300 
attacks  daily. 

Diagnosis  of  the  Site  of  the  Lesion. — It  is  not  difficult  to  recognize 
partial  epilepsy,  but  this  is  only  the  first  step  in  the  diagnosis.  There  are 
two  other  steps,  the  topographical  diagnosis  and  the  pathogenic  nature  of 
the  original  lesion.     These  facts  are  indispensable  in  treatment. 

In  general,  attacks  of  Jacksonian  epilepsy  have  their  origin  in  a  cortical 
lesion  of  the  ascending  frontal  and  parietal  convolutions,  separated  by  the 
fissure  of  Rolando. 

This  motor  area  may  be  divided  into  three  chief  motor  centres  :  one  for 
the  face  and  the  tongue,  another  for  the  arm,  and  a  third  for  the  leg.  The 
motor  centre  of  the  face  and  of  the  tongue  corresponds  to  the  lower  extremity 
of  the  convolutions,  and  more  particularly  to  the  ascending  frontal  convolu- 
tion. The  motor  centre  of  the  arm  is  placed  higher  in  the  ascending,  frontal, 
and  parietal  convolutions.  The  motor  centre  of  the  leg  corresponds  to  the 
upper  portion  of  the  ascending  convolutions,  which,  on  the  internal  surface 
of  the  hemisphere,  form  the  paracentral  lobule.     The  paracentral  lobule 


1-186 


TEXT-BOOK  OF  MEDICINE 


is  a  narrow  and  circumscribed  area  of  tlie  internal  surface  of  the  cerebral 
hemispheres.  It  is  bounded  in  front  by  the  first  frontal  convolution,  and 
behind  by  the  quadrate  lobe,  below  by  the  convolution  of  the  corpus 
callosum,  and  above  by  the  upper  edge  of  the  hemisphere. 

As  Charcot  has  pointed  out,  we  must  extend,  at  least  above,  the  classic 
limits  of  the  paracentral  lobule,  and  join  to  it  the  terminal  extremity  of  the 


Fig.  74. — ^Motor  Area  of  BRArsr. 

Fa,  Ascending  frontal  convolution ;  Pa,  ascending  parietal  convolution ; 
F,  H,  centres  for  face  and  tongue ;  B,  centre  for  speech. 

ascending,  frontal,  and  parietal  convolutions  which  form  a  part  of  the 
external  surface  of  the  hemispheres.  In  other  words,  the  region  of  the  para- 
central lobule,  or  the  crural  centre,  must  comprise,  on  the  one  hand,  the 
paracentral  lobule,  and,  on  the  other  hand,  the  upper  extremity  of  the 
ascending  frontal  and  parietal  convolutions  which  bend  over  the  upper 
edge  of  the  hemisphere  prior  to  entering  the  paracentral  lobule,  properly 


Fig.  75. — Inner  Aspect  of  HEMismERB. 
PcL,  Paracentral  lobula, 

so  called.  "  In  this  circumscribed  crural  region  arise  the  anatomo-physio- 
logical  changes  which  govern  the  execution  of  the  usual  movements  of  the 
lower  limb  "  (Charcot). 

The  lesions,  limited  to  each  of  these  motor  regions,  may  give  rise  to 
svmptoms  which  are  also  limited  to  the  face,  to  the  arm,  and  to  the  leg. 
According  to  the  degree  of  destruction,  or  of  irritation  of  the  affected  region, 


NEUROSES  1487 

the  corresponding  symptoms  assume  the  f(jrm  of  paralysis,  of  contractures, 
or,  finally,  of.  attacks  of  Jacksonian  epilepsy.  It  is,  indeed,  not  rare  to  find 
these  differcjit  forms  ap])earing  together  or  in  succession. 

In  order  to  bo  thoroughly  convinced  of  the  value  of  these  cerebral 
localizations,  I  shall  quote  cases  in  which  the  Jacksonian  epilepsy  and  the 
cerebral  localization  are,  so  to  say,  superposed.  Let  us  first  deal  with 
lesions  of  the  paracentral  lobule. 

Potain :  A  carman,  walking  bosido  his  cart,  suddenly  felt  a  sharp  ]y,im  in  liis  riglit 
foot.  He  gripjicd  a  neighbouring  tri'lliswork  to  prevent  iiimself  fioni  f;illijig,  and  after 
his  boot  had  boon  taken  oil  by  a  friend,  ho  noticed  that  the  muscles  of  the  calf  were 
hard,  as  in  cramp,  that  the  foot  was  extended,  and  that  the  muscles  of  the  leg  were 
affected  with  painful  jerks.  This  attack  of  Jacksonian  epilepsy  lasted  for  icn  minutes. 
Four  days  later,  at  ten  o'clock  in  the  morning,  a  similar  attack  occurred,  and  the 
patient  was  admitted  under  Potain.  The  convulsive  attack  reappeared  on  his  admis- 
sion into  hospital ;  it  was  strictly  confined  to  the  left  leg.  When  the  attack  was  over, 
it  was  noticed  that  the  leg  was  pai'alyzed,  the  sensibility  was  diminished,  and  the 
reflexes  were  sluggish.  After  this  time  the  Jacksonian  epilepsy  did  not  reappear,  but 
erysipelas  invaded  the  buttocks,  and  a  bed-sore  developed  on  the  sacrum.  Signs  of 
tuberculosis  were  foimd  in  both  lungs,  and  the  patient  soon  died  in  coma. 

At  the  post-mortem  examination  the  limgs  were  foimd  to  be  infiltrated  with  tubercles, 
but  the  interest  was  centred  in  the  cerebral  lesion.  This  lesion,  except  for  some  tuber- 
cular granulations  over  the  convexity  of  the  hemispheres,  was  clearly  localized  in  the 
left  paracentral  lobule,  which  was  capped  by  a  patch  of  meningitis  as  hard  as  cartilage. 
This  patch  not  only  covered  the  paracentral  lobule,  properly  speaking,  but  almost  the 
whole  paracentral  region — that  is  to  say,  the  upper  portion  of  the  parietal  convolution. 

This  case  is  an  example  of  a  tubercular  lesion  of  the  paracentral  region,  followed 
by  Jacksonian  epilepsy  of  the  lo-\\^r  limb. 

Charcot :  A  patient  suffering  from  pulmonary  tuberculosis  was  admitted  under 
Charcot.  Three  months  previously  she  had  felt  numbness  in  the  left  leg,  which  made 
walking  diflficult.  A  fortnight  later  an  attack  of  Jacksonian  epilepsy  suddenly  super- 
vened ;  it  commenced  in  the  left  leg,  and  extended  to  the  arm  and  to  the  face  on 
the  same  side.  A  second  attack  occurred  a  week  later,  followed  in  four  days' 
time  by  a  third  attack,  and  the  left  arm  became  paralyzed.  Charcot  diagnosed 
meningeal  tuberculosis  of  the  paracentral  lobule.  The  patient  died  a  fortnight 
later. 

At  the  post-mortem  examination  pulmonary  tuberculosis  was  foimd.  The  para- 
central region  only  was  attacked.  On  the  paracentral  lobule  and  on  the  upper  part 
of  the  ascending  frontal  and  parietal  convolutions  of  the  right  hemisphere  a  patch  of 
thick,  yellowish  meningitis  was  found,  infiltrated  with  tubercular  granulations  and 
with  pus.  This  patch,  clearly  limited  to  the  paracentral  region,  was  firmly  adherent 
to  the  brain  tissue,  which  also  showed  tubercular  infiltration. 

This  case  proves  that  tubercular  meningitis  may  occur  as  a  circumscribed  patch. 
It  shows,  furthermore,  the  relation  of  crural  Jacksonian  epilepsy  to  lesions  of  the 
paracentral  region. 

Rendu :  The  patch  of  tubercular  meningitis  may  be  bilateral,  affecting  the  para- 
central region  of  both  hemispheres.  The  symptoms  then  affect  both  lower  limbs  in 
the  same  manner  as  an  attack  of  paraplegia,  caused  by  a  lesion  of  the  spinal  cord. 
Rendu  has  published  a  case  of  this  kind.  He  had  in  his  wards  a  patient  with  para- 
plegic symptoms  simulating  a  disease  of  the  spinal  cord.  The  patient  died,  and  "  instead 
of  the  supposed  spinal  meningitis,  we  found  circumscribed  and  symmetrical  tubercular 
meningitis  strictly  confined  to  the  area  supplied  by  the  anterior  cerebral  arteries.     The 


1488  TEXT-BOOK  OF  MEDICINE 

progressive  and  simultaneous  destruction  of  the  paracentral  lobule  on  both  sides  had 
caused  the  special  symptomatology  in  this  case." 

Charcot:  A  physician  requested  Charcot  to  give  him  his  opinion.  While  he  was 
dining  two  evenings  previously  at  a  friend's  house,  he  had  been  acutely  troubled  with 
headache,  from  which  he  had  suffered  for  several  days.  He  started  to  walk  home,  but 
he  had  only  taken  a  few  steps  when  his  right  leg  became  suddenly  rigid,  and  was  at 
the  same  time  shaken  by  violent  rhythmical  convulsions.  Almost  immediately  the 
arm  of  the  same  side  was  invaded  in  a  similar  manner,  and  the  patient  fell  senseless. 
He  was  carried  home,  the  loss  of  consciousness  lasting  for  an  hour.  During  the  night 
and  the  next  morning  more  epileptiform  attacks  occurred. 

These  attacks  were  not  accompanied  by  loss  of  consciousness,  and  the  patient  was 
able  to  witness,  n,ot  without  alarm,  the  progressive  and  regular  invasion  of  the  con- 
vulsions, which  always  started  in  the  left  leg,  and  then  spread  to  the  arm  and  to  the 
corresponding  side  of  the  face.  He  had  had  syphilis,  and  as  his  attack  of  Jacksonian 
epilepsy  always  commenced  in  the  leg,  Charcot  diagnosed  a  syphilitic  lesion  of  the  right 
paracentral  lobule,  and  consequently  prescribed  treatment  with  mercury  and  iodide. 
Speedy  recovery  followed. 

Personal  case :  A  man  was  brought  into  my  ward  on  November  6,  1899.  He  had 
hardly  got  there  when  he  had  an  attack  of  Jacksonian  epilepsy.  The  head  was  turned 
to  the  left,  the  left  leg  and  the  arm  were  extended,  and  were  almost  immediately  affected 
by  shght  convulsions  ;  the  right  leg  was  also  affected  by  convulsions.  The  crisis  lasted 
for  half  a  minute  without  the  patient  losing  consciousness,  and  without  the  face  par- 
ticipating. The  man  had  always  been  well.  For  the  past  year  he  had  only  been 
troubled  with  shght  headache,  which  had  recently  increased  in  severity.  Partial 
epilepsy  had  suddenly  made  its  appearance  on  the  previous  evening.  The  patient  had 
had  since  that  time  about  300  crises  in  twenty-four  hours.  In  spite  of  all,  he  remained 
quite  conscious,  but  his  anxiety  was  extreme.  Although  the  arm  seemed  to  be  attacked 
at  the  same  time  as  the  leg,  I  placed  the  lesion  at  the  top  of  the  right  paracentral  lobule, 
thinking,  too,  that,  convulsions  being  present  in  the  right  leg,  the  left  paracentral  lobule 
was  also  affected.  It  was  impossible  for  me  to  state  the  nature  of  this  lesion.  As 
mercurial  treatment  gave  no  result,  I  asked  Marion  to  operate,  and  the  topographical 
diagnosis  was  absolutely  verified.  In  the  highest  portion  of  the  motor  convolutions, 
near  the  upper  extremity  of  the  fissure  of  Rolando,  in  the  right  paracentral  lobule,  on 
the  surface  of  the  cortex,  there  was  a  hard  tumour  of  the  size  of  a  cherry.  Its  removal 
was  easy.  The  microscopic  examination  of  this  tiunour  had  nothing  characteristic. 
The  absence  of  adhesions  to  the  dura  mater,  the  seat,  the  size,  the  mulberry-hke  appear- 
ance, and  the  delimitation  found  in  my  case  are  seen  in  the  most  varied  cases.  The 
liistological  examination  did  not  reveal  the  exact  nature  of  this  tumour.  It  was 
markedly  fibromatous. 

We  are  now  clear,  I  think,  as  to  the  relations  between  Jacksonian  epilepsy 
of  the  crural  type  and  the  lesions  of  the  paracentral  lobule.  When  the  attack 
commences  in  the  leg,  whether  it  remains  there,  or  whether  it  extends,  the 
cerebral  lesion  (tuberculoma,  syphiloma,  glioma,  osteoma,  fibroma,  or 
parasitic  tumour)  is  localized  in  the  paracentral  region. 

Let  us  next  study  the  localization  of  the  motor  convolutions  in  which  a 
lesion  causes  brachial  epilepsy.  The  following  case  gives  a  very  clear  idea 
of  it : 

Chantemesse :  A  woman,  twenty-eight  years  of  age,  in  good  health,  said  that  one 
day,  on  rising,  she  felt  twitchings  and  jerks  in  the  left  arm.  The  jerks  then  invaded 
the  leg  on  the  same  side,  and  the  patient  became  unconscious.     Next  day  a  similar 


NEUROSES  1480 

attack  of  Jacksonian  epilepsy  commenced  in  the  left  arm,  and  was  followed  by  paralysis. 
On  her  admission,  we  noticed  paralysis  of  the  left  arm,  with  contracture  and  flexion  of 
the  elbow.  Those  s\'ni{)tnms  wore  much  less  marked  in  the  leg.  The  fate  and  tongue 
were  slightly  doviatotl  to  the  right.     A  few  days  later  the  jKitient  died  in  coma. 

At  the  post-mortem  examination  we  found  tubercular  mt-ningo-encephalitis  over 
the  right  ascending  frontal  and  parietal  convolutions  ;  the  paracentral  region  was 
healtliy.  This  localization  was  in  dose  relation  with  the  appearance  of  the  BjTnptoms, 
the  epilepsy  always  commencing  in  the  left  arm. 

Charcot  has  published  the  case  of  a  man  of  fifty  years  of  age  Buffering  from 
Jacksonian  epilepsy  beginning  in  the  right  arm,  and  accompanied  by  paresis.  The 
post-mortem  examination  showed  a  sarcoma  in  the  left  upper  portion  of  the  fissure  of 
Rolando,  invading  the  upper  two-thirds  of  the  ascending  frontal  convolution  and  the 
anterior  half  of  the  upper  two-thirds  of  the  ascending  parietal  convolution.  The 
paracentral  lobule  was  healthy. 

These  cases  and  many  others  which  I  might  quote  show  the  relations 
between  Jacksonian  epilepsy  of  the  brachial  type  and  lesions  in  the  ascending 
frontal  and  parietal  convolutions.  "WTien  the  epilepsy  commences  in  the 
arm,  the  cerebral  lesion  (syphilis,  tuberculosis,  glioma,  sarcoma,  etc.)  may 
be  localized  in  this  portion  of  the  motor  zone. 

In  conclusion,  there  are  cases  in  which  Jacksonian  epilepsy  commences 

in  the  face. 

jMilion  has  published  a  case  of  Jacksonian  epilepsy  commencing  on  the  left  side  of 
the  face.  The  post-mortem  examination  revealed  a  large  subcortical  tumour,  seated 
on  the  right  side  at  the  jimction  of  the  foot  of  the  ascending  frontal  with  the  foot  of 
the  ascendtng  parietal  convolutions,  the  cortical  centre  of  the  movements  of  the  face. 

All  that  I  have  just  said  with  regard  to  the  relations  between  the  varieties 
of  partial  epilepsy  and  the  localizations  of  the  lesions  in  Rolando's  region 
is  applicable  to  the  great  majority  of  cases.  Unfortunately  this  topo- 
graphical diagnosis  has  often  been  found  at  fault,  as  will  be  seen  in 
the  section  dealing  with  these  errors. 

Pathogenic  Diagnosis. — Let  us  now  study  the  diagnosis  of  the  cause, 
which  has  provoked  the  Jacksonian  epilepsy.  "We  must  always  think  of 
syphilis  (bony,  gummatous,  or  sclero-gujnmatous  lesions),  and  this  diagnosis 
must  not  be  abandoned  until  it  has  been  absolutely  proved  by  rigorous 
treatment  that  the  patient  is  not  syphilitic.  Patches  of  chronic  tubercular 
meningitis  often  give  rise  to  partial  epilepsy.  If  we  are  not  acquainted  with 
this  question,  we  are  surprised  to  hear  of  such  limited  tubercular  meningitis. 
Syphilis  at  first  sight  seems  more  likely  to  be  so  limited  ;  periostosis,  gumma, 
and  sclero-gummatous  meningitis  are  more  limited  than  tubercular 
meningitis,  which  in  its  nature  is  more  diffuse.  This  argument  is  true,  but, 
after  all,  such  argimients  are  of  little  value.  We  must  remember  that  local 
tuberculosis  of  the  brain  may  confine  itself,  as  elsewhere,  to  a  certain 
region  (Ballet,  Chantemesse). 

Charcot  dwells  on  these  cases  of  localized  meningitis :  "  Wlien  we 
considei  tuberculosis  of  the  brain  in  general,  we  notice  that  diffuse  granular 


1490  TEXT-BOOK  OF  MEDICINE 

meningitis,  with  its  seat  of  election  at  the  base  of  the  brain  and  in  the 
fissure  of  Sylvius,  is  the  most  common  form.  Next  comes  patchy  meningitis, 
which  is  usually  localized  in  the  psychomotor  zone,  and  especially  in  the 
paracentral  region.  This  patchy  meningitis,  which  is  clearly  circumscribed, 
is  much  more  frequent  in  adults  than  in  children.  Eemember,  too,  that 
here  everything  seems  made  to  lead  the  observer  astray  if  he  is  not  fore- 
warned as  to  the  diagnosis  of  this  localized  meningitis.  In  fact,  it  is  the 
rule  that  in  this  form  of  meningitis  headache,  vomiting,  delirium,  and  fever 
are  wanting,  and  if,  in  some  rare  cases,  the  evolution  is  rapid  and  febrile,  and 
ends  in  coma,  there  are  other  and  more  common  cases  in  which  the  disease 
runs  a  chronic  course  lasting  for  months  and  even  for  years."  And  as  a 
proof  of  this  assertion,  Charcot  quotes  the  case  of  a  patient  in  whom 
localized  tubercular  meningitis  lasted  for  fourteen  months,  without  provoking 
any  other  symptom,  except  attacks  of  Jacksonian  epilepsy.  Pulmonary 
tuberculosis  caused  death. 

When  the  provoking  lesion  of  the  Jacksonian  epilepsy  is  neither  syphilitic 
nor  tubercular,  it  is  a  question  of  one  of  the  numerous  tumours — sarcoma, 
glioma,  fibroma,  parasitic  tumour,  etc. — which  are  really  difficult  to 
diagnose. 

Treatment. — In  a  case  of  Jacksonian  epilepsy,  we  must  always  think  of 
syphilis.  Mercury  and  iodides  (especially  mercury)  must  be  immediately 
given.  If  the  cerebral  lesion  is  tubercular  in  nature,  surgery  has  little  chance 
of  successful  intervention.  In  other  cases  (parasitic  tumours,  glioma, 
sarcoma,  etc.)  an  operation  is  indicated  ;  it  must  be  performed  without  delay. 
The  precision  of  the  topographical  diagnosis  made  by  the  physician  will 
enable  the  surgeon  to  direct  his  attention  with  certainty  to  the  proper 
cerebral  region. 

III.  TRAUMATIC  EPILEPSY. 

Description. — Epilepsy  may  follow  any  head  injury,  such  as  blows, 
bruises,  depressed  fractures,  and  wounds  caused  by  sabres  or  by  firearms. 
Splinters,  sequestra,  exostoses,  abscesses,  subcranial  adhesions,  cortical 
lesions,  and  thickenings  of  the  dura  mater  may  induce  cerebral  irritation 
expressed  as  epilepsy. 

An  individual  may  become  epileptic  as  the  result  of  a  lesion  affecting 
the  parietal,  frontal,  or  occipital  regions.  The  time  at  which  the  epilepsy 
appears  is  very  variable ;  it  may  set  in  a  short  while  after  the  injury,  or  it 
may  not  appear  until  months  and  years  later.  Nevertheless,  the  patient 
usually  suffers  from  cerebral  troubles,  such  as  headache  or  vertigo,  during 
the  period  between  the  injury  and  the  appearance  of  the  epilepsy.  Trau- 
matic epilepsy  is  often  partial,  but  this  is  by  no  means  the  only  form ;  injury 
may  give  rise  to  the  grand  mal,  to  the  petit  mal  with  vertigo  and  mental 


NEUROSES  1491 

aberration,  to  intellectual  troubles,  inaniu,  delirium,  and  iiresistible 
impulses.  Traumatic  epilepsy,  says  Echeverria,  may  lead  to  raadncHS  ; 
in  his  statistics  we  find  eight  men  and  four  women  with  homicidal 
impulses ;  one  man  and  one  woman  kleptomaniacs,  and  three  women 
pyroraaniacs. 

■\Ianv  cases  of  so-called  essential  e])ilepsy  are  doubtless  due  to  a  cranial 
injury  which  has  escaped  notice.  It  is  therefore  necessary  in  every  case 
to  make  a  minute  examination  for  a  cicatrix,  caused  by  a  recent  or  an  old 
injury,  which  may  have  produced  the  epilepsy.  Epilepsy  may  also  recur 
or  appear  after  trephining — a  proof  that  the  cause,  either  cicatrix  or  ad- 
hesions, still  persists  in  spite  of  the  operation. 

Treatment. — Medical  measures  are  at  times  insufficient  in  traumatic 
epilepsy.  Surgical  intervention  must  then  be  employed.  In  the  following 
cases  surgical  measures  were  successful : 

A  child,  six  years  of  age,  fell  and  cut  himself  over  the  left  side  of  the  occipital  pro- 
tuberance. Ten  years  later  he  suffered  every  morning  from  spasms  and  shocks  in  the 
arms.  An  attack  of  grand  mal  appeared  thirteen  years  after  the  injury.  The  attacks 
recurred  every  tliree  or  four  days,  and  then  twice  daily.  The  frequency  of  the  attacks 
made  the  patient  irritable  and  impulsive ;  he  lost  his  memory.  An  exostosis,  due  to 
the  former  injur3-,  was  found  on  the  occiput,  and  was  held  to  be  the  cause  of  the  attacks. 
The  exostosis,  which  was  pressing  on  the  dura  mater  and  the  brain,  was  removed. 
Recovery  followed. 

A  girl  was  struck  on  the  head  by  a  shutter,  and  fell  down  imconscious.  A  depres- 
sion of  the  right  parietal  bone  was  found.  The  injury  was  followed  by  headache, 
vertigo,  nocturnal  epilepsy,  rapid  mental  decay,  and  suppression  of  menstruation. 
The  depressed  fragment  of  bone  was  removed  by  trephining.  The  attacks  of  epilepsy 
ceased,  and  complete  restoration  of  the  mental  faculties  followed. 

Operations  on  the  cranial  bones  and  the  dura  mater  are  not  always 
successful,  and  epilepsy  often  persists  in  spite  of  more  than  one  operation. 
Horsley  has  proposed  tbe  more  radical  operation  of  removing  the  cerebral 
centre  producing  the  attacks.  Removal  of  a  portion  of  the  motor  cortex  is 
especially  indicated  in  Jacksonian  epilepsy,  and  electrical  excitation  of  the 
ascending  parietal  and  frontal  convolutions  is  employed  in  order  to  ascertain 
the  part  to  be  removed.  The  objection  has  been  made  that  removal  of  a 
portion  of  the  motor  area  would  produce  paralysis  on  the  opposite  side  of  the 
body.  Experience  has  shown  that  the  removal  may  be  accomplished  with- 
out inducing  paralysis  as  a  necessary  result ;  substitution  takes  place,  and 
the  movements  soon  reappear ;  they  may  be  marked  by  inco-ordination, 
known  as  cortical  ataxy,  but  paralysis  is  not  present.  Although  this  opera- 
tion has  given  some  good  results,  its  true  worth  cannot  yet  be  stated. 
Operations  upon  the  cranial  bones  and  the  dura  mater  alone,  and  also  opera- 
tions for  removal  of  a  portion  of  the  brain,  have  been  successful,  and  the 
reverse.  A  factor  to  be  reckoned  with  is  the  presence  and  the  extent  of  his- 
tological lesions  in  the  cerebral  focus.     Thus,  in  a  case  of  extirpation  of  the 


1492  TEXT-BOOK  OF  MEDICINE 

motor  centre  for  the  upper  limb,  histological  examination  of  the  fragment 
removed  shows  degeneration  of  the  large  pyramidal  cells  and  condensation 
of  the  neuroglia. 

IV.  HYSTERIA. 

Hysteria  is  a  neurosis  more  frequent  in  women  than  in  men,  and  appearing 
in  two  principal  forms — the  one  convulsive,  the  other  non-convulsive.  In 
some  women,  in  a  third  of  the  cases,  according  to  Briquet,  convulsive 
hysteria  appears  without  having  been  announced  by  other  symptoms ;  but 
often,  especially  at  an  early  age,  hysteria  is  most  often  announced  a  long 
time  in  advance — the  little  girl  becomes  impressionable  and  nervous ;  she 
is  subject  to  attacks  of  suffocation,  palpitation,  headache  ;  her  character 
changes,  her  appetite  becomes  capricious,  and  she  gradually  goes  on  to 
confirmed  hysteria. 

The  convulsive  attack  is  often  preceded  by  certain  stigmata  of  hysteria, 
such  as  the  clavus  hystericus  and  the  globus  hystericus.  Sometimes,  on 
the  contrary,  hysteria,  whether  it  is  or  is  not  convulsive,  occurs  in 
persons  free  from  any  nervous  taint,  and  in  men  who  were  apparently 
quite  unlikely  to  suffer  from  hysteria.  Careful  investigation,  however, 
into  the  antecedents  of  these  people  generally  reveals  some  precursory 
signs. 

According  to  Babinski,  "  hysteria  is  a  psychical  condition,  rendering  the 
patient  capable  of  auto-suggestion.  It  manifests  itself  principally  by  primary 
troubles,  and  to  a  minor  degree  by  secondary  symptoms.  The  characteristic 
feature  of  these  primary  troubles  is  the  possibility  of  reproducing  them  by 
suggestion  in  certain  subjects,  and  of  causing  their  disappearance  by  the  sole 
influence  of  persuasion.  The  secondary  troubles  are  characterized  by  the 
fact  that  they  are  strictly  subordinate  to  the  primary  troubles." 

According  to  Babinski,  suggestion  is  the  act  by  which  we  seek  to  make 
others  accept  an  idea  that  is  obviously  unreasonable,  while  persuasion  is  the 
act  by  which  we  seek  to  make  others  accept  an  idea  that  is  eminently 
reasonable. 

The  hysterical  symptoms  are  therefore  said  to  be  the  result  of  suggestion 
or  of  auto-suggestion  ;  they  are  phenomena  which  the  wiU  can  reproduce. 
In  the  same  way  they  will  disappear  under  the  exclusive  influence  of  per- 
suasion, and  this  character  is  practically  essential  to  hysteria,  since  the  other 
psychical  troubles,  insanity  of  doubt  and  neurasthenia,  may  be  improved 
by  persuasion,  while  they  cannot  be  cured  by  it. 

Convulsive  Hysteria. — This  form  comes  on  in  attacks.  The  hysterica] 
attacks  behave  differently,  according  to  the  case,  and  two  varieties  may  be 
described  :  the  one  is  ordinary  hysteria  {'petite  hysterie).;  the  other,  which  is 
more  rare,  is  grande  hysterie  or  epileptiforme  hysterie. 


NEUR08ES  149;) 

1.  Ordinary  llytitcrin.-  The  attack  is  almost  iilways  announced  .some 
hours  or  some  days  in  advance  by  prodromata,  such  as  palpitation,  yawning, 
lassitude,  malaise,  unreasonable  crying  or  laughter,  constriction  of  the  thorax 
and  of  the  neck  (globus  hystericus).  The  attack  commences  in  most  cases 
with  an  aura.  The  aura  may  be  complete  or  incomplete.  The  complete 
aura  is  characterized  by  a  painful  sensation,  which  starts  from  the  ovary, 
reaches  the  pit  of  the  stomach,  ascends  along  the  sternum,  reaches  the 
pharynx  and  the  larjmx  {strangulation),  and  ends  in  cerebral  phenomena 
(whistlings  in  the  ears,  dimness  of  the  sight),  which  are  more  marked  on  the 
side  where  the  aura  commenced.  The  attack  then  commences,  and  the 
patient  falls  dowm  ;  but,  unlike  the  epileptic  patient,  she  has  time  to  select 
the  place  where  she  is  going  to  fall,  and  she  does  not  lose  consciousness — at 
least,  at  the  commencement  of  the  attack.  She  utters  cries,  and  feels  as 
though  she  were  being  suffocated.  Her  face  is  congested,  and  the  cervical 
veins  are  distended.  She  puts  her  hand  on  her  throat  as  if  to  tear  away 
something  which  is  impeding  respiration,  and  the  convulsions  are  accom- 
panied by  sighs  and  hiccough. 

The  convulsive  movements  are  essentially  clonic.  They  are  very 
extensive  and  disordered ;  contortions  sometimes  agitate  the  limbs,  and 
move  the  body  as  a  whole  ;  sometimes  the  convulsive  movements  are  more 
rhythmical,  and  affect  chiefly  the  muscles  of  the  pelvis  (libidinous  hysteria). 
The  trunk  shows  a  kind  of  rocking  movement.  Sometimes  the  head  is 
jerked  violently,  and  hits  neighbouring  objects.  The  face  is  not  grunacing 
as  in  epilepsy,  the  abdomen  is  distended  with  gas,  and  the  loss  of  conscious- 
ness is  generally  absolute.  After  a  duration  of  some  minutes  to  several 
hours,  according  to  the  number  of  fits,  the  movements  calm  down,  the 
physiognomy  betrays  the  various  expressions  of  fear,  anger,  or  voluptuous- 
ness, and  the  attack  ends  in  copious  tears,  and  in  the  emission  of  colourless 
urine. 

The  attacks  of  hysteria  are  not  always  so  acute  and  so  complete.  In 
some  cases  the  patients  hear  what  is  said,  and  understand  what  is  going  on 
round  about  them.  In  hysteria,  as  in  epilepsy,  the  attacks  may  follow  one 
after  the  other  for  several  days  ;  the  evacuations  which  mark  the  termination 
of  the  attack  are  absent,  and  the  patient  feels  that  the  attack  wUl  recur.  The 
attacks  of  hysteria  do  not  take  place  at  night.  It  is  often  possible  to  provoke 
or  arrest  at  will  an  attack  of  hysteria  ;  it  is  sufficient  to  press  firmly  on  the 
ovaries,  the  left  ovary  principally,  or  else  over  a  hysterogenous  zone.  The 
attack  of  hysteria  is  not  always  complete  ;  it  is  sometimes  preceded  by  a 
tonic  stage,  with  spasms  of  the  cesophagus,  of  the  glottis,  or  of  the  masseters, 
and  this  stage  may  per  se  constitute  the  whole  attack. 

2.  Ejnleptiform  Hysteria. — Ordinary  hysteria,  as  above  described,  may 
be  considered  as  a  mild  kind  of  epileptiform  hysteria.     The  latter,  which  is 
II.  95 


1494  TEXT-BOOK  OF  MEDICINE 

very  uncominon,  differs  from  the  sligM  attack,  in  tliat  it  commences  with  an 
epileptiform  phase.  The  crisis,  preceded  by  an  aura  and  by  the  prodromata 
already  described,  consists  of  four  periods,  which  occur  in  the  following 
order  : 

(a)  The  first,  or  epileptoid,  period  simulates  an  attack  of  epilepsy,  with 
tonic  and  clonic  convulsions  and  resolution. 

(6)  After  this  epileptoid  period,  which  lasts  three  or  four  minutes,  the 
other  periods  are  pure  hysteria.  There  is  at  first  a  phase  of  contortions  or 
clownism  (Charcot).  The  patient  rests  on  her  head  and  on  her  feet  in 
the  form  of  a  bridge,  or  performs  a  rhythmical  rocking  motion  with  the 
upper  part  of  her  body,  a  sort  of  salutation,  etc. 

(c)  Then  the  phase  of  passionate  attitudes  supervenes  ;  they  manifest 
themselves  under  the  influence  of  sad  or  gay  hallucinations  (fear,  love, 
voluptuousness). 

(d)  The  terminal  period  comprises  hallucinations  with  terrifying  visions 
(rats,  snakes,  black  animals). 

The  succession  of  these  attacks  constitutes  a  status  hystericus,  which 
may  last  for  several  weeks,  with  a  hundred  attacks  a  day ;  there  is  no  rise 
of  temperature,  such  as  occurs  in  the  status  epilepticus,  and  compression 
of  the  ovary  may  arrest  a  severe,  as  well  as  a  mild,  attack  of  hysteria. 

Epileptiform  hysteria  assumes  other  less  common  forms  ;  these  are  the 
syncopal  form  (Briquet),  syncope  constituting  the  entire  attack,  the  cata- 
leptic form  (Lasegue),  and  the  lethargic  form,  coma  and  lethargy  supervening 
at  the  termination  of  the  attack. 

Non-convulsive  Hysteria. — The  manifestations  of  this  form  are  many : 
paralyses,  trophic  troubles,  muscular  atrophy,  contractures,  tremors,  anaes- 
thesia, neuralgia,  congestion  with  or  without  haemorrhage,  respiratory, 
digestive,  and  urinary  troubles,  disorders  of  the  genital  organs  and  of  the 
organs  of  the  senses,  and  intellectual  troubles.  AU  these  are  met  with  in 
hysteria. 

Paralysis. — The  involuntary  and  the  voluntary  muscles  were  involved 
139  times  in  430  patients  (Briquet).  Hemiplegia  and  paraplegia  are  the 
most  frequent  forms.  Sometimes  only  one  limb  is  attacked  (monoplegia), 
especially  the  upper  limb.  The  paralyses  either  follow  an  attack  or  super- 
vene apart  from  any  convulsive  manifestation  ;  slight  injury,  emotion,  and 
fright  are  often  the  determining  cause.  According  to  circumstances,  their 
appearance  is  sudden  or  gradual;  they  are  mobile,  appearing  and  disappearing 
with  equal  faciUty  ;  they  may  persist  indefinitely,  or  may  recover  suddenly. 
Paralyses,  accompanied  by  anaesthesia,  the  anaesthesia  taking  the  form  of 
outlines  perpendicular  to  the  longitudinal  axis  of  the  limb,  with  normal 
electrical  contractility,  and  exaggerated,  normal,  or  diminished  reflexes,  are 
the  characteristics  of  hysterical  paralysis. 


NEUROSES  1495 

Amongst  other  distinctive  characteristics  hysterical  hemiplegia  differs 
from  hemiplegia,  caused  by  cerebral  lesions,  in  that  it  rarely  attacks  the  face. 
This  distinctive  sign  is  of  great  im[)ortance,  although  it  is  not  absolute, 
because  in  some  cases  of  hysterical  hemiplegia  the  face  was  slightly  deviated. 
"  But,"  says  Charcot,  "  a  mistake  has  been  made,  facial  hemiplegia  having 
been  mistaken  for  hemispasm."  In  hysterical  hemiplegia  the  inferior  facial 
nerve  is  never  affected,  as  it  is  in  ordinary  hemiplegia.  The  deviations  of 
the  face  associated  with  hysterical  hemiplegia  are  the  consequence  of  hemi- 
lateral  glossolabial  spasm  on  the  opposite  side  to  the  hemiplegia,  or  on  the 
same  side.  In  this  glossolabial  spasm  the  angle  of  the  lips  and  the  tongue 
are  drawn  over  to  the  convulsed  side  ;  the  cheek  is  sometimes  affected  by 
convulsive  jerks."  Charcot,  later,  withdrew  this  statement,  and  hysterical 
facial  hemiplegia  is  now  proved.  It  seems  only  to  supervene  in  the  grave 
forms  of  hysteria. 

Contractures. — Nearly  all  the  voluntary  and  involuntary  muscles  may 
be  attacked.  We  find  monoplegic,  hemiplegic,  and  paraplegic  forms ;  they 
may  involve  the  four  limbs,  the  lumbar  muscles,  the  muscles  of  the  neck, 
of  the  jaws,  of  the  tongue,  of  the  eyeballs,  etc.  ;  at  other  times  they  are 
limited  to  a  muscle  or  a  group  of  muscles.  The  contractures  are  permanent. 
They  are  generally  very  painful,  and  last  for  months  and  years,  appearing 
gradually  or  suddenly,  and  disappear  in  some  cases  with  equal  suddermess. 
They  may  follow  the  paralyses,  or  may  set  in  apart  from  any  paralytic 
condition.  They  do  not  relax  during  sleep,  although  they  yield  for  the  time 
being  to  chloroform.  Intermission  of  the  contractures  is  exceptional ;  it 
was  well  marked  in  one  of  Benon's  cases,  with  total  facial  hemispasm  : 
the  crises  occurred  seventy  or  eighty  times  during  the  day. 

These  features  distinguish  hysterical  contractures  from  those  due  to 
sclerosis  of  the  lateral  columns  of  the  spinal  cord.  The  latter  establish 
themselves  slowly  and  progressively,  and  are  not  modified  by  chloroform. 
It  appears  nevertheless  that  the  hysterical  contracture  may,  in  the  long  run 
and  in  very  exceptional  cases,  be  associated  with  a  lesion  of  the  lateral 
columns  of  the  spinal  cord  (Charcot).  This  condition  must  be  very  ex- 
ceptional, for  in  a  remarkable  case  seen  by  Vulpian  no  spinal  lesions  were 
found  in  a  hysterical  patient,  who  for  five  years  had  suffered  from  general 
contractures,  with  trophic  troubles,  muscular  atrophy,  and  fibrillary  con- 
tractions of  the  muscles  (Klumpke). 

The  arm  is  in  the  position  of  forced  flexion,  the  leg  is  in  extension  with 
talipes  equino-varus.  Every  attempt  to  overcome  the  contracture  is 
accompanied  by  severe  pains.  If,  during  contracture  of  the  lower  limb,  the 
point  of  the  foot  is  forcibly  straightened,  an  epileptoid  tremor  is  provoked 
in  the  limb  ;  the  tremor  lasts  for  some  time,  and  may  be  arrested  by  sudden 
flexion  of  the  foot.     The  application  of  a  magnet  sometimes  causes  the 

95—2 


1496  TEXT-BOOK  OF  MEDICINE 

transfer  of  the  contracture  to  the  opposite  side.  I  shall  next  enumerate 
certain  hysterical  contractures  :  contracture  of  the  extremities  (tetanus) ; 
periarticular  contractures  of  the  knee  and  of  the  shoulder,  which  are  often 
very  painful  (Brodie). ;  contractures  of  the  muscles  of  the  hip,  which  simulate 
coxalgia  ;  contracture  of  the  muscles  of  the  neck  (torticollis) ;  of  the  masti- 
cator muscles  (trismus)  ;  of  the  motor  muscles  of  the  eye  (strabismus) ; 
of  the  muscles  of  the  tongue,  without  counting  contracture  of  the  sphincters 
(retention  of  urine),  spasms  of  the  oesophagus,  which  may  last  for  weeks 
and  months  (spasmodic  stricture);  spasms  of  the  glottis,  with  consequent 
dyspnoea,  etc.,  which  will  be  studied  under  each  of  these  organs. 

The  hysterical  contractures  sometimes  supervene  spontaneously;  at 
other  times  they  are  occasioned  by  insignificant  causes,  by  a  slight  injury 
(fall,  contusion,  sprain,  prick  with  a  needle),  and  it  is  remarkable  that  the 
contracture  caused  by  traumatism  is  often  the  first  manifestation  of  hitherto 
latent  hysteria. 

Tremors. — Hysterical  tremors  generally  supervene  suddenly  in  conse- 
quence of  emotion,  fright,  or  of  a  complete  or  incomplete  attack  of  hysteria. 
According  to  circumstances,  the  tremor  is  partial  or  general ;  it  assumes  the 
hemiplegic,  paraplegic,  or  monoplegic  form.  The  tremor  may  improve  and 
disappear  after  a  few  hours  or  a  few  days,  but  it  may  be  continuous,  inter- 
rupted only  during  sleep,  and  lasting  for  months.  The  excitation  of  a 
hysterogenous  zone  may  sometimes  cause  the  tremor  to  reappear.  The 
intensity  varies  from  the  least  tremor  to  such  violent  agitation  as  to  interfere 
with  walking  and  with  the  grasping  of  objects.  The  rhythm  of  the  tremor 
is  regular.  Dutil  has  divided  them  into  three  groups  :  (1)  Tremors  with 
rapid  or  vibratory  oscillations,  numbering  eight  to  twelve  per  second,  and 
resembling  the  tremor  of  Basedow's  disease,  of  general  paralysis,  and  of 
alcoholic  poisoning  ;  (2)  tremors  of  five  to  seven  oscillations  per  second, 
resembling  the  tremor  of  mercurialism  and  of  spasmodic  paraplegia,  and 
more  rarely,  when  they  are  intentional,  imitating  the  tremor  of  insular 
sclerosis  ;  (3)  slow  tremors  of  four  to  five  oscillations  per  second,  resembling 
the  senile  tremor  and  paralysis  agitans. 

HemiancBsthesia. — The  anaesthesia  of  hysterical  patients  may  be  general 
and  disseminated;  it  is  more  often  local  in  the  form  of  hemiansesthesia. 
It  is  especially  frequent  on  the  left  side,  and  has  been  noted  93  times  in 
400  cases  by  Briquet.  The  insensibility  affects  the  whole  of  one  side 
of  the  body  as  far  as  the  median  line,  and  invades  the  superficial  and 
deep  planes,  the  skin,  the  mucosae,  the  muscles  (loss  of  muscular  sensa- 
tion), and  the  joints.  It  is  a  strange  fact  that  many  hysterical  patients 
are  not  aAvare  of  this  anaesthesia.  Total  hemianaesthesia  not  only  afiects 
tactile  sensibility,  but  also  the  sensations  of  pain  and  of  temperature,  and 
the  special  senses  (taste,  smell,  hearing,  sight).     Pharyngeal  anaesthesia  is 


NEUROSES  149'7 

very  common.  The  anaesthetic  akin  is  pale,  cold,  and  bloodless,  and  may 
be  pricked  without  the  loss  of  a  drop  of  blood.  The  musfles  of  the  paralyzed 
side  are  much  weaker  (amyosthenia)  than  those  of  the  healthy  side.  This 
hemiansBsthesia  is  quite  analogous  with  that  described  in  diseases  of  the 
brain,  caiised  by  a  lesion  of  the  posterior  part  of  the  internal  capsule. 

Burcq's  researches  on  hysterical  hemiana;sthesia  have  brought  to  light 
some  very  interesting  facts  (metalloscopy  and  metallotherapy).  If  discs 
of  gold,  tin,  or  copper  are  applied  to  the  anaesthetic  skin,  the  anesthesia 
disappears  after  an  application,  ranging  in  duration  from  a  few  seconds  to 
fifteen  minutes.  As  the  sensation  reappears  in  the  anaesthetic  regions,  the 
skin  regains  its  colour,  the  circulation  is  re-established,  and  the  amyosthenia 
disappears  :  a  patient  who  only  registered  30  pounds  on  the  dynamometer 
actually  registers  double.  Whilst  these  changes  are  taking  place  on  the 
anaesthetic  side,  the  other  side,  which  was  healthy,  becomes  anaesthetic  in 
the  s\'mmetrical  regions  :  a  phenomenon  of  transference  takes  place. 

The  results  obtained  with  discs  of  copper  in  one  patient  are  not  obtained 
in  another  one,  except  by  the  application  of  discs  of  gold  or  of  tin.  One 
patient  is  "  sensitive  to  gold,  another  to  copper."  These  metals  develop  a 
current,  and  only  act  when  impurities  are  present.  A  similar  result  is 
obtained  by  the  application  of  a  galvanic  current  or  of  a  magnet. 

These  various  means  are  not  limited  to  the  hemianaesthesia  of  hysterical 
patient^;  ;  thev  act  also  on  the  hemianaesthesia  which  accompanies  intoxi- 
cations (alcoholism  and  plumbism)  and  cerebral  lesions.  It  must  also  be 
noted  that  the  improvement  which  is  generally  transient  in  hysterical 
hemianaesthesia  may  be  permanent  in  the  other  varieties. 

EyfercEstliesia — Neuralgia. — Hysterical  patients  are  subject  to  various 
pains  afEecting  the  skin,  the  muscles,  the  joints,  and  the  \'iscera.  The 
clavus  hystericus  is  a  lancinating  pain,  situated  at  the  sagittal  suture. 
The  headache  of  hysterical  patients  is  said  to  be  a  muscular  hyperaesthesia 
(Briquet),  a  neuralgia,  or  a  migraine.  It  is  sometimes  characterized  by  a 
painful  spot  on  the  temple  ;  but  whatever  the  variety  of  this  headache,  its 
appearance,  as  an  obstinate  symptom  in  young  girls  near  the  age  of  puberty, 
is  a  frequent  index  of  hysteria.  The  backache  is  due  to  hyperaesthesia  of 
the  muscles  of  the  back  and  of  the  spine  ;  it  may  extend  to  the  whole  mass 
of  the  sacro-hmibar  muscles  and  to  the  longissimus  dorsi,  or  it  may  be  limited 
to  one  of  the  regions  of  the  back  ;  the  pain  is  readily  provoked  by  pressure 
on  the  spinous  processes,  or  on  the  muscles. 

In  hysterical  patients  we  find  hysterogenous  zones — that  is  to  say, 
regions  endowed  with  a  special  and  permanent  sensibility.  Prior  to  the 
attack,  these  points  are  the  seat  of  increased  pain,  which  forms  a  part  of 
the  aura.  The  aura  may  also  be  provoked  by  pressure,  or  by  rubbing  of 
the  hysterogenous  patches,  and,  if  we  keep  on,  the  attack  of  hysteria  may  be 


1498  TEXT-BOOK  OF  MEDICINE 

as  certainly  provoked  as  by  exerting  pressure  on  the  ovary.  Conversely, 
the  hysterical  attack  may  be  arrested  .by  firm  pressure  on  the  hysterogenous 
zones.  These  zones  are  very  numerous  ;  they  are  found  at  the  bregma,  the 
xiphoid  cartilage,  under  the  breasts,  at  the  angle  of  the  scapula,  in  the  lumbar 
region,  in  the  ovarian  region,  in  the  testicle,  in  the  arms,  in  the  legs,  etc. 

Ideogenous  zones  have  also  been  described  ;  as  a  rule,  they  are  only 
active  in  the  hypnotic  condition.  The  excitation  of  the  zone  of  ecstasy, 
situated  on  both  sides  of  the  vertex,  places  the  patient  in  an  attitude  of 
ecstasy.  The  excitation  of  the  zones  of  chattering,  situated  over  the  mastoid 
processes,  causes  the  patient  to  talk  volubly.  The  excitation  of  the  zone 
of  laughter  over  the  external  occipital  protuberance  causes  convulsive  and 
noisy  laughter,  which  it  is  impossible  to  interrupt. 

Hysterical  women  are  subject  to  attacks  of  intercostal  neuralgia,  and 
to  visceral  pains,  gastralgia,  hepatalgia,  ovaria,  hysteralgia.  They  have 
painful  crises  comparable  with  angina  pectoris,  abdominal  pains  due  to 
hypersesthesia  of  the  ovary,  and  neuralgia  of  the  abdominal  wall.  These 
symptoms,  joined  to  exaggerated  meteorism  of  the  belly,  are  called  false 
peritonitis.  Care  must  be  taken  not  to  confound  this  condition  with 
appendicitis. 

ApJwnia — Mviism — Aphasia. — I  have  grouped  hysterical  aphonia, 
mutism,  and  aphasia  in  the  same  paragraph,  in  order  the  better  to  oppose 
these  various  troubles,  and  to  show  their  differences.  This  description  is 
taken  from  Charcot's  lectures.  Hysterical  aphonia,  like  all  other  forms 
of  aphonia,  is  characterized  by  loss  of  voice  ;  the  larynx  can  no  longer  emit 
the  sounds  necessary  for  the  voice.  The  patient  can  still  speak  in  a  whisper, 
which  is  produced  by  the  tongue  and  the  lips,  and  has  nothing  to  do  with 
the  larynx.  The  aphonia  is  due  to  the  paralysis  of  the  vocal  muscles ;  the 
sound  is  absolutely  lost,  but  this,  however,  does  not  prevent  the  cough  from 
being  noisy.  Hysterical  aphonia  supervenes  suddenly  as  the  result  of  some 
moral  cause,  or  after  a  convulsive  attack  ;  it  lasts  for  several  days  or  weeks, 
and  disappears  as  it  came,  sometimes  as  the  result  of  a  moral  emotion. 
Patients  suffering  from  hysterical  aphonia  often  have  a  cutaneous  patch  of 
anaesthesia  iti  the  supra-  and  subhyoid  regions.  Hysterical  aphonia  may  be 
cured  by  almost  any  measure  (electricity,  magnetization,  or  metaUotherapy), 
or  it  may  resist  aU  means. 

Hysterical  mutism  commences  suddenly  in  consequence  of  a  fright,  an 
emotion,  or  a  convulsive  attack,  or  even  without  apparent  cause.  It  may 
last  for  weeks,  for  months,  or  for  years.  It  is  always  cured,  and  suddenly, 
but  it  is  subject  to  recurrences.  Like  all  the  manifestations  of  hysteria, 
it  is  more  frequent  in  women,  but  it  is  also  met  with  in  men.  The  hysterical 
mute  is  aphonic  and  mute  at  the  same  time ;  aphonic,  that  is  to  say,  her 
larvTx  can  produce  no  sound ;   mute,   that  is  to  say,  she  is  absolutely 


NEUROSES  1499 

deprived  of  speech,  being  unable  to  articulate  a  sinpjle  word  even  in  a  low 
voice  ;  she  cannot  whisper,  and  yet  she  has  not  lost  any  of  the  movements 
of  the  tongue  and  of  the  lips  ;  she  can  whistle  and  blow,  but  she  can  neither 
co-ordinate  nor  imitate  the  movements  necessary  for  the  articulation  of 
words.  Tn  this  respect  hysterical  mutism  resembles  organic  motor  aphasia, 
but  it  differs  from  organic  aphasia  in  many  respects,  and  without  speaking 
of  other  troubles,  such  as  agraphia,  word-deafness,  and  word- blindness, 
which  enter  more  or  less  into  the  domain  of  aphasia,  a  patient  with  com- 
plete organic  aphasia  can  utter  cries  or  even  a  few  words. 

Tiie  hysterical  mute  retains  his  intelligence,  writes  with  facility,  and  con- 
trives to  make  himself  understood  by  gestures — two  things  which  are  rare 
in  a  person  suffering  from  organic  aphasia.  Accordingly,  the  preservation 
of  writing,  of  mimicry,  and  of  intelligence  in  a  man  or  woman  who  has 
suddenly  become  mute  shows  the  hysterical  nature  of  the  mutism.  This 
diagnosis  is  almost  always  confirmed  by  other  stigmata  of  hysteria, 
hemiansesthesia,  pharyngeal  anaesthesia,  sensory  troubles,  ocular  troubles, 
hysterogenous  zones,  facility  of  provoking  contracture  in  a  limb  by  the 
application  of  a  circular  ligature.  On  the  other  hand,  the  union  or  the 
absence  of  these  various  signs  allows  us  to  recognize  cases  of  simulation. 
Mutism  may  be  readily  provoked  in  hypnotizable  hysterical  patients  ;  this 
artificial  syndrome,  produced  during  the  period  of  somnambulism,  persists 
when  the  subject  is  awakened.  "  We  must  look  in  the  grey  cortex  of  the 
cerebral  hemispheres  for  the  dynamic  lesion  from  which  the  symptoms  in 
question  are  derived,  and  the  mechanism  which  must  be  here  invoked  is 
none  other  than  that  which  accounts,  in  my  opinion,  for  the  production  of 
so-called  cases  of  psychic  or  mental  paralysis  "  (Charcot). 

Typical  aphasia  has  sometimes  been  observed  in  hysterical  patients  ;  it 
is  generally  associated  with  hysterical  apoplexy. 

Hysterical  Ajjoplexy. — Hysterical  apoplexy  has  all  the  clinical  characters 
of  apoplexy  of  organic  origin  (Debove)  ;  apoplexy  with  or  without 
aphasia,  with  hemiplegia,  and  almost  always  with  hemiansesthesia.  Hemi- 
anaesthesia  is  a  prominent  symptom,  whilst  the  hemiplegia  is  not  so  marked. 
The  sequelae  of  the  attack — hemianaesthesia,  hemiplegia,  hemichorea,  and 
contracture — are  readily  curable  by  esthesiogenic  measures. 

Psychic  Troubles. — The  hysterical  woman  always  exaggerates,  and  loves 
to  make  an  exhibition  of  herself  in  order  to  excite  interest ;  she  indulges 
in  every  kind  of  simulation,  and  is  capable  of  the  most  repugnant  acts. 
Hysterical  women  are  often  malicious  and  untruthful ;  some  of  them  lie 
with  unheard-of  effrontery  ;  they  sow  disagreement  and  discord  everywhere  ; 
they  are  at  a  loss  what  to  invent  in  order  that  they  may  be  talked  about. 
They  threaten  suicide,  and  worry  their  family  by  announcing  that  they 
intend  to  make  away  with  themselves.     They  accuse  themselves  of  acts 


1500  TEXT-BOOK  OF  MEDICINE 

which  they  have  never  committed,  and  bear  false  witness  against  others  of 
theft  and  murder.  They  profess  to  be  the  victims  of  assaults  and  of  rape, 
and  they  cause  innocent  people  to  be  arraigned  before  a  court  of  justice, 
when  they  do  not  succeed  in  having  them  burnt  at  the  stake,  as  was  that 
unfortunate  man,  Urbain  Grandier,  whom  the  Ursuline  sisters  of  Loudun 
accused  of  imaginary  crimes.  Most  hysterical  women  have  hallucinations 
during  the  convulsive  attack ;  in  some  women  these  hallucinations  persist 
outside  the  attack ;  thus,  a  woman  who  is  quietly  reading  or  working  rises 
suddenly,  and  utters  cries,  fancying  that  she  sees  fantastic  animals  on  the 
wall  or  on  the  floor.  Erotic  and  religious  delirium  is  common  to  them,  and 
sometimes  leads  to  dementia. 

Hysteria  renders  patients  particularly  liable  to  neurasthenia,  and  makes 
them  good  subjects  for  hypnotism. 

A  rabid  form  of  hysteria  has  been  described  by  Grasset. 

An  important  medico-legal  question  is  associated  with  the  mental 
condition  of  hysterical  patients,  and  hysteria  has  been  more  than  once  a 
prominent  feature  in  certain  causes  cdehres.  With  regard  to  this  subject, 
Grasset's  interesting  case,  published  under  the  title  "  Roman  d'une 
hysterique,"  should  be  read. 

Trofhic  Troubles.  —  Numerous  trophic  troubles  are  associated  with 
hysteria.  The  cutaneous  troubles  include  zona,  falling  out  of  the  hair, 
shedding  of  the  nails,  spontaneous  ecchymoses,  and  sweating  of  blood.  To 
the  troubles  of  the  cellular  tissue  belongs  oedema,  which  is  sometimes 
cyanotic.  In  hysterical  oedema  we  find  a  hard  swelling  of  the  skin,  which 
does  not  pit  on  pressure.  The  skin  is  cyanosed,  whence  the  name  of  blue 
oedema.  This  oedema  may  be  limited  to  a  hand  or  to  a  limb  ;  it  is  almost 
always  associated  with  contracture,  or  with  paralysis  of  the  invaded  limb. 

In  some  patients  we  find  painful  swelling  of  the  breasts,  with  secretion 
of  milk.  Chipault  has  seen  a  case  of  haemorrhage  from  the  breast,  and  he 
has  succeeded  in  collecting  several  similar  cases.  I  must  add  that  the  fore- 
going trophic  troubles  are  no  longer  admitted  as  being  functional  of 
hysteria. 

Soon  nothing  will  remain  of  so-called  trophic  troubles  taught  us  in 
our  medical  education.  This  is  my  conviction,  and  we  may  well  agree 
with  Babinski  that  the  trophic  troubles  of  hysteria  are  non-existent. 
Simulation  accounts  for  the  so-called  hysterical  vesicular  eruptions,  pem- 
phigus, ulcers  of  the  limbs  and  breasts,  phlyctense  and  gangrene.  It 
matters  little  whether  the  person,  commonly  spoken  of  as  being  hysterical, 
does  or  does  not  find  any  tangible  profit  in  fabricating  such  lesions  ;  he  is 
the  victim  of  this  peculiar  mental  abnormality  which  makes  him  capable 
of  any  roguery  or  any  simulation. 

Cases  exist  in  proof  of  this  statement : 


NEUROSES  1501 

A  liystprioal  pirl  was  aflmiifod  for  hulln*  on  llio  muffnis  niotnl)ran«  of  tlif  mouth; 
she  wjis  imiuaski'd,  aucl  it  was  I'ouiid  iliat  tlio  builiu  wcro  produoeU  by  lawiiis  of 
cuutharides  (Daiilos). 

A  hystei'ioal  jjfirl  was  .suffering  from  multiple  ulcers  on  the  limbs;  it  was  shown 
that  she  produced  them  with  nitric  acid. 

The  muscular  atrophies  belong  to  the  trophic  disorders  of  hysteria. 
The  atrophy  is  usually  present  in  the  regions  attacked  by  paralysis,  con- 
tracture, and  anEesthesia ;  it  is  very  rarely  independent.  The  atrophy 
attacks  the  hand,  the  arm,  or  the  leg.  In  some  cases  it  has  an  ascendmg 
course,  commencing  in  the  hand  and  spreading  to  the  arm.  Hysterical 
muscular  atrophy  differs  considerably  from  myelopathic  amyotrophy.  It 
does  not  attain  the  degree  of  wasting  seen  in  progressive  muscular  atrophy, 
and  is  not,  as  a  rule,  accompanied  by  fibrillary  tremors.  The  electrical  con- 
tractility is  diminished  in  proportion  to  the  atrophy,  and  there  is  in  most 
cases  no  reaction  of  degeneration.  These  distinctive  signs  are,  however, 
not  absolute,  because  in  some  cases  fibrillary  contractures  and  slight  reaction 
of  degeneration  have  been  noted.  The  onset  is  rapid,  and  as  soon  as  an 
improvement  supervenes  recovery  speedily  follows.  The  pathogenesis  of 
this  atrophy  is  obscure  ;  it  may  perhaps  be  due  to  a  dynamic  change  in  the 
nerve  centres,  and  it  is  said  to  be  comparable  with  the  amyotrophy  which 
follows  joint  injuries  (Vulpian). 

Viscera. — The  respiratory  system  shows  various  disorders.  Spasms  of 
the  glottis  provoke  attacks  of  dyspnoea.  Paralysis  of  the  posterior  crico- 
arytenoid muscles  is  accompanied  by  dyspnoea,  with  inspiratory  stridor. 
Convulsions  of  the  laryngeal  muscles  and  spasms  of  the  diaphragm  provoke 
barking  and  grumbling  noises,  which  may  occur  in  attacks,  or  may  follow 
one  another  incessantly.  The  spasmodic  movements  of  the  diaphragm 
cause  uncontrollable  fits  of  yawning,  hiccough,  and  laughter.  Some 
hysterical  women  suffer  from  broncho-pulmonary  congestion,  with  haemop- 
tysis ;  others,  especially  young  girls,  have  an  incessant,  dry  cough,  which 
tires  the  family  more  than  the  patient.  This  cough  diminishes  or  disappears 
at  night ;  it  is  very  obstinate,  lasting  for  weeks  and  months. 

Digestive  Troubles. — Gastralgia,  dyspepsia,  and  perverted  appetite  are 
of  common  occurrence  ;  hysterical  patients  frequently  vomit  water  or  food  ; 
they  may  have  attacks  of  hsematemeses.  The  vomiting  of  food  is  painless  ; 
it  may  last  for  several  months  without  injuring  health,  and  without 
causing  marked  loss  of  flesh.  Constipation  is  the  rule ;  intestinal  pneuma- 
tosis is  frequent,  and  abdominal  meteorism  consequently  results.  This 
abdominal  swelling  and  the  abdominal  pains  constitute  the  false  peritonitis 
of  hysteria. 

Some  patients  lose  their  appetite  completely.  A  young  girl  with  anorexia 
delights  in  fasting,  and  the  phenomena  of  disassimilation  are  so  slow  that 


1502  TEXT-BOOK  OF  MEDICINE 

she  can  fast  for  a  long  time,  and  apparently  without  losing  flesh.     Grave 
complications  may,  however,  result. 

Tuberculosis  may  attack  hysterical  patients  with  anorexia.  The  ali- 
mentary canal  is  frequently  the  seat  of  spasms — spasms  of  the  pharynx,  of 
the  oesophagus  (spasmodic  stricture),  of  the  stomach  (cramps),  of  the 
intestine,  which  may  lead  to  fsecal  vomiting. 

Eructations  and  borborygmi  are  very  frequent  in  hysterical  patients. 
The  sounds  may  be  irregular  or  regular,  and  coincident  with  the  respiratory 
movements.  Pitres  attributes  the  rhythmic  borborygmus  in  hysterical 
patients  to  a  spasmodic  contraction  of  the  respiratory  muscles. 

Urinary  System. — The  urinary  troubles  may  be  excretory  or  secretory. 
The  former  (retention  of  urine)  are  due  to  a  contraction  of  the  sphincter  of 
the  bladder,  or  to  paralysis  of  the  viscus.  The  latter,  oliguria  or  anuria, 
are  more  difficult  to  explain.  Hysterical  patients  may  go  for  several  weeks 
without  passing  water,  not  from  retention,  but  because  the  kidneys  do  not 
act.  And  in  spite  of  this  suppression  we  find  no  ursemic  symptoms, 
doubtless  because  the  processes  of  metabolism  are  almost  at  a  standstill. 

Hysterical  polyuria  has  long  been  recognized.  To  make  a  diagnosis 
Babinski  advises  hypnotic  suggestion ;  by  this  means  the  polyuria  can  be 
made  to  appear  and  to  disappear  at  will.  Hysterical  polyuria  is  only  seen 
in  men ;  it  usually  begins  with  excessive  thirst. 

On  cryoscopic  examination  the  freezing-point  of  the  urine  may  be  lower 
than  that  of  the  blood  (0-56°  C.) ;  it  may  faU  to  017°  0. 

The  urine  may  amount  to  twenty  litres  or  more.  In  time  the  patient 
loses  flesh,  and  the  prognosis  becomes  grave.  Hysterical  polyuria  is  a 
most  obstinate  condition:  valerian,  opium,  antipyrine,  and  suggestion 
yield  some  results,  but  they  are  rarely  permanent. 

Organs  of  the  Senses. — The  organs  of  the  senses  may  be  attacked 
separately  by  hy perse  sthesia,  anaesthesia,  paralysis,  or  contracture.  Hard- 
ness of  hearing  is  frequent,  but  deafness  is  rare.  I  have  seen  a  young  girl 
with  such  marked  hypersesthesia  of  the  lingual  mucosa  that  everything 
tasted  like  vinegar. 

The  ocular  troubles  of  hysteria  are  so  characteristic  that  it  is  customary 
to  unite  them  under  the  term  "  hysterical  eye."  The  amblyopia  is  character- 
ized by  anaesthesia  of  the  retina,  and  by  contracture  of  the  ciliary  muscle. 

Anaesthesia  of  the  retina  is  revealed  by  two  symptoms :  constriction  of  the 
field  of  vision  and  dyschromatopy.  The  contracture  shows  itself  by  mono- 
cular polyopia,  micropsia,  and  megalopia.  The  constriction  of  the  field  of 
vision  commences  at  the  circumference,  and  becomes  regularly  concentric ; 
it  may  reduce  the  sight  to  central  vision  alone.  The  constriction  of  the 
field  of  vision  is  often  complicated  by  disturbance  of  colour  vision.  The 
perception  of  colours  disappears  in  the  following  order  :  violet,  green,  blue. 


NTEUROSES  1503 

yellow,  and  finally  red.  As  in  the  normal  condition,  it  is  the  blue  field 
which  is  the  most  extended  (white  being  excluded),  so,  on  the  other  hand, 
in  hysteria  the  perception  of  red  is  the  last  one  affected.  The  following 
paradox  results — viz.,  the  red  field  becomes,  from  the  outset,  more  extended 
than  the  blue  (Parinaud).  This  phenomenon  has  received  the  name  of 
change  in  the  relative  extent  of  the  fields  of  the  different  colours.  If  a 
magnet  or  a  plate  of  gold,  copper,  or  tin  be  applied  to  the  temple  of  the 
patient,  tlie  colours  reappear  in  the  inverse  order  of  their  disappearance, 
according  to  the  metallic  idios}^Ticrasy  of  the  hysterical  patient. 

These  symptoms  are  most  important ;  they  belong  especially  to  hysteria, 
and  they  allow  us  to  distinguish  hysterical  amblyopia  from  tabetic  and 
alcoholic  amblyopia.  In  alcoholic  amblyopia  the  red  and  the  green  dis- 
appear first,  whilst  a  central  scotoma  develops.  In  tabetic  amblyopia  the 
red  also  disappears  first ;  the  constriction  of  the  field  of  vision  is  peripheral, 
but  it  is  notched  and  not  regularly  concentric.  Finally,  the  ophthalmoscope 
reveals  atrophy  of  the  optic  nerve,  whereas  the  fundus  is  always  normal 
in  hysteria. 

Monocular  diplopia  and  polyopia  are  very  curious  symptoms.  If  an 
object  is  held  vertically  in  front  of  the  hysterical  eye  (the  other  eye  being 
closed),  the  object  is  distinct  only  at  a  certain  distance.  Within  this 
distance,  or  beyond  it,  the  object  becomes  blurred,  and  at  the  same  time 
it  appears  double  or  triple,  although  seen  with  only  one  eye.  This  variety 
of  diplopia  is  due  to  defective  accommodation,  which  varies  in  hysterical 
patients  in  the  three  segments  of  the  crystalline  lens,  and  therefore  repro- 
duces a  separate  image  for  each  of  the  three  segments  (Parinaud).  Defective 
accommodation  also  produces  micropsy  and  megalopsy — symptoms  which 
often  accompany  monocular  diplopia.  This 'monocular  diplopia,  in  which 
two  images  are  perceived  by  one  eye  (the  other  eye  being  closed)  must  be 
distinguished  from  the  diplopia  due  to  paralysis  of  the  motor  muscles  of 
the  eye,  in  which  case  each  of  the  two  images  is  perceived  by  the  eye  of  the 
corresponding  side,  or  by  the  eye  of  the  opposite  side  (homonymous,  or 
crossed  diplopia). 

Hysterical  amblyopia  may  be  limited  to  one  eye  ;  it  is,  however,  almost 
always  double,  and  more  marked  on  the  side  of  the  hemiansesthesia. 
Amaurosis  may  follow  amblyopia,  or  may  appear  suddenly. 

I  have  already  said  that  the  fundus  always  remains  normal  in  hysteria. 
Let  me  add,  while  the  pupU  reflex  is  absent  in  tabes  and  in  the  other  cases 
of  amblyopia  due  to  an  organic  lesion,  it  remains  present  in  hysterical 
amaurosis,  because  the  impression,  although  it  is  not  perceived  by  the 
subject,  nevertheless  reaches  the  brain. 

We  may  also  find  motor  troubles  of  the  eye  ;  they  are,  however,  of  minor 
importance.     Spasm  of  the  eyelids   (blepharospasm)   betrays  itself  by  a 


1504  TEXT-BOOK  OF  MEDICINE 

drooping  of  tlie  eyelid,  which  simulates  ptosis  (pseudo-paralytic  ptosis), 
or  by  clonic  movements,  with  continual  winking  of  the  half-closed  lids. 
This  symptom  is  associated  with  a  zone  of  anaesthesia  or  of  hyperaesthesia, 
which  afiects  the  eyelid  and  the  conjimctiva,  but  respects  the  cornea.  On 
the  side  of  the  blepharospasm  the  eyebrow  is  lowered.  We  must  also  notice 
contractures  of  the  recti  muscles,  especially  of  the  internal  rectus,  causing 
strabismus  and  diplopia  which  at  first  sight  simulate  paralysis.  Paralysis 
of  the  motor  muscles  of  the  eye  has  yet  to  be  proved. 

Blindness. — I  have  given  two  clinical  lectures  *  on  hysterical  blindness ; 
I  shall  give  a  resume  of  them. 

I  have  collected  over  sixty  cases  of  hysterical  blindness.  In  five  instances 
it  was  the  only  symptom  of  hysteria  present,  the  patients  being  apparently 
free  from  any  stigmata  of  hysteria.  The  blindness  is  usually  associated 
with  other  manifestations  of  hysteria.  It  sometimes  follows  an  attack  of 
hysteria.  Hemiansesthesia,  anaesthesia  of  the  cornea  and  of  the  pharynx, 
hemiplegia,  loss  of  the  senses  of  taste  and  smell,  deafness,  mutism,  oeso- 
phagism,  contractures,  etc.,  are  often  satellites  of  the  blindness.  One  patient 
is  blind  and  hemiplegic ;  a  second  is  blind  and  deaf ;  and  a  third  is  blind, 
mute,  deaf,  and  paralyzed. 

One  of  the  features  of  hysterical  blindness  is  its  sudden  onset  without 
warning.  In  one  of  my  patients  the  loss  of  sight  came  on  in  less  than  a 
quarter  of  an  hour ;  another  patient  became  suddenly  blind.  Abadie's 
patient  went  to  bed,  and  woke  up  next  day  quite  blind ;  a  young  man,  of 
whom  Marlow  speaks,  became  suddenly  blind  as  he  was  entering  his  house. 
A  rapid  or  sudden  onset  is  therefore  characteristic  of  hysterical  blindness. 
In  some  patients  the  amaurosis  may  not  become  complete  for  several  hours, 
and  in  exceptional  instances  it  afiects  one  eye  before  the  other. 

Hysterical  blindness  is  absolute.  Cases  in  which  the  patient  retains  some 
perception  of  hght  are  very  rare  ;  the  patient  is  in  total  darkness,  no  matter 
how  bright  a  light  is  placed  in  front  of  the  eyes. 

A  special  feature  of  hysterical  blindness  is  the  preservation  of  the  light 
reflex  both  to  natural  and  artificial  light,  even  though  the  patient  has  no 
perception  of  light. 

A  fundamental  characteristic  of  hysterical  blindness  is  the  integrity  of 
the  media  and  of  the  retina.  The  information  yielded  by  the  ophthalmo- 
scope is  of  capital  importance. 

I  have  said  that  prodromata  are  usually  absent  in  hysterical  blindness. 
Headache  is,  however,  an  important  precursory  symptom.  One  of  my 
patients  had  severe  headache  before  he  became  bUnd,  and  as  he  had  had 
syphilis  it  was  not  unnatural  to  consider  the  headache  as  syphilitic.     In  a 

*  Dieulafoy,  "  La  Cecite  Hysterique  "  {Clinique  Medicate  de  V H otel-Dieu,  1907, 
5me  gt  6""^  lejons). 


NEUJIOSES  lo05 

woman  uiidor  my  care  the  blindness  was  accompanied  l)v  intense  headaclie. 
lasting  ten  months. 

Headache  has  been  noticed  repeatedly  in  cases  of  hysterical  blindness. 
It  has  no  fixed  seat ;  we  must  be  careful  not  to  put  it  down  to  a  cerebral 
tumour  or  to  meningitis,  when  it  accompanies  hysterical  blindness. 

Contracture  of  the  oculo-motor  muscles  frequently  accompanies  hysterical 
blindness.  Many  patients  keep  their  eyes  tightly  closed,  like  persons  who 
suffer  from  keratitis  and  keep  their  eyes  shut  because  they  dread  the  light. 

My  patient  in  the  Sainte-Jeanne  Ward  was  a  typical  case.  Not  only  did  she  keep 
her  eyes  closed,  but  the  eyelids  were  contracted  from  spasm  of  the  orbicularis.  When 
she  was  told  to  open  her  eyes,  she  tried  to  overcome  the  contracture  of  the  orbicularis, 
and  the  eyeUds  were  raised  to  a  slight  extent.  The  eyes  did  not  open  completely. 
During  this  effort  a  well-marked  frown  was  noticeable.  At  the  same  time  the  eyeballs 
were  deviated  to  the  right  side  by  the  jerky  contraction  of  the  right  external  rectus 
and  the  left  internal  rectus.  Tliis  deviation  was  accompanied  by  a  jerky  contracture 
of  the  muscles  of  the  neck,  which  drew  the  head  to  the  right.  Her  position  and  her 
appearance  were  so  characteristic  that  I  at  once  diagnosed  hysterical  blindness. 

The  blindness  has  a  duration  varjdng  from  some  days  to  several  months. 
Relapses  are  common,  and  we  may  see  several  attacks  of  blindness  at  variable 
intervals. 

The  poor  sufferers  ask  anxiously  as  to  the  probable  duration  of  the 
blindness ;  an  answer  is  impossible,  because  we  have  no  means  of  telling 
whether  recovery  .will  be  prompt  or  tardy.  It  appears  to  be  a  question 
of  chance.  The  blindness  sometimes  disappears  suddenly  without  apparent 
cause  ;  at  other  times  it  ceases  after  an  attack  of  hysteria.  In  some  patients 
the  sight  gradually  returns. 

The  prognosis  is  good  in  hysterical  blindness ;  the  duration  may  vary, 
but  recovery  finally  ensues.  It  is  important,  therefore,  to  make  a  diagnosis. 
In  some  cases  the  diagnosis  is  easy.  When  an  individual,  whose  \dsion  has 
previously  been  normal,  becomes  blind  after  an  attack  of  hysteria,  the 
blindness  is  obviously  hysterical.  This  diagnosis  also  holds  good  if  we 
find  sensitivo-sensory  hemianaesthesia,  hysterogenic  zones,  contractures,  etc. 

The  question  is  by  no  means  so  simple  in  every  case.  The  blindness  may 
supervene  in  persons,  showing  but  few  stigmata  of  hysteria  ;  it  may  appear 
as  the  only  symptom  of  hysteria.  On  the  other  hand,  a  patient  with  hysteria 
may  also  be  suffering  from  syphilis,  alcoholism,  or  lead-poisoning,  conditions 
in  which  visual  troubles  are  common. 

Under  the  name  of  "  symptomatic  triad  of  hysterical  blindness,"  I  have 
collected  the  symptoms  by  which  a  diagnosis  may  be  made.  These  s}Tnptoms 
are  sudden  onset  of  the  blindness,  preservation  of  the  light  reflex,  and 
integrity  of  the  media  and  of  the  retina.  When  a  blind  patient  presents 
this  triad,  we  can  state  that  the  blindness  in  hysterical,  although  the  patient 
appears  to  be  free  from  any  trace  of  hysteria. 


1506  TEXT-BOOK  OF  MEDICINE 

Is  it  possible  to  find  tliis  triad  in  blindness  due  to  other  causes  ?  Let  us 
examine  tbe  question.  Blindness  due  to  tumours  and  lesions  of  the  brain, 
LQcludiiig  syphilis,  is  far  from  presenting  the  fundamental  characters  of  the 
triad  ;  the  loss  of  sight  is  not  so  sudden,  the  light  reflex  is  lost,  and  the  media 
show  abnormahties,  apart  from  the  fact  that  other  symptoms  (paralysis  of 
the  cranial  nerves,  hemiplegia)  often  accompany  a  brain  lesion. 

Some  lesions  of  the  brain,  however,  may  cause  bliudness,  which  resembles 
in  character  the  triad  of  hysterical  blindness ;  they  are  combined  lesions 
(haemorrhage,  softening,  etc.)  of  both  occipital  lobes  at  the  cortical  origin, 
or  in  the  course  of  the  two  optic  tracts.  Chaufiard  has  employed  the  term 
"  cortical  anopsia."  Hemianopia  appears  suddenly  on  one  side  without  the 
patient's  knowledge,  and  is  followed  by  hemianopia  on  the  other  side.  This 
bilateral  hemianopia  gives  rise  to  anopsia — that  is  to  say,  sudden  blindness, 
with  normal  light  reflex  and  normal  media.  Cortical  anopsia  occurs  in  elderly 
persons  and  in  general  paralytics  ;  they  may  sufier  from  other  cerebral 
lesions  (foci  of  softening),  with  organic  hemiplegia,  aphasia,  epileptiform 
attacks,  and  rapid  cachexia — a  striking  contrast  to  the  person  with  hysterical 
blindness. 

I  need  not  discuss  the  diagnosis  of  hysterical  blindness  and  of  blindness 
in  tabes,  because  the  latter  shows  totally  difierent  characteristics.  Alco- 
holism and  tobacco-poisoning  may  give  rise  to  amaurosis.  The  amaurosis, 
however,  comes  on  slowly,  and  lesions  of  the  optic  nerve  are  constant — a 
condition  quite  opposite  to  that  found  in  hysterical  blindness.  Lead- 
poisoning  may  lead  to  blindness,  but  in  this  event  optic  neuritis  is  found. 

Ursemic  amaurosis  may  resemble  hysterical  blindness.  In  hysteria  we 
find  signs  from  which  we  can  deduce  the  nature  of  the  disease,  and  yet  these 
signs  may  be  absent.  In  uraemia  we  find  albuminuria  and  oedema,  the  two 
great  symptoms  of  nephritis  ;  they  may,  however,  be  absent,  at  any  rate  for 
a  time,  in  Bright's  disease,  as  I  have  already  pointed  out.  On  what  facts, 
then,  are  we  to  base  a  diagnosis  ?  We  must  inquire  carefuUy  into  the 
patient's  history.  If  the  blindness  is  uraemic,  the  patient  will  have  shown 
some  of  the  symptoms  of  Brightism :  the  arterial  tension  is  high,  a  hruit  de 
galop  is  heard  on  examining  the  heart,  the  ursemic  poisoning  has  already 
been  shown  by  dyspnoea,  etc. — ^in  short,  uraemic  blindness  appears  in  a 
patient  already  sick,  and  subject  for  some  time  past  to  symptoms  of 
Brightism  or  of  uraemia.  Hysterical  blindness  appears  in  a  healthy  individual, 
or  in  one  who  has  so  far  shown  only  the  nervous  stigmata  of  hysteria.  We 
have  a  diagnostic  method  of  supreme  importance.  Even  after  the  disap- 
pearance of  hysterical  bhndness  the  perimeter  shows  narrowing  of  the  visual 
field  and  overriding  of  the  coloured  circles. 

What  is  the  treatment  of  hysterical  blindness  ?  In  some  cases  it  defies 
every  method  :  magnetization,  static  electricity,  metaUotherapy,  blisters, 


NEUR0SH:3  1507 

collyria,  hydrotherapy,  douches  to  the  cycH,  su^^fstion,  isolation,  broiuides, 
and  injection  of  ovarian  extract.  In  other  cases  it  disappears  without  any 
treatment  after  an  attack  of  hysteria,  or  after  some  violent  emotion,  for  no 
reason  at  all. 

Genital  Functions.  —  Besides  false  peritonitis,  which  I  have  already 
mentioned,  hysterical  patients  may  suffer  from  spontaneous  or  provoked 
pain  in  the  iliac  region  :  the  pain  is  due  to  hypera3sthesia  of  the  ovary. 
Compression  of  the  painful  ovary  may  cut  short  or  bring  on  an  attack.  The 
genital  troubles  also  include  vaginismus  and  hypersesthesia  of  the  breast 
(mastodpiia). 

Troubles  of  the  Circulation — Fever. — The  vasomotor  nerves  play  a  large 
part  in  the  circulatory  troubles.  At  the  present  time,  however,  we  do  not 
admit  that  the  congestions  may  go  as  far  as  haemorrhage,  haemoptysis, 
haematemesis,  haematuria,  tears  of  blood,  and  sweating  of  blood. 

Is  there  such  a  thing  as  hysterical  fever  ?  Certain  cases  tend  to  prove 
that  hysterical  patients  may  suffer  from  fever  which  is  continuous,  like 
typhoid  fever,  and  which  may  last  for  several  weeks.  I  have  seen  several 
cases  of  this  kind  ;  the  temperature  may  exceed  106°  F. 

Diagnosis. — The  diagnosis  must  include  (1)  convulsive  hysteria,  (2)  non- 
convulsive  hysteria. 

Convulsive  hysteria  {petite  hysterie)  differs  from  epilepsy  in  the  char- 
acters I  have  enumerated.  In  certain  cases  epilepsy  is  associated  with  hys- 
teria, but  the  association  of  these  two  neuroses  is  sometimes  real,  sometimes 
apparent.  It  is  real  when  the  attacks  of  hysteria  and  of  epilepsy  remain 
distinct.  Thus,  a  young  epUeptic  girl,  who  becomes  hysterical  at  puberty, 
may  have  definite  attacks  of  hysteria  or  of  epilepsy.  In  other  cases  the 
association  of  the  two  neuroses  is  only  apparent :  this  is  grande  hysterie, 
or  the  epileptoid  attack,  but  it  is  not  true  epilepsy  (Charcot).  In  fact,  the 
attack  of  hystero-epUepsy  may  be  stopped  by  the  compression  of  the  ovary ; 
the  temperature  does  not  rise  after  a  series  of  attacks,  as  it  does  in  epilepsy. 
Babinski's  sign  is  not  met  with  in  hysteria,  while  it  exists  in  epilepsy  as  weU 
as  in  hemiplegia  of  organic  origin.  Hysteria  differs  from  catalepsy — a 
neurosis  characterized  by  momentary  loss  of  intellect  and  by  exaggeration  of 
the  muscular  contractions,  the  limbs  remaining  immovable  in  the  position 
in  which  they  have  been  placed.  Catalepsy  is,  however,  frequently  asso- 
ciated with  hysteria. 

The  diagnosis  of  local  (non-convulsive)  hysteria  comprises  the  diagnosis 
of  the  innumerable  symptoms  which  I  have  mentioned.  Hysterical  hemi- 
plegia must  not  be  confounded  with  the  hemiplegia  due  to  cerebral  lesions  ; 
the  diagnosis  is  discussed  under  Cerebral  Haemorrhage.  Hysterical  contrac- 
tures must  be  distinguished  from  the  contractures  due  to  lateral  scleroses 
of  the  spinal  cord.     Certain  hysterical  syndromes  may  simulate  insular 


1508  TEXT-BOOK  OF  MEDICINE 

sclerosis,  syringomyelia,  tabes,  and  paraplegia.     The  diagnosis  is,  in  general, 
possible  even  wben  there  are  hystero-organic  associations  (Souques). 

We  must  distinguish  hysterical  gastralgia  and  hsematemesis  from  similar 
symptoms,  due  to  a  lesion  of  the  stomach.  Cough  and  hsemoptysis  due  to 
hysteria  must  be  differentiated  from  pulmonary  lesions  of  a  tubercular  nature. 
In  these  difl&cult  cases  we  must  try  to  find  out  if  the  patient  has  not  had 
attacks  of  convulsive  hysteria,  or  if  m  her  condition  there  is  not  some  sus- 
picious stigma,  such  as  the  globus  hystericus,  hemiansesthesia,  ovarian 
hypersesthesia,  pharyngeal  ansesthesia,  hysterogenous  zones,  ocular  troubles, 
etc.  Finally,  the  special  characters  of  the  symptom  in  question  must  be 
carefully  analyzed.  We  shall  not  then  look  upon  ovarian  hypersesthesia  in 
a  hysterical  patient  as  appendicitis. 

JEtiology — Prognosis — Treatment. — Hysteria  may  occur  in  children,  but 
it  generally  makes  its  appearance  about  the  age  of  puberty,  and  it  becomes 
much  less  frequent  at  the  menopause.  Heredity  prepares  the  soil.  According 
to  certain  writers,  it  is  said  to  be  intimately  connected  with  tuberculosis 
(Grasset).  Emotions,  grief,  unfortunate  love-afEairs,  imitation,  and  chlorosis 
are  the  usual  causes.  It  often  coexists  with  exophthalmic  goitre,  with 
neurasthenia,  with  astasia-abasia,  and  with  Sydenham's  chorea. 

The  great  predisposing  cause  of  hysteria  is  nervous  heredity,  and  the 
provoking  agents  are  numerous.  Amongst  the  latter  I  would  mention  the 
infectious  fevers  (typhoid,  pneumonia,  malaria,  acquired  and  hereditary 
syphilis,  rheumatism),  the  chronic  intoxications  (lead,  mercury,  alcohol), 
genital  diseases,  pregnancy,  accouchement,  and  trauma. 

With  respect  to  trauma,  I  must  make  some  restrictions.  Trauma  is 
no  doubt  the  occasional  cause  of  many  hysterical  complications — but  are 
not  these  complications  sometimes  hysteriform  ?  The  proof  is  that  auto- 
suggestion, which  has  such  a  happy  influence  on  certain  hysterical  complica- 
tions—for example,  on  flaccid  paralysis — has  no  effect  on  hysteriform  para- 
lysis of  traumatic  origin.  Many  of  these  cases  might  be  described  as  cases  of 
secondary  or  symptomatic  hysteria,  just  as,  side  by  side  with  epilepsy,  we 
find  secondary  or  symptomatic  epilepsy.  The  syndrome  of  hysteria  may  be 
realized,  with  some  of  its  most  marked  characteristics,  in  poisoning  by  lead, 
mercury,  alcohol,  and  sulphide  of  carbon. 

Hysteria  is  far  from  being  as  serious  as  epilepsy.  It  may,  however,  lead 
to  dementia,  and  to  suicide  ;  it  may  cause  paralyses  and  contractures,  the 
results  of  which  we  can  never  foresee  ;  and,  in  conclusion,  it  is  a  source  of 
torment  to  the  patient,  a  source  of  constant  worry  to  the  family.  In  some 
exceptional  cases  death  supervenes  during  an  attack  of  hysteria. 

Male  Hysteria.— Rjstena,  is  more  frequent  in  men  than  was  at  first  sup- 
posed ;  it  is  frequently  observed  in  the  Army.  It  does  not  only  develop  in 
men  who  have  the  characteristics  of  feminism,  but  it  is  also  seen  in  robust 


NEUROSKS  J  009 

adult  Mini,  wliH  arc  not  of  an  rllrmiiiah'  f  \'[io  ;  malciiial  licrt'<lit,y  plavs  u 
great  part  in  its  development.  In  nicn,  as  in  women,  hysteria  may  he  non- 
convulsive  or  convulsive,  and  the  attacks  assume  the  forms  of  pHlilc  ut  of 
grande  htjderie.  Paralysis  (monoplegia,  hemiplegia,  paraplegia),  hemianes- 
thesia, anaesthesia  of  the  pharynx,  and  constriction  of  the  field  of  vision  are 
frequent  symptoms.  Contractures,  with  or  without  muscular  atrophy, 
aphonia,  and  mutism,  are  also  met  with  in  male  hysteria.  Hysterogenous 
and  hypnogenous  zones  are  also  met  with  ;  the  patients  are  susceptible  to 
suggestion  and  to  hypnotism.  Ovarian  hyperajsthesia  is  replaced  by  irrita- 
tion of  the  testicle  ;  pressure  may  provoke  or  arrest  the  attack  of  hysteria. 

In  men,  as  in  women,  hysteria  may  simulate  Sydenham's  chorea  and 
every  disease  of  the  spinal  cord.  Many  complications,  such  as  hysterical 
apoplexy,  which  simulates  true  apoplexy,  tympanites  with  acute  pain,  which 
simulates  peritonitis,  insomnia,  and  trophic  troubles,  are  seen  not  only  in 
women,  but  also  in  the  most  robust  men,  who  from  their  previous  life  and 
social  position  would  not  seem,  at  first  sight,  to  be  in  the  least  predisposed 
to  hysteria.  In  men,  as  in  women,  hysteria  may  be  associated  with  astasia- 
abasia. 

The  treatment  of  hysteria  must  be  palliative  and  curative.  In  a  pre- 
disposed child  education  plays  a  large  part ;  every  cause  of  excitation  and  of 
emotion  must  be  avoided.  A  country  life  and  somewhat  vigorous  exercise 
are  to  be  recommended.  Marriage  has  no  drawbacks,  when  it  takes  place 
under  favourable  circumstances  ;  in  certain  cases  it  is  beneficial.  When 
hysteria  has  declared  itself,  use  is  made  of  anti-spasmodics ;  isolation  is  an 
excellent  remedy.  Hydrotherapy,  change  of  air,  and  a  sea-voyage  should 
be  prescribed,  and  any  causes  which  may  assist  its  development  should  be 
carefully  looked  for. 

Hydrotherapy  is  certainly  one  of  the  most  powerful  remedies  against 
certain  manifestations  of  hysteria.  The  paralysis,  the  contractures,  and  the 
anaesthesia  generally  yield  to  the  application  of  electricity,  but  the  disappear- 
ance of  these  disorders  is  often  only  temporary. 

Suggestion  may  render  great  service,  and  in  several  cases  attacks  of 
hystero-epilepsy,  paralyses,  and  contractures  of  many  months'  duration, 
which  had  resisted  every  measure,  have  been  completely  cured  by  suggestion. 


V.  HYPNOTISM— LETHARGY— CATALEPSY— SOMNAMBULISM. 

Braid  has  defined  hypnotism  {v'kvo';,  sleep)  as  "  a  peculiar  condition  of 
the  nervous  system,  brought  about  by  artificial  manoeuvres."  This  condition 
is  also  called  nervous  sleep,  in  order  to  distinguish  it  from  natural  sleep, 
with  which  it  has  only  the  most  coarse  resemblance.  According  to  Babinski, 
"  hypnotism  is  a  psychical  condition,  rendering  the  subject  capable  of  sub- 
u.  96 


1510  TEXT-BOOK  OF  MEDICINE 

mitting  to  external  suggestion.  It  manifests  itself  by  phenomena,  which 
suggestion  calls  into  being.  These  phenomena  disappear  as  the  result  of 
persuasion,  and  are  identical  with  hysterical  symptoms.  Hypnotism  was 
for  a  long  time  practised  by  quacks  under  the  name  of  animal  magnetism ; 
it  was  placed  on  a  scientific  basis  by  Braid  (1843).  It  may  show  itself  in 
three  different  forms  (Charcot)— lethargy,  catalepsy,  and  somnambulism. 

etiology. — Nervous,  impressionable  women  and  boys  are  more  readily 
hypnotized  than  men.  Hysterical  people  are  hypnotized  even  more  easily  ; 
and  yet  aU  hysterical  people  cannot  be  hypnotized,  and  all  hypnotizable 
subjects  are  not  hysterical.  Grief,  deep  emotions,  and  convalescence  from 
acute  diseases  predispose  towards  it. 

The  will-power  of  the  subject  is  of  great  importance.  In  order  to  be  put 
to  sleep  rapidly  and  deeply,  the  subject's  whole  attention  must  be  given  to 
the  operator.  The  patient  must  wiU  to  be  put  to  sleep.  Certain  subjects 
can  only  be  sent  to  sleep  when  they  resist  mentally,  and  they  then  succeed, 
on  the  contrary,  in  hj^pnotizing  themselves  when  they  wish  to  do  so. 

When  we  try  to  put  a  person  to  sleep  for  the  first  time,  sleep  has  often 
to  be  waited  for.  If  the  patient  is  submitted  to  further  experiments,  the 
hypnosis  will  be  produced  much  more  rapidly.  Education  (Richet)  is, 
therefore,  of  great  importance. 

Contrary  to  the  generally  accepted  opinion,  any  person  can  be  put  to 
sleep.  There  is,  m  this  case,  no  fluid  or  divining  influence.  We  merely 
acquire,  by  habit,  more  authority  over  the  persons  who  are  to  be  put  to  sleep, 
and  more  still  over  those  who  have  been  already  put  to  sleep. 

The  artificial  means  used  to  provoke  nervous  sleep  are  numerous  (Cham- 
bard).  The  most  simple  one  consists  in  seating  the  subject  face  to  face 
with  the  operator,  in  taking  hold  of  his  hands  so  as  to  keep  him  quiet  still, 
and  in  making  him  fix  his  eyes  on  the  latter.  After  three  or  four  minutes  the 
eyelids  move,  slight  convulsive  jerks  appear  in  the  muscles  of  the  face  and 
of  the  limbs,  the  respiration  is  sighuig,  the  head  falls  on  the  shoulder,  and 
the  result  is  obtained.  The  act  of  looking  at  a  shining  object  held  12  to  15 
inches  from  the  root  of  the  nose,  so  as  to  make  the  eyeballs  converge  at  the 
same  time  as  they  look  upwards,  may  lead  to  the  same  result,  provided  the 
subject  fixes  the  object  and  devotes  all  his  attention  to  it  (Braid).  Subjects 
accustomed  to  hypnotic  seances  often  put  themselves  to  sleep  by  compressing 
the  eyeballs,  by  closing  of  the  eyes,  or  by  looking  at  a  shining  object.  Others 
are  easily  influenced  by  auditory  sensations — an  unexpected  noise,  the 
sound  of  the  diapason,  the  tick  of  a  watch,  music,  etc.  Hypnosis  is  some- 
times produced  under  the  influence  of  psychical  phenomena — faith,  expecta- 
tion, emotion,  and  intellectual  fatigue  ;  or  is  consequent  on  the  action  of 
certain  substances — ether,  chloroform,  alcohol,  and  Indian  hemp.  Cuta- 
neous friction  and  touching  of  the  so-called  hypnogenous  zones  (Pitres)— 


NEUROSES  1511 

vertex,  angle  of  the  scapula,  etc. — also  lead  to  nervous  sleep.  Finally,  an 
experienced  subject  can  go  to  sleep  by  merely  thinkiiijj;  of  the  fact  that  he 
or  she  is  about  to  be  put  to  sleep.  It  is  sufficient  to  say  to  some  of  them, 
"  In  an  hour,  or  to-morrow  at  such-aud-such  an  hour,  you  will  go  to  sleep," 
for  them  to  be  soundly  asleep  iit  the  time  named,  even  in  the  absence  of  the 
operator  (Hernheim). 

Symptoms. — The  process  of  hypnotization  just  described  does  not  pro- 
duce the  same  phenomena  in  all  subjects  ;  but  the  condition  provoked  may 
always  be  classitied  in  one  of  the  three  forms  described  by  Charcot. 

Lethargy.— In  the  condition  of  lethargy  the  patient  appears  to  be  in  a 
deep  sleep  :  the  eyes  are  closed,  the  muscles  are  relaxed,  and  the  uplifted 
aim  falls  down  inert ;  the  general  sensibility  is  abolished  ;  the  tendon 
reflexes  are  exaggerated,  and  every  effort  to  rouse  the  patient  by  shaking  him 
fails.  Charcot  has  shown  that,  in  this  condition,  there  is  very  marked 
muscular  hyperexcitability.  If  we  touch  the  cutaneous  points  corresponding 
to  the  course  of  the  superficial  nerves  (uhiar  or  facial)  with  the  point  of  a 
pencil,  the  muscles  supplied  by  these  nerves  contract,  just  as  they  do  with 
the  electric  current.  By  continuing  the  excitation,  we  cause  contractures, 
which  persist  even  when  the  subject  is  awakened.  Gentle  friction  to  the  skin 
over  the  antagonistic  muscles  makes  them  cease.  Richet  and  Brissaud  have 
shown  that  in  the  limbs  rendered  anaemic  by  Esmarch's  bandage,  the  muscular 
hyperexcitability  disappears.  Certain  excitants  may,  on  the  contrary,  act 
at  a  distance  ;  thus,  the  application  of  an  electrical  current  to  one  side  of 
the  skuU  may  cause  muscular  contractions  on  the  opposite  side  of  the  body — 
a  phenomenon  not  seen  in  the  waking  condition.  If  the  Kght  falls  on  one 
eye,  the  whole  of  the  corresponding  side  is  seen  to  become  cataleptic,  so 
that  the  subject  is  at  the  same  time  hemilethargic  and  hemicataleptic.  If 
the  right  eye  has  been  open,  aphasia  may  be  met  with.  As  soon  as  the  eye- 
lid is  closed,  the  limbs  again  relax. 

Catalepsy. — If  both  eyes  are  opened  in  the  presence  of  a  bright  light, 
lethargy  is  replaced  by  catalepsy.  The  same  result  may  be  obtained  directly 
by  one  of  the  procedures  mentioned  above,  especially  those  which  act  sud- 
denly, such  as  an  imexpected  noise.  The  eyes  are  then  open,  and  the 
limbs  are  not  contracted,  but  keep  the  position  in  which  they  have  been 
placed.  If  the  arm  is  raised,  it  remains  so  for  a  long  time.  Through  this 
peculiar  condition  of  the  muscles,  the  subject  may  be  placed  in  the  most 
extraordinary  positions.  The  general  anaesthesia  is  complete,  the  tendon 
reflexes  are  dimmished  or  abolished,  and  the  pulse  is  accelerated,  but  the 
respiration  is  not  altered ;  whereas  in  the  malingerer  the  effort  necessary 
to  maintain  the  arm  in  the  given  position  increases  the  respiration  rate, 
while  the  muscles  concerned  show  fatigue  tremors.  By  placing  the  limbs  in 
a  position  which  corresponds  to  a  passionate  attitude,  we  excite  or  suggest 

96—2 


1512  TEXT-BOOK  OF  MEDICINE 

an  expression  of  the  face  corresponding  to  a  similar  sentiment  or  a  similar 
passion.  The  muscular  system  is  in  a  condition  which  is  the  counterpart  of 
that  seen  in  lethargy.  Gentle  friction  of  a  muscle  produces  paralysis  which 
may  persist  when  the  experiment  is  finished. 

Somnamhulism.  —  Sonmambulism  is  the  condition  most  often  seen  in 
h5rpnotic  seances,  and  is  produced  most  readily  in  certain  subjects.  It 
consists  in  a  kind  of  intellectual  torpor,  with  preservation  of  the  muscular 
activity.  The  patient,  in  a  condition  of  provoked  somnambulism  (Barth), 
can  therefore  walk  and  talk  as  in  the  waking  condition  ;  he  often  replies  only 
to  questions  put  by  the  operator.  The  general  sensibility  is  abolished,  but 
cutaneous  hypersesthesia  is  often  present  to  such  a  degree  that  contact  with 
certain  metals  may  cause  a  burn.  The  special  senses  are  usually  rendered 
more  acute.  A  patient  of  Azam  heard  the  ticking  of  a  watch  at  a  distance  of 
nine  metres. 

In  somnambulists  there  is  often  a  cataleptoid  condition  of  the  muscles ; 
in  this  case  the  hyperexcitability  is  as  marked  as  in  the  lethargic  patient. 
When  the  somnambulist  or  the  cataleptic  patient  is  told  to  fix  an  object, 
and  when  he  cannot  turn  his  eyes  away  from  it,  he  is  said  to  be  in  an  ecstasy, 

A  similar  phenomenon  is  produced  when  a  person  is  concerned,  the 
somnambulist  imitating  aU  his  or  her  movements.  From  the  intellectual 
■point  of  view,  the  sonmambulist  is  an  automaton.  We  can  suggest  to  him 
a  certain  act  which  we  wish  to  see  him  perform.  He  often  resists,  but  if  we 
insist,  he  ends  by  giving  way.  We  can,  at  will,  provoke  illusions,  hallucina- 
tions, and  memory  troubles ;  by  means  of  suggestion  we  can  even  cause 
paralyses  and  contractures.  The  suggestion,  instead  of  referring  to  some- 
thing which  has  to  be  accomplished  immediately,  may  refer  to  something 
which  has  to  be  performed  some  time  hence  ;  thus  arise  hallucinations, 
or  irresistible  impulses  which  appear  long  after  the  order,  and  unknown  to 
the  subject.  The  question  of  suggestion  is  being  studied  to-day ;  it  has 
only  entered  the  sphere  of  science  during  the  last  few  years  (Bernheim, 
Pitres,  Charcot,  Dumontpallier,  etc.).  From  the  medico-legal  point  of  view, 
it  is  pregnant  with  consequences  ;  the  question  arises  how  far  hypnotizable 
subjects  are  responsible,  especially  if,  as  Bernheim  asserts,  we  can  make 
suggestions  to  certain  trained  individuals,  even  in  the  waking  condition. 

Whatever  the  hypnotic  condition  produced,  it  suffices  to  open  the  eyes 
of  the  patient,  and  to  blow  vigorously  on  them  in  order  to  awaken  him. 
When  he  has  come  round,  he  loses  the  recollection  of  what  has  happened, 
and  of  the  orders  which  he  has  received  to  carry  out  at  a  specified  date. 
Certain  cataleptic  patients,  however,  remember  the  seances  at  which  they 
were  present,  but  maintain  that  they  were  unable  to  prevent  them  or  to. 
withdraw  from  them. 

Much  has  been  Avritten  during  the  past  few  years  on  the  advantages  of 


NEUROSES  ir,i3 

hypnotism  fii»iii  a  therapeutic  point  of  view.  Rrona,  Vemeuil,  and  Pozzi 
havo  made  uso  of  the  an<t»sthesia  of  letharsry  in  order  to  perform  operations 
of  sliort  duration,  but  this  means  is  uncertain.  Certain  hysterical  paraly.scs, 
or  contractures,  and  hystero-epileptic  attacks  have  been  cured  by  these 
means.  We  must,  however,  be  guarded  in  our  practice,  becau.se  the 
inconveniences  might  be  greater  than  the  advantages.  The  repetition  of 
the  stances  causes  great  excitability  of  the  nervous  system,  and  the  latter 
often  brings  about  hysterical  complications. 


VI.— PATHOMIMIA. 

Clinical  Case.— In  April,  190i:s  a  man,  thirty  years  of  age,  was  admitted  to  the  Hotel- 
Dieu  for  gangrenous  trouble  of  two  and  a  half  years'  standing.  The  right  arm  was 
covered  with  slougli.-^.  wounds,  and  cicatrices.  The  patches  of  gangrene  varied  in  size  ; 
some  were  as  large  a.s  a  crown-piece.  The  gangrene  was  dry  and  odourless  ;  the  patches 
were  black  and  hard,  involving  the  whole  thickness  of  the  derma.  A  well-marked  line 
of  demarcation  was  present.  Where  the  sloughs  had  become  detached,  the  wounds 
showed  healthy  granulations.  The  recent  scars  were  of  a  violet  colour ;  others  were 
white  and  puckered.  In  some  places  the  scars  showed  keloid  formation.  Fresh  sloughs 
had  appeared  in  the  scar  tissue.  Lymphangitis  and  oedema  were  absent.  The  arm 
was  muscular. 

He  gave  the  following  history  :  Some  years  before  he  had  suffered  from  nervous 
crises  with  loss  of  consciousness.  In  a  fall  against  a  piece  of  furniture  he  injtu-ed  his 
left  wi'ist.  The  trivial  wound  was  dressed  with  carbolic  lotion;  but  it  gradually 
became  gangrenous  and  showed  no  sign  of  healing.  Scraping,  under  chloroform,  was 
advised.  The  patient  refused,  though  he  afterwards  felt  he  was  wrong  and  thought 
the  scrajiing  might  have  stopped  the  trouble.  Fresh  patches  of  gangi-ene  appeared  on 
the  arm. 

He  never  suffered  any  pain,  having  simply  an  acute  itching,  which  heralded  the 
apj)earance  of  a  patch  of  gangrene.  A  blister  formed,  and  in  two  or  three  hours  a 
gangrenous  patch  woidd  make  its  appearance.  In  a  few  days  a  line  of  demarcation 
formed  around  the  patch,  the  slough  came  away  in  a  week  or  two,  granulations 
appeared,  and  in  a  fortnight  healing  was  complete.  There  was  no  regularity  in  the 
appeai'ance  of  the  sloughs  ;  sometimes  they  came  one  after  another,  at  other  times  an 
interval  of  some  days  would  elapse.  Several  physicians  and  surgeons  were  consulted 
and  made  divergent  diag-noses ;  but  he  gained  no  reHef . 

In  May,  1906,  he  consulted  a  surgeon  who  diagnosed  trophic  changes,  consecutive  to 
neuritis,  and  advised  stretching  the  nerves  of  the  brachial  plexus.  The  operation  saw 
performed  on  June  21,  and  was  followed  by  such  acute  pain  that  free  injection  of 
morphine  was  necessary.  The  gang*renous  condition  did  not  show  any  change,  fresh 
sloughs  appearing. 

He,  therefore,  again  consulted  the  surgeon,  who  advised  amputation  of  the  arm. 
He  consented,  and  the  arm  was  amputated  in  the  upper  third.  The  wound  healed  weU 
and  he  resumed  his  employment. 

Nevertheless,  in  February,  1907,  patches  of  gangrene  appeared  on  the  right  arm, 
and  ran  a  similar  course  to  those  on  the  left  arm.  The  surgeon,  who  had  removed  tlie 
left  arm,  was  consulted  for  the  third  time  and  advised  nerve  stretching.  The  patient 
refused  and  came  to  the  Hutel-Dieu  on  April  28,  1908.  We.  then,  found  the  condition 
already  described.     In  two  years  and  a  half  the  sloughs  had  numbered  ninety  eight. 


1514  TEXT-BOOK  OF  MEDICINE 

Some  days  later  a  siioiliar  condition  appeared  on  tlie  left  foot  and  ankle.  Reddish 
streaks  like  tliose  of  lympliang-itis  appeared.     Walkiag  was  very  painful. 

Diagnosis. — The  lesions  were  not  syphilitic.  Syphilis  may  cause  gangrene ;  but 
it  does  not  cau^e,  in  an  hour,  sloughs,  having  the  characters  above  mentioned  and 
appearing  so  frequently  as  a  hundred  times  in  two  years  and  a  half. 

There  was  no  question  of  diabetes  ;  furthermore,  the  lesions  of  diabetes — perforat- 
ing ulcer  and  gangrene  of  the  limbs — show  no  resemblance  to  the  rapidly  appearing  and 
recurrent  patches  of  gangrene  seen  in  the  present  case. 

"Was  the  condition  trophic  and  secondary  to  neuritis  ?  He  was  not  an  alcoholic  and 
he  had  never  suffered  from  lead  poisoning.  And,  again,  the  trophic  troubles  referable 
to  neuritis  and  polyneuritis  do  not  mummify  the  whole  thickness  of  the  skin  in  an  hour. 
Tabes  could  not  be  held  guilty ;  the  patient  had  none  of  the  symptoms  of  this  disease. 
Trophic  troubles  of  a  hysterical  nature  alone  remained.  As  I  have  said  before,  it 
is  hardly  logical  to  admit  the  existence  of  trophic  disorders  in  hysteria.  This  view  is 
amply  confirmed  by  the  researches  of  Babinski,  and  by  certain  communications  to  the 
Societe  de  INeurologie.  We  could,  therefore,  exclude  sypMlis,  diabetes,  tabes,  hysteria, 
and  neuritis ;  and  accordingly  we  made  the  following  diagnosis :  Simulatimi,  the 
sloughs  being  caused  hy  caustic  potash.  We  made  this  diagnosis  even  in  the  face  of 
the  fact  that  the  patient  had  submitted  to  two  operations,  one  of  which  was  amputa- 
tion of  the  arm. 

The  fii'st  point  to  notice  in  the  history  of  the  case  is :  the  rapidity  with  which  the 
lesions  occxu-red,  a  slough  forming  in  less  than  an  hour.  Chemical  substances  alone 
can  produce  such  rapid  gangrene.  In  this  case  the  lesions  produced  were  exactly 
similar  to  those  produced  by  Yienna  paste,  which  contains  caustic  potash. 

It  was  now  a  question  of  exposing-  the  fraud.  As  we  could  not  catch  the  offender 
flagrante  delictu,  the  following  m,ise  en  scene  was  arranged. 

The  managing  director  of  the  insurance  company  for  which  the  patient  worked, 
called  him  into  his  office.  My  assistant.  Dr.  Cronzon,  and  myself  were  also  present. 
The  patient  was  then  told  that  he  must  give  up  the  simulation  he  had  been  practising 
for  the  past  two  years.  The  patient  denied  the  accusation  on  his  word  of  honour,  and 
pointed  out  that,  as  he  had  undergone  two  severe  operations,  such  a  charge  was 
obviously  groundless. 

If  an  expert  physician  had  been  present  in  his  defence,  the  situation  would  have 
been  most  difficult.  He  might  have  suggested  Raynaud's  disease,  and  pointed  out  the 
fact  that  in  this  strange  disease  the  limbs  are  attacked  by  gangrene,  and  that  the 
duration  of  the  malady  is  often  a  question  of  many  years.  "  Can  you  state  that  this 
case  is  not  one  of  some  undescribed  form  of  spontaneous  gangrene  ?  "  was  a  possible 
question. 

We  had  considered  these  points,  and  yet  remained  firm  in  our  conviction  that  the 
man  was  a  simulator. 

Accordingly,  I  faced  him  and  spoke  to  him,  "  So  far  you  have  been  the  dupe  of 
a  peculiar  mental  condition.  Tou  have  been  compelled  by  an  irresistible  impulse  ;  in 
short,  you  have  not  been  responsible,  and  we  have  come  to  your  assistance.  If,  from  now 
on,  you  persist  in  your  denials,  you  are  a  rogue  and  an  impostor,  and  you  wiU  foi-feit 
the  regard  of  honest  men.     Tou  can  make  your  choice." 

He  broke  down  completely,  admitted  the  deception,  and  gave  us  a  signed  statement 
to  the  effect  that  the  sloughs  had  been  made  with  caustic  potash.  He  has  often  been 
to  see  me  since  his  confession,  and  is  now  free  from  the  obsession  which  had  rendered 
his  life  a  burden.     His  gratitude  has  been  most  profound. 

The  history  of  this  case  is  truly  astounding.  An  intelligent  man,  free  from  any 
nervous  taint,  starts  without  any  good  reason  to  make  sloughs  by  means  of  caustic 
potash  for  two  years,  and  a  half!  He  submits  to  the  loss  of  his  left  arm,  and  then 
attacks  his  right  arm  and  his  left  leg.     In  what  category  is  this  to  be  placed  ? 


NEUROSES  ir.l5 

Dupu'.  nndor  the  natne>  of  mythomania,  has  (lesoribctl  a  most  reraarkahlf  psycho- 
log-ical  anil  uuMlico-leg-jii  ooiulitiuu.  This  patient,  liowever,  wan  not  a  mythomaniac  ; 
his  fabrication  was  niaikod  by  acts.  My  friend,  Paul  I5«)r)/et,  lias  suggested  the 
excellent  term  "  palhomimia  "  for  the  morbid  condition. 

Pathominies  can  be  divided  into  <wo  cla.sses :  those  who  simulate  a  disease  with 
fraudulent  intent  for  gain,  and  those  who  do  so  simply  for  their  »iwn  satisfaction.  (Jur 
patient  was  one  of  the  latter  class.  Othf^r  examples  are  given  in  C'liniques  de  I'llutd. 
Dii'u.  When  we  examine  the  mental  i-oudition  of  fliose  pathominies  whoso  object  is 
ut'ifher  fraud  nor  gaiu.  we  are  almost  at  a  loss  to  find  an  explanation  for  their  mental 
condition.  Leniontin  has  noted  the  case  of  a  young  girl  who  produced  disfiguring 
scars  on  herself  for  two  and  a  half  years.  No  reason  could  be  found  for  such  a 
peculiar  aberration.  I  have  published  the  case  of  a  woman  who  produced  ulcers 
in  her  legs,  and  submitted  to  amputation  through  the  thigh,  under  the  impression 
that  some  day  a  fresh  amputation  might  be  performed.  Thoriot  and  Mosny  speak  of 
a  man  who.  for  no  reason  at  all,  had  his  abdomen  opened  on  three  occasions.  He  did  all 
he  could  to  have  laparotomy  jierformed  a  foiu'th  time. 

My  patient  underwent  nerve-stretching  and  amputation  of  the  arm ;  but  yet 
he  did  not  reveal  his  secret,  although  a  word  would  have  stopped  the  surgeon's  knife 
and  cleared  np  the  WTong  diagnoses  previously  made.  And  the  man  was  neither 
demented,  degenerate,  nor  alcoholic ;  he  did  not  suffer  from  hereditary  taint,  neuras- 
thenia, or  hysteria ;  on  the  contrary,  he  was  intelligent  and  well-read.  The  patho- 
mimes  of  this  class  experience  much  satisfaction,  in  making  themselves  the  object 
of  interest  and  mystery  to  their  friends.  They  guard  their  secret  jealously,  and, 
once  started  on  their  wretched  journey,  they  lose  the  will-power  to  leave  the  track. 


YII.  NEURASTHENIA. 

.ffitiology. — The  affection  usually  develops  between  the  ages  of  twenty- 
five  and  fifty  years  of  age,  affecting  men  and  women  in  equal  proportions. 
Uterine  affections  play  a  great  part  as  provoking  agent.  Intellectual  efforts, 
mental  overwork,  and  emotions  favour  its  appearance,  and  explain  its 
frequency  in  authors,  scientists,  doctors,  speculators,  etc. ;  hence  the 
frequency  of  neurasthenia  in  the  Jewish  and  the  Anglo-Saxon  races,  whose 
intellectual  life  is  very  active.  Charcot  has  laid  especial  stress  on  injuries, 
accompanied  by  shock,  by  excessive  emotion  (railway  accidents,  explosions). 
Sexual  excesses,  masturbation,  and  diseases  of  the  genital  organs  are  also 
a  frequent  cause  of  neurasthenia.  Digestive  troubles  have  been  regarded 
as  the  result  and  also  the  cause  of  neurasthenia  ;  such  is  said  to  be  the  mode 
of  action  of  dilatation  of  the  stomach  and  of  the  resulting  auto-intoxication 
(Bouchard),  of  enteroptosis  (G-hssard),  and  of  chronic  gastritis  (Hayem). 
It  is  certain  that  neurasthenia  develops  especially  in  people  of  neurotic 
stock  and  in  arthritic  subjects  (Huchard).  This  fact  explains  its  frequency 
in  hysterical  and  diabetic  patients ;  its  coexistence  with  gravel,  gall-stones, 
rheumatism,  gout ;  and  its  association  with  tabes,  exophthalmic  goitre, 
general  paralysis,  etc. 

De  Fleury,  who  has  published  some  interesting  work  on  this  question, 
thus  states  his  conception  of  neurasthenia.     The  gastro-intestinal  theory 


1516  TEXT-BOOK  OF  MEDICINE 

does  not  appear  to  him  to  be  admissible.  The  digestive  troubles  so  frequent 
in  neuropathic  patients  undoubtedly  have  a  secondary  action  on  the  brain ; 
but  they  themselves  arise  from  a  faulty  innervation.  Neither  is  neurasthenia 
a  disease  of  the  imagination  ;  its  symptoms  are  not  comparable  with  those 
of  hysteria,  which  result  from  a  fixed  idea,  and  gradually  disappear  under 
the  influence  of  suggestion.  According  to  De  Fleury,  neurasthenia  is 
primarily  a  fatigue  of  the  nerve  centres,  producing  in  all  the  organs  a  diminu- 
tion of  the  muscular  tonicity  and  of  the  glandular  secretion.  As  each  part 
of  the  economy  performs  its  functions  sluggishly,  the  sensory  nerves  carry 
to  the  brain  the  continuous  idea  of  poor  vitality,  and  it  is  the  consciousness 
of  this  ph3^sical  condition  which  constitutes  the  mental  state  of  neurasthenia. 

Symptoms. — Neurasthenia  shows  certain  fixed  symptoms  or  stigmata 
by  analogy  with  the  equivalent  sjrmptoms  of  hysteria  (Bouveret). 

In  this  group  must  be  included  headache,  the  most  constant  of  all 
the  stigmata.  It  is  generally  frontal  and  occipital,  and  is  comparable  with 
the  pressure  of  a  heavy  and  narrow  helmet  (Charcot's  neurasthenic  helmet) ; 
it  follows  a  circular  line  passing  round  the  temples.  In  other  cases  it  is 
limited  to  the  occiput,  is  seated  between  the  eyebrows,  or  is  hemilateral. 
It  manifests  itself  on  awakening,  and  continues  the  whole  day,  with  slight 
diminution  after  meals.  It  ceases  at  night,  even  though  the  patient  is  troubled 
with  insomnia.  It  is  increased  by  sensory  stimuli — noises,  strong  odours, 
and  by  intellectual  fatigue.  It  is  sometimes  accompanied  by  hyperaesthesia 
of  the  scalp  and  by  creaking  in  the  occipital  articulations.  Rachialgia  is 
often  associated  with  neurasthenia.  At  times  the  rachialgia  exists  alone ; 
it  may  be  limited  to  the  sacrum  or  to  the  coccyx.  It  betrays  itseK  by  a  sensa- 
tion of  pressure  or  of  heat,  brought  on  by  percussion  of  the  vertebral  column. 

Mental  depression  is  never  wanting.  The  patient  has  no  longer  the 
same  faculty  of  attention  nor  the  same  will-power.  The  least  work  becomes 
difficult ;  the  memory  fails,  especially  for  proper  names.  The  neurasthenic 
patient  becomes  depressed,  seeks  isolation,  and  often  passes  his  time  in 
reading  works  on  medicine,  or  in  writing  long  monographs  intended  for  his 
physician.  In  the  morning  he  feels  fatigued,  and  this  fatigue  is  often  real, 
because  it  betrays  itself  by  a  diminution  of  the  muscular  force  appreciable 
with  the  dynamometer. 

The  gastric  troubles  are  also  constant.  Flatulent  dyspepsia,  distension 
after  food,  hot  flushes,  somnolence,  .constipation,  and  pseudo-membranous 
colic  may  cause  us  to  think  of  cancer  of  the  rectum,  or  of  dilatation  of  the 
stomach.  These  gastric  manifestations  are  generally  accompanied  by  loss 
of  flesh  and  by  decoloration  of  the  skin. 

We  also  find  numerous  morbid  manifestations,  varying  according  to  the 
subject,  and  involving  all  the  systems;  such  are  insomnia,  vertigo,  agora- 
phobia, claustrophobia,  disturbance  of  the  cutaneous  sensibility,  neuralgic 


NEUROSES 


ir,i7 


pains,  spnsations  of  boat  and  of  cold,  JiRavino.ss  of  tlu-  exdids,  accoiiiinoda- 
tiori  a.stli(Mio]>ia,  liy])(>racoii.sia,  l)uzzin<^  and  wliisllin^'  in  the  ears,  iniiscular 
jerks,  and  giving  way  of  the  legs. 

Tn  the  circulatory  system  wo  find  |)eriodic.  attacks  of  ]>soudo-angina 
pectoris,  with  restlessness  and  dyspiujea.  Tachycardia,  palpitation,  and 
coldness  and  ])alIor  (tf  the  extremities  are  also  comnu>n. 

Profuse  swcalinirs,  or,  on  the  contrary,  dryness  of  the  skin  arul  of  the 
mucosiP,  seminal  emissions,  impotence,  and  increase  of  the  urates  and  of 
the  uric  acid  in  the  urine  must  also  be  mentioned. 

Pitres  describes  six  forms  of  neurasthenia,  according  to  the  system, 
most  affected  :  (1)  Cerebral  form  ;  (2)  spinal  form  ;  (3)  neuralgic  form  ; 
(4)  cardialgic  form  ;  (5)  gastro-intestinal  form  ;  (6)  general  form.  Blocq 
describes  in  addition  a  local  form,  often  characterized  by  painful  zones, 
without  organic  lesions.  It  is  needless  to  say  that  these  forms  are  often 
combined.  Neurasthenia  rarely  occurs  in  an  acute  form ;  it  generally 
assumes  "  a  circular  form,"  even  when  it  is  due  to  injury.  It  lasts  for 
months  and  years,  but  it  is  susceptible  to  complete  cure,  excepting  in 
hereditary  cases  ;  it  then  leads  to  hypochondria,  which  is  often  irremediable. 

Diagnosis. — The  diversity  of  the  forms  and  of  the  symptoms  of  neuras- 
thenia cause  it  to  resemble  many  diseases.  It  may  simulate  general  paralysis, 
but  it  is  not  accompanied  by  pupillary  troubles,  embarrassment  of  speech 
and  tremors  ;  the  diagnosis  may  be  in  doubt  until  the  case  is  far  advanced. 
Cerebral  tumours,  and  in  particular  cerebral  syphilis,  lead  to  confusion. 
Neurasthenic  pseudo-tabes  is  distinguished  from  true  tabes  by  the  presence 
of  the  reflexes,  by  the  absence  of  pupillary  troubles,  and  by  the  less  intensity 
of  the  pains. 

The  gastro-intestinal  form  is  at  times  most  difficult  to  diagnose.  Not 
only  may  cancer  of  the  stomach  or  of  the  intestine, in  the  absence  of  a  tumour, 
be  confounded  with  neurasthenia,  but  chronic  gastritis  and  dyspepsia  have 
many  symptoms  in  common  with  neurasthenia,  thus  explaining  why  a  case 
is  regarded  by  one  physician  as  gastric,  and  by  another  physician  as  nervous. 
The  examination  of  the  gastric  juice  does  not  always  settle  the  question. 

Treatment. — Tonics,  kola,  coca,  injections  of  cacodylate  of  sodium, 
the  glycero-phosphates,  absolute  rest,  isolation,  massage,  electrical  methods, 
and  hydrotherapy,  together  with  the  use  of  iron  and  of  bromide  of 
potassium,  are  the  means  generally  employed  in  neurasthenia.  The  bowels 
should  be  regulated  by  the  daily  use  of  a  laxative.  The  hours  of  meals 
should  be  regulated,  and  the  diet  should  be  carefully  selected  in  every  case. 
When  the  lost  flesh  and  strength  are  being  regained,  moderate  exercise  and 
subcutaneous  injections  of  organic  extracts  (Brown-Sequard)  and  of 
artificial  serum  should  be  prescribed. 

"  Neurasthenic  patients ,  properly  so  called,  are  not  amenable  to  sug- 


1518  TEXT-BOOK  OF  MEDICINE 

gestion.  Their  condition  may  be  almost  always  improved,  and  they  are  at 
times  cured  by  a  diet  from  which  alcohol  and  indigestible  foods  are  eliminated, 
and  by  systematic  mechanical  stimulation  of  the  nervous  system  (douches, 
change  of  air,  massage,  saline  injections,  static  electricity).  Drugs  should  be 
used  as  little  as  possible.  After  a  period  of  rest,  permitting  the  restoration  of 
the  energy  in  the  nerve  centres,  the  lost  habit  of  physical  and  intellectual 
work  must  be  gradually  resumed.  Isolation  in  an  asylum  is  only  necessary 
in  the  most  serious  cases  "  (De  Fleury), 

VIII.  ASTASIA-ABASIA. 

Description. — These  terms  were  applied  by  Blocq  to  a  syndrome, 
characterized  by  impossibility,  or  difficulty  in  standing  erect  (ao-racri?)  and 
in  walking  {a^aatq),  while  the  muscular  power,  the  sensibility  and  co-ordina- 
tion of  the  other  movements  of  the  lower  limbs  are  perfect.  In  1864  Jaccoud 
had  given  to  this  condition  the  name  of  "  ataxy  from  want  of  automatic 
co-ordination." 

Apart  from  the  difficulty  in  standing  erect  and  walking  normally,  the 
patient  when  lying  down  can  execute  all  the  movements  he  is  asked  to 
perform  without  hesitation,  weakness,  or  want  of  co-ordination.  He  has 
an  exact  idea  of  the  position  of  his  legs,  and  when  he  has  risen  he  sometimes 
succeeds  in  walking  by  means  of  certain  subterfuges  ;  thus  some  patients 
manage  to  walk  on  all  fours,  or  with  their  legs  crossed,  or  with  very  small 
steps,  or,  on  the  contrary,  with  large  steps  (actor's  walk) ;  some  can 
even  run. 

In  some  patients  the  trouble  appears  as  soon  as  they  try  to  stand  up, 
and  they  sink  down  unless  they  are  held  up.  Others  have  recourse  to  crutches , 
and  drag  their  seemingly  inert  legs  after  them. 

In  most  cases  the  abasia  predominates;  it  may  be  divided  into  three 
varieties : 

1.  Paretic  Abasia,  characterized  especially  by  the  diminution  in  the 
muscular  force.  Walking  is  difficult ;  it  is  only  possible  by  means  of  the 
greatest  efforts,  and  it  very  rapidly  becomes  impossible. 

2.  Choreiform  Abasia  (Grasset). — When  the  patient  stands  up,  the 
legs  are  seized  with  sudden  movements  of  flexion  and  extension  ;  at  the 
same  time  the  trunk  is  flexed  or  extended  on  the  pelvis,  and  the  movements 
are  thus  propagated  to  the  arms.  It  seems  as  though  the  contortions  would 
throw  the  patient  down,  but  nothing  of  the  kind  happens ;  on  the  other 
hand,  normal  progression  forwards  is  rendered  absolutely  impossible. 

3.  Trembling  Abasia. — In  this  form  the  contradictory  movements  pre- 
dominate ;  the  legs  become  entangled  just  as  in  certain  forms  of  incomplete 
spasmodic  paraplegia. 


NETT710SR3  ISi^ 

As  astasia-abasla  13  almost  always  of  an  hysterical  nature,  the  strange 
forms  which  it  may  assume  will  be  readily  understood.  In  general,  it  is  a 
syndrome  of  long  duration,  persisting  for  months  or  years,  and  subject  to 
relapses  ;  it  disappears  and  reappears  suddenly.  Patients  auflering  from 
abasia  sometimes  show  hysterical  stigmata  :  ovarian  or  testicular  pains, 
various  hysterogenic  zones,  anaesthesia  in  patches,  convulsive  attacks,  etc. 
Seglas  is  of  opinion  that  it  is  connected  with  insanity,  and  Charcot  with  an 
indeterminate  lesion  of  the  brain.  As  a  rule,  however,  astasia-abasia  mu.st 
be  attributed  to  some  d}'Tiamic  trouble  in  the  brain  or  in  the  spinal  cord, 
either  because  the  cerebral  cells  which  transmit  to  the  spinal  cells  the  stimuli 
necessary  for  the  performance  of  normal  walking  have  lost  their  power,  or 
because  the  spinal  cells,  receiving  a  normal  stimulus  from  the  brain,  are  no 
longer  capable  of  transmitting  it  properly  to  the  nerves  of  the  lower  limbs. 
Stasobasophobia  is  abasia  accompanied  by  emotional  troubles. 

Diagnosis. — Astasia-abasia  was  for  a  long  time  confounded  with  para- 
plegia and  ataxy.  It  differs  from  the  former  in  the  preservation  of  the 
muscular  force  when  the  patient  is  l}'ing  down,  in  the  integrity  of  the 
sphincters,  and  in  the  possibility  of  walking  other  than  normal  walking. 
It  must  not  be  confounded  with  ataxy,  because  the  co-ordination  of  the 
movements  is  intact  when  the  patient  is  lying  down,  and  the  muscular  sense 
is  preserved.  Chorea,  and  especially  rhythmical  chorea,  show  some  analogy 
with  astasia-abasia,  but  here  the  upper  limbs  and  the  face  show  their  own 
proper  movements,  and  not  the  propagated  movements  found  in  astasia- 
abasia.  Furthermore,  we  have  to  deal  with  extensive  movements,  either 
forwards  or  backwards,  and  but  little  comparable  with  the  movements  of 
sudden  flexion  and  extension  of  the  legs. 

The  giving  way  of  the  legs  in  cases  of  neurasthenia  and  of  ataxy  might 
also  lead  to  confusion,  but  in  patients  suffering  from  ataxy  the  want  of  co- 
ordination exists  when  they  are  in  bed,  and  the  neurasthenic  patient  often 
refuses  to  stand  erect  or  to  leave  the  room.  Every  attempt  to  over- 
come the  resistance  of  the  patient  is  accompanied  by  a  characteristic 
agony. 

In  Thomsen's  disease  the  rapidity  with  which  the  spasms  produced  on 
attempting  to  wallc  disappear  is  an  excellent  means  of  diagnosis  ;  besides, 
the  upper  limbs,  the  neck,  the  jaw,  and  the  tongue  are  sometimes 
attacked. 

Paramyoclonus  multiplex  is  accompanied  by  jerks,  which  extend  to  the 
whole  body,  or  to  a  great  part  of  the  body,  and  which  supervene  as  the 
result  of  very  slight  stimuli.  Nothing  of  this  kind  occurs  in  astasia- 
abasia. 


1520  TEXT-BOOK  OF  MEDICINE 

IX.   CEREBRO-CARDIAC  NEUROPATHY— KRISHABER'S 

DISEASE. 

Description.— Under  tlie  name  of  cerebro-cardiac  neuropathy,  Krishaber 
has  described  a  neurosis  witli  such  definite  symptoms  and  characters  that 
it  may  be  looked  upon  as  a  morbid  entity. 

The  onset  may  be  slow  or  rapid,  and  the  slowness  of  the  onset  is  generally 
a  favourable  sign.  The  rapid  onset  is  very  rare.  The  disease  supervenes 
almost  without  prodromata.  The  subject  has  a  distressing  sensation  of  a 
cerebral  void.  He  complains  of  vertigo,  insomnia,  nightmares,  photopsia, 
palpitation,  and  tightness  in  the  chest ;  he  is  liable  to  attacks  of  syncope. 

These  troubles,  instead  of  appearing  suddenly,  supervene  gradually  in  the 
slow  form  of  this  neuropathy ;  they  follow  and  replace  one  another  until  the 
disease  is  completely  established.  Whether  the  symptoms  come  on  slowly 
or  suddenly,  a  time  comes  when  the  descriptions  of  the  two  forms  of  the 
disease  may  be  blended  together.  Vertigo  is  one  of  the  earliest  and  also 
the  most  obstinate  symptom  ;  it  lasts  for  months  and  for  years.  The  organs 
of  the  senses  are  affected,  especially  those  of  sight  and  hearing,  which  become 
very  acute  ;  a  bright  light  is  intolerable,  and  the  sense  of  hearing  is  increased 
to  such  a  degree  that  the  slightest  noise  causes  genuine  distress.  The  tactile 
sensibility  is  increased. 

The  patient  lives  in  a  world  of  dreams  :  the  aspect  of  the  exterior  world 
seems  changed  to  him  ;  his  own  voice  is  strange  to  him.  He  finds  himself 
so  changed  that  he  hardly  recognizes  himself,  and  would  readily  take  himself 
for  somebody  else  if  reason  did  not  rectify  the  aberration  of  his  senses. 
Insanity  is  never  present,  and  the  patient  is  conscious  that  "  his  senses 
are  perverted,  and  give  him  incorrect  ideas  of  the  external  world " 
(Krishaber). 

The  heart  troubles  consist  in  palpitation,  angina  pectoris,  and  s5nicope  ; 
they  are  often  accompanied  by  sensations  of  strangulation. 

The  neuralgia  is  multiple,  and  affects  the  head,  the  face,  the  ear,  and 
the  sciatic  nerve. 

Insonmia  is  one  of  the  most  painful  symptoms  in  the  grave  form.  The 
patient  cannot  enjoy  a  moment's  rest,  and  if  he  goes  to  sleep,  it  is  only  to  be 
awakened  by  nightmares,  accompanied  by  angina  and  palpitations.  The 
duration  of  cerebro-cardiac  neuropathy  varies  from  a  few  months  to  several 
years.  It  is  almost  always  cured  ;  it  never  ends  in  mental  alienation,  but 
the  nature  and  the  persistence  of  the  symptoms  render  the  disease  most 
distressing.  It  is  provoked  by  all  kinds  of  excesses,  especially  in  a  predis- 
posed person.  The  intimate  cause  of  the  symptoms  seems  to  be  cerebral 
anaemia,  produced  by  a  permanent  contraction  of  the  vessels  of  the  brain 
(Krishaber' s  experiments). 


NEUROSES  1521 

Diagnosis.  Cenhro-cardiao  neuropathy  difiurs  fnun  the  nervous  condi- 
tions known  us  ^cju^ral  (H'liriil^iii,  s[)irial  irritation,  and  nervosism. 

In  general  neuralgia  (VuIIimx)  the  principal  phenomenon  is  pain,  dis- 
seminated tiirouf^hout  the  whole  surface  of  the  body,  and  complicated  by 
neuralgia  of  various  nerves.  Dizziness,  dimness  of  sight,  and  more  or  less 
marked  weakness,  feebleness,  and  depression  complete  the  picture  of  this 
morbid  condition. 

Spinal  irritation  is  characterized  by  a  general  nervous  condition,  in  which 
racliialgiu  is  the  chief  feature.  This  rachialgia,  which  is,  according  to  circum- 
stance, most  marked  in  the  cervical,  dorsal,  or  lumbar  regions,  is  accom- 
panied by  muscular  weakness,  by  spermatorrhoea,  and  by  hypochondria. 
This  nervous  condition  is  said  by  Hammond  to  be  due  to  an  anaemia  of  the 
posterior  columns  of  the  spinal  cord. 

X.  PARALYSIS  AGITANS— PARKINSON'S  DISEASE. 

Paralysis  agitans  is  a  neurosis  characterized  by  a  special  tremor,  which 
is  absent  in  some  cases,  by  a  peculiar  rigidity  of  the  muscular  system,  and  by 
a  paralytic  condition  which  appears  late,  and  is  simply  an  accessory  element 
in  the  disease. 

Description. — In  some  cases  the  disease  appears  suddenly  after  fright, 
emotion,  or  trauma,  and  the  tremor  at  once  declares  itself  ;  but  this  is  the 
exception.  As  a  rule,  the  onset  is  insidious,  and  the  course  is  slowly  progres- 
sive. The  tremor  first  affects  the  hand,  the  thumb,  the  foot,  but  this  tremor 
is  so  slight  that  the  patient  hardly  notices  it.  It  disappears,  and  then  returns 
with  renewed  intensity.  It  becomes  general,  or  else  in  certain  subjects  it 
assumes  the  hemiplegic  and  paraplegic  forms. 

The  tremor  of  paralysis  agitans  has  characteristics  distinguishing  it  from 
other  tremors.  The  hand  looks  as  if  it  were  holding  a  pen.  The  fingers 
are  stretched  out  and  tremble  as  a  whole,  while  the  thumb  moves  on  them 
with  isochronic  and  rh^-thmical  tremors,  though  the  hand  as  a  whole  seems 
to  be  spinning  wool  or  crumbling  bread  (Gubler).  The  tremor  of  the  wrist 
on  the  forearm  is  produced  by  movements  of  flexion  and  extension,  and 
sometimes  extends  to  the  whole  Of  the  upper  limb.  The  writing  shows  the 
effect  of  these  tremors  ;  the  down-strokes  are  sinuous.  In  the  lower  limbs 
the  tremor  of  the  toes  and  of  the  feet  is  produced  by  successive  movements 
of  flexion  and  extension. 

All  the  tremors  occur  when  the  muscles  are  at  rest ;  they  cease  during 
sleep  ;  they  diminish  and  may  cease  under  the  influence  of  the  ^vill — an 
essential  difference  from  the  tremor  of  insular  sclerosis,  which  only  takes 
place  during  voluntary  movements.  The  head  is  at  times  affected  by  the 
movements  of  the  body  :  there  is  a  borrowed  tremor  ;  but  the  head  may  also 


1522  TEXT-BOOK  OF  MEDICINE 

be  afiected  by  spontaneous  tremors.  Amongst  the  muscles  which  partici- 
pate in  the  tremor,  I  would  especially  mention  those  of  the  jaw,  of  the 
tongue,  and  of  the  eyelids. 

Muscular  rigidity  is  an  essential  element  in  paralysis  agitans,  and  it  may 
be  the  chief  element ;  it  commences  with  transient  cramps,  and  gradually 
becomes  permanent.  As  the  result  of  this  muscular  rigidity,  the  head,  the 
trunk,  and  the  limbs  assume  special  attitudes.  The  patient's  head  is 
stretched  forward  and  fixed  in  this  position  ;  the  eye  is  fixed,  the  features 
lose  their  mobility,  and  the  physiognomy  has  a  dull  look. 

In  the  erect  position  the  trunk  is  bent ;  the  elbows  are  slightly  separated 
from  the  body  ;  the  hands  rest  on  the  waist,  and  show  tremors  ;  the  legs  are 
slightly  bent  on  the  thighs  ;  the  movements  are  slow  and  occur  together, 
the  patient  looking  as  though  he  were  soldered  together.  When  the  patient 
commences  to  walk,  he  starts  with  his  head  and  his  trunk  forward,  taking 
small  steps  and  hopping,  as  though  he  were  running  after  his  centre  of 
gravity  (Trousseau),  and  he  quickens  his  pace,  as  if  he  were  moved  by  some 
irresistible  impulse.  Certain  patients,  impelled  by  a  backward  movement 
(retropulsion),  would  fall  down  if  they  were  not  prevented. 

At  a  later  period  the  muscular  rigidity  causes  adduction  of  the  thighs, 
but  we  observe  neither  the  true  contracture  nor  the  epileptoid  tremor  of 
lateral  sclerosis.  The  rigidity  of  the  muscles  may  in  the  long  run  cause 
deformity  of  the  hands,  analogous  to  those  of  chronic  rheumatism,  but  with- 
out the  bony  swellings,  and  also  without  the  characteristic  deformity  of  the 
thumb,  which  in  Parkinson's  disease  presents  both  in  front  and  behind  a 
flattening,  due  to  its  permanent  apphcation  to  the  index-finger, 

Besides  the  above  symptoms,  the  patient  experiences  painful  cramps, 
and  has  to  change  his  position  constantly ;  he  complains  of  a  sensation  of 
excessive  heat.  In  some  cases  the  tremor  is  absent,  and  the  muscular 
rigidity  constitutes  the  chief  symptom  of  the  disease.  At  times  symmetrical 
spontaneous  ecchymoses,  probably  of  myelopathic  origin,  are  noticed 
(Carriere). 

The  disease  makes  incessant  progress,  and  ends  in  a  kind  of  paresis, 
which  has  been  called  the  paralytic  period,  although  there  is  no  paralysis, 
in  the  true  sense  of  the  word,  and  the  tremor  disappears  in  proportion  as  the 
muscular  weakness  increases.  This  incomplete  and  disseminated  paralysis 
has  been  variously  interpreted  :  Charcot  thinks  that  it  is  a  question  of 
muscular  rigidity  rather  than  a  true  weakness  of  the  muscles ;  there  are, 
however,  cases  in  which  the  paresis  is  evident.  Trousseau  admits  that  the 
paralysis  is  due  to  the  continual  loss  of  nervous  stimulus  in  the  muscles,  which 
no  longer  store  the  force  necessary  to  produce  true  contractions. 

The  terminal  period  of  the  disease  supervenes  after  ten,  twenty,  or 
thirty  years.     This  cachectic  period  is  characterized  by  disorders  of  nutrition, 


NEUROSES  1523 

and  by  psychic  troubles.  The  patient  loses  fiosli  and  falls  into  marasmus, 
with  anasarca,  diarrluea,  incontineuce  of  urine,  and  weakenin^^  of  the  intel- 
lectual faculties.  Prior  to  this  period  death  is  often  broiij^ht  about  by  some 
intercurrent  disease  (pneumonia). 

Diagnosis  yEtiolagy.  -The  co-ordinated  tremor  of  tlie  hands  in  para- 
lysis a<;itans  in  no  way  resembles  the  short  and  isochronic  oscillations  of  the 
so-called  senile  tremor.  It  also  differs  from  the  toxic  tremors  (alcohol, 
mercury,  lead),  and  from  the  tremor  of  insular  sclerosis,  which  appears  only 
on  the  occasion  of  voluntary  movement.  Finally,  in  no  other  disease  do  we 
find  the  special  attitudes  of  the  face  and  trunk  which  characterize  paralysis 
agitans.  There  are  defaced  cases  in  which  the  tremor  is  slight,  and  the 
diagnosis  is  made  by  means  of  the  rigidity  of  the  muscles  and  the  special 
attitude  of  the  patients.  Paralysis  agitans  is  rare  before  the  age  of  forty. 
Its  causes  are  most  frequently  unknown  :  great  emotions,  terror,  cold,  and 
traumatism  of  a  nerve  have  at  times  caused  it ;  heredity  has  played  a  part  in 
some  cases. 

Pathological  Anatomy. — The  lesion  of  paralysis  agitans  has  still  to  be 
found,  and  the  disease  at  present  deserves  to  be  placed  amongst  the 
neuroses,  although  various  changes  have  been  noted,  such  as  :  diffuse  sclerosis 
in  the  bulb,  the  pons,  and  the  lateral  columns  of  the  spinal  cord ;  obliteration 
of  the  central  canal  of  the  spinal  cord ;  fragility  of  the  protoplasm  of  the 
cells  in  the  posterior  cornua  (Ballet) ;  and  lesions  of  the  peduncle,  or  of  the 
suboptic  region. 

XI.  SYDENHAM'S  CHOREA— ST.  VITUS'S  DANCE. 

Description. — Chorea  (Bouteille),  which  has  been  called  by  Sydenham 
St.  Vitus's  dance  (xopela,  dance),  is  a  disease  especially  frequent  at  an  early 
age,  and  more  common  in  the  female  sex.  This  disease  has  derived  its  name 
from  the  remarkable  intervention  which  St.  Vitus  seemed  to  have  in  con- 
juring certain  epidemic  affections  of  the  Middle  Ages — affections  which  were 
evidently  hysterical,  and  characterized,  among  other  symptoms,  by  frenzied 
dancing. 

Chorea  may  commence  suddenly  as  the  result  of  a  deep  emotion,  but  it  is 
more  often  announced  by  precursory  signs,  such  as  changes  of  character, 
symptoms  of  spinal  irritation,  pains  in  the  limbs,  and  continual  restlessness  ; 
the  subject  becomes  capricious,  impressionable,  forgetful,  and  inattentive. 
At  times  motor  troubles  open  the  scene,  the  voluntary  movements  being 
affected  before  the  involuntary  movements.  The  child  is  scolded  because 
he  has  dropped  his  food  or  spilt  his  milk.  He  is  scolded  because  he  has 
broken  a  certain  object,  and  it  is  not  seen  that  this  awkwardness,  for  which 
he  is  not  responsible,  must  be  ascribed  to  the  want  of  co-ordination  of  the 


1524  TEXT-BOOK  OF  MEDICINE 

voluntary  movements  which  so  often  precedes  confirmed  chorea  (Jaccoud). 
The  choreic  movements  commence  in  the  face  with  grimaces,  in  the  arm,  or 
in  the  hand.  At  the  same  time,  involuntary  jerks  in  the  shoulders,  neck, 
and  face  supervene,  and  the  patient  tries  to  hide  these  jerks  by  various  volun- 
tary movements.  The  choreic  movements  soon  increase  in  intensity,  and 
become  general,  afiecting  more  especially  the  left  side. 

In  the  choreic  patient  the  muscular  system  shows  arrhythmical  move- 
ments, quite  different  from  the  rhythmical  movements  of  hysterical  chorea, 
and  having  nothing  in  common  with  the  short  oscillatory  tremors  of 
paralysis  agitans.  The  choreic  patient  rises  suddenly,  stumbles,  and 
sometimes  falls  ;  the  gait  is  strange  and  hopping,  because  he  throws  out 
his  legs  in  different  directions.  He  finds  a  difficulty  in  grasping  an  object, 
because  the  arms  execute  the  most  varied  movements  of  flexion,  extension, 
rotation,  etc.,  without  order,  and  one  after  the  other.  There  are  incessant 
contortions  of  the  trunk  and  of  the  head.  The  muscles  of  the  face  work  in 
a  thousand  different  ways  :  the  forehead  is  wrinkled  and  unwrinlded  ;  the 
eyebrows  are  drawn  and  separated  ;  the  eyes  turn  in  their  sockets ;  the 
tongue  is  suddenly  protruded  from  the  mouth,  or  smacks  against  the  palate  ; 
the  lips  are  pulled  in  every  direction,  so  that  the  subject  shows  almost  at 
the  same  instant  "  the  contradictory  expressions  of  joy,  grief,  or  anger  " 
(Simon).  The  muscles  of  the  tongue,  of  the  larynx,  and  of  the  pharynx 
participate  in  the  want  of  muscular  co-ordination  ;  the  result  is  a  kind  of 
stuttering  and  barking.  Mastication  and  deglutition  are  difficult,  and  the 
speech  is  jerky.  The  restlessness  is  incessant,  whether  the  patient  is  seated 
or  is  lying  down,  whether  he  wish  to  perform  some  movement  or  not.  It  is 
a  case  of  muscular  madness  (BouUlaud),  and,  notwithstanding  these  con- 
tinual movements,  the  patient  is  but  little  fatigued. 

Every  voluntary  movement  exaggerates  the  chorea,  and  yet  the  object 
is  always  gained  ;  thus  the  patient  at  last  succeeds  in  lifting  a  glass  of  water 
to  his  mouth,  but  it  is  only  after  "  a  thousand  gestures  and  a  thousand 
contortions  "  (Sydenham),  which  bear  no  relation  to  the  object  in  view. 
When  the  chorea  is  violent,  sleep  is  impossible.  When  it  is  of  moderate 
severity,  the  restlessness  ceases  during  sleep,  provided  the  patient  does  not 
dream  (Marshall  Hall). 

The  muscular  force  diminishes  during  the  disease,  and  reappears  imme- 
diately. In  some  cases  the  paretic  or  paraljrfcic  troubles  predominate,  the 
choreic  movements  being  of  minor  importance,  and  passing  unnoticed  in 
the  absence  of  a  careful  examination.  This  variety  has  received  the  name 
of  chorea  mollis.  The  paresis  may  be  limited  to  an  arm  or  a  leg,  or  may 
become  general.  It  may  invade  the  muscles  of  the  upper  and  lower  limbs, 
of  the  neck,  of  mastication,  of  deglutition,  and  of  phonation.  The  patient 
lies  motionless  in  bed,  incapable  of  making  the  slightest  movement.     The 


NEUR08KS  1525 

tcii<l()ii  n'll(>xi^s  art>  irciu'rally  |tr<'S('rv('(l  ;  llici'c  is  nriihcr  nnisciilar  atrophy 
nor  loss  of  sensation.  Cliorea  mollis  may  rocovcr  directly,  or  may  end  in 
ordinary  eliorea.  Cliorea  is  sometimes  accompanied  by  anesthesia  or 
hypersesthesia  ;  hemiansesthesia  is  frequent  in  hemichorea,  symptomatic  of 
a  cerebral  lesion.  In  women  chorea  is  often  associatetl  with  chloro-anseraia 
and  dyspeptic  troubles  (gastralgia,  constipation). 

Psychical  disorders  are  frequent.  In  a  general  way  it  may  be  said  that 
the  intellectual  faculties  are  more  or  less  aflecited  in  most  patients.  The 
mental  condition  in  chorea  has  been  very  carefully  studied  by  many  writers 
(Trousseau,  Marce,  Ball).  Raymond  and  Joffroy  have  reviewed  all  its 
phases.  In  the  choreic  patient  the  psychic  troubles  vary  from  the  slightest 
symptoms  to  the  most  pronounced  mental  disorders.  In  children  the 
character  becomes  changed  several  weeks  prior  to  the  appearance  of  the 
chorea.  These  children  become  irascible,  wilful,  disobedient,  lazy,  taciturn, 
or  emotional,  A  child  who  was  studious  and  diligent  becomes  absent- 
minded,  and  falls  to  the  lowest  place  in  his  class.  Another  child  is  moved 
by  a  trifle,  and  cries  without  a  motive.  A  child  who  was  fond  of  his  family 
becomes  indifferent  to  all  around  him.  One  child  loses  his  memory,  and 
no  longer  remembers  his  lessons  ;  another  is  restless  and  excited  :  his  sleep 
is  disturbed  by  dreams  and  nightmare.  The  face  may  have  a  dull  look, 
the  eye  groAvs  haggard,  and  the  intellectual  faculties  become  weak.  Some 
choreic  patients  have  speech  troubles,  due  to  chorea,  properly  so  called 
(stuttering,  want  of  co-ordmation  between  the  tongue  and  the  lips) ;  others 
suffer  from  a  sort  of  mutism  due  to  mental  idleness. 

Marce  has  well  described  this  intellectual  condition  in  choreic  patients  : 
"  In  most  choreic  patients  we  meet  with  that  nervous  instability  wliich 
accompanies  all  the  neuroses.  The  subjects  are  impressionable  ;  their  sleep 
is  light ;  they  are  troubled  with  vertigo,  fits  of  suffocation,  and  other 
hysteriform  symptoms.  .  .  .  We  may  observe,  especially  in  children, 
sometimes  an  unusual  gaiety  or  a  silly  laugh,  brought  on  by  the  most  futUe 
causes  ;  sometimes  sadness,  tendency  to  cry,  or  else  alternate  excitation  and 
depression.  At  the  same  time  the  character  is  changed,  and  the  most  docile 
children  become  irascible,  impatient,  and  wrangling ;  they  lie  about  every- 
thing, and  strike  those  who  approach  them.  Adults  suffer  from  these 
changes,  but  in  a  less  degree  ;  some  become  extravagant,  strange  in  their 
mamier,  and  intolerant  of  any  contradiction."  We  shall  see  in  the  next 
section,  referring  to  fatal  chorea,  the  importance  of  the  mental  condition  of 
choreic  patients. 

Duration — Complications. — Chorea  in  youth  recovers  after  an  average 

duration  of  two  to  three  months  ;  it  often  leaves  tics  behind,  and  it  is  subject 

to  recurrences,  which  break  out  on  the  occasion  of  emotion,  at  the  approach 

of  puberty,  or  in  pregnancy.      An  intercurrent  febrile  disease  (pneumonia, 

II.  97 


1526  TEXT-BOOK  OF  MEDICINE 

eruptive  fever)  may  modify  or  arrest  tlie  chorea  {febris  accedens  spasmos 
solvit). 

St.  Vitus' s  dance  has  its  complications.  Some  patients  suffer  from  such 
severe  movements  that  they  are  compelled  to  keep  their  bed,  and  in  their 
incessant  movements  they  literally  wear  away  their  skin.  The  result  is 
excoriations,  ulcerations,  sores,  and  abscesses.  Others  suffer  from  terrible 
insomnia,  from  nightmare,  from  hallucinations,  accompanied  by  delirium, 
and  from  attacks  of  acute  mania,  which  may  cause  death  in  a  few  days. 

The  cardiac  complications,  and  especially  endocarditis,  will  be  discussed 
under  the  .etiology. 

Chronic  chorea  is  especially  met  with  in  adults  and  old  persons ;  the 
motor  troubles  are  those  of  ordinary  chorea,  but  they  are,  however,  slower, 
less  extensive,  and  more  subordinated  to  the  influence  of  the  will.  Chronic 
chorea  has  a  slow  and  progressive  course,  does  not  recover,  and  it  is  often 
accompanied  by  mental  decay.  Nervous  heredity  is  the  most  common 
cause  of  chronic  chorea.  It  must  not  be  confounded  with  symptomatic 
chorea,  with  the  convulsive  tics,  or  with  double  athetosis.  Here,  as  in 
acute  chorea,  pathological  anatomy  is  stiU  silent. 

iEtioIogy. — St.  Vitus's  dance  is  especially  a  disease  of  early  age,  and  is 
more  common  in  the  feminine  sex.  It  supervenes  at  the  period  of  dentition, 
during  the  course  of  second  infancy,  and  at  puberty ;  it  has,  nevertheless, 
been  observed  in  old  people.  Chorea  in  the  aged  presents  some  special 
characteristics.  The  onset  is  fairly  sudden  ;  it  leaves  the  intellectual  faculties 
intact;  but  it  persists  in  the  condition  of  infirmity,  and  does  not  recover 
like  chorea  ia  early  age.  Heredity  has  a  manifest  influence  on  the  develop- 
ment of  chorea.  Epileptic  or  hysterical  parents  beget  choreic  children. 
This  transformation  of  neuroses  by  heredity  is  seen  every  day  (Trousseau). 
The  most  common  determiuiag  causes  are  emotions,  fright,  anger,  ansemia, 
pregnancy,  imitation,  and  rheumatism.  Imitation,  which  is  frequent  in 
children's  hospitals,  accounts  for  epidemics  of  chorea. 

The  relations  between  chorea  and  rheumatism  must  detain  us  longer. 
These  relations  were  clearly  established  by  Botrel  ia  1850.  According  to 
See,  the  rheumatic  diathesis  causes  chorea,  in  the  same  manner  as  it  causes 
the  articular  pains  or  the  endocarditis.  The  chorea  may  directly  attack  the 
heart  without  the  patient  showing  the  phase  of  articular  pains.  In  other 
words,  chorea,  endocarditis,  and  articular  rheumatism  are  manifestations  of 
the  rheumatic  diathesis.  In  a  lecture  on  St.  Vitus's  dance.  Trousseau 
reports  a  series  of  cases,  showing  the  association  of  rheumatism,  chorea,  and 
endocarditis.  "  In  many  circumstances,"  says  he,  "  I  have  been  able  to 
predict  that  St.  Vitus's  dance  would  affect  children  whom  I  attended  for 
rheumatism.  Furthermore,  I  have  been  able  to  predict  conversely  that 
children  who  were  brought  to  me  with   St.  Vitus's  dance  would  sooner  or 


NKl'ROSKS  1517 

liitor  have  rheiunatisrn.  You  will,  however,  rarely  see  chorea  pnM-erliii;^ 
rlieuinatisiii,  whilst  it  often  follows  it,  and  that  hi  the  proportion  of  a  third 
of  the  cases." 

Broadhent  has  opposed  another  theory  to  the  preceding  •;onclusion.s. 
He  holds  that  the  relations  of  chorea  and  of  the  uflections  of  the  heart 
follow  quite  a  different  course.  Rlieumatic  endocarditis  is  the  first,  as 
far  as  date  is  concerned  ;  this  endocarditis  gives  rise  to  capillary  emboli, 
which  lodge  in  the  brain  and  cause  chorea.  This  theory  cannot  be 
accepted,  because  in  most  cases  chorea  appears  without  previous  endo- 
carditis. 

According  to  some  writers,  rheumatism  does  not  play  in  chorea  the 
predominant  part  which  has  been  attributed  to  it.  In  many  choreic 
patients  the  rheumatic  diathesis  is  absent,  and  besides,  whatever  may  be 
the  causes  contributing  to  the  development  of  the  chorea,  it  is  especially 
a  cerebro-spinal  neurosis  of  growth,  having  this  feature  in  common  with 
chlorosis,  which  also  appears  in  most  cases  at  the  time  of  puberty  (Joffroy). 
Marie  is  of  opinion  that  chorea  is  most  intimately  allied  with  hysteria. 
Marfan  replies  to  this  statement :  "I  have  attended  a  large  number  of 
children,  and  I  have  never  met  with  hysteria,  or  with  a  single  stigma  of 
hysteria."  According  to  Marfan,  chorea  almost  always  follows  some  other 
disease.  It  is  generally  preceded  by  an  acute  infectious  disease  :  typhoid 
fever,  measles,  influenza,  mumps,  or  more  often  by  rheumatism. 

The  question  may,  I  think,  be  thus  stated :  It  is  undeniable  that  the 
association  of  chorea  with  rheumatism,  with  or  without  endocarditis,  is  VDry 
common,  but  I  would  point  out  that  in  this  association  we  are  dealing 
especially  with  rheumatism  in  children  or  in  youths.  This  clause  seems  to 
me  to  be  important.  I  do  not  believe  that  an  adult  attacked  by  rheumatism 
is  on  that  account  a  candidate  for  chorea.  He  is  suffering  from  endo- 
carditis, but  not  from  chorea.  I  have  attended  many  patients  of  twenty, 
thirty,  or  forty  years  of  age  for  acute  articular  rheumatism,  and  I  have 
scarcely  ever  seen  the  rheumatism  followed  by  chorea.  Nevertheless,  some 
had  had  chorea  in  their  infancy.  In  short,  the  choreigenic  rheumatism  is 
the  rheimiatism  of  childhood.  When  I  see  a  child  with  articular  rheumatism,  I 
think  of  the  chorea  which  may  come  later.  This  idea  does  not  occur  to  me  in 
the  case  of  an  adult. 

The  cardiac  compUcations  of  chorea  consist  in  mitral  and  in  aortic  endo- 
carditis ;  the  endocarditis  is  often  vegetative.  An  attack  of  articular 
rheumatism  is  not  the  indispensable  intermediary  between  chorea  and  endo- 
carditis ;  we  meet  with  choreic  patients  who  have  never  had  rheumatism, 
chorea  alone  having  brought  on  the  endocarditis.  It  is,  therefore,  necessary 
to  auscultate  the  chest  in  patients  with  chorea,  so  that  we  may  not  miss 
any  cardiac  complications. 

97-2 


1528  TEXT-BOOK  OF  MEDICINE 

Pregnancy  has  a  marked  influence  on  the  development  of  chorea 
{chorea  gravidarum),  but  some  determining  cause,  such  as  fright,  emotion, 
imitation  or  traumatism,  is  frequently  present  as  well.  The  disease  makes  its 
appearance  during  the  first  four  months  of  gestation,  though  it  may  not 
appear  until  lactation,  and  it  is  not  rare  for  it  to  reappear  at  each  subsequent 
pregnancy.  Primiparse  are  particularly  predisposed  to  it.  Chorea  generally 
disappears  after  delivery  ;  nevertheless,  the  prognosis  in  a  pregnant  woman 
with  chorea  must  be  reserved,  in  view  of  the  possibihty  of  a  miscarriage  or 
of  a  premature  birth.  We  must  also  remember  that  mental  troubles  are 
frequent. 

Diagnosis. — Chorea  must  be  distinguished  from  sjnnptomatic  hemi- 
chorea.  This  hemichorea,  which  is  generally  associated  with  hemiplegia  and 
hemiansesthesia,  appears  to  result  from  a  lesion  in  the  foot  of  the  corona 
radiata,  close  to  the  region  where  a  lesion  produces  hemiansesthesia. 

Athetosis  (Hammond)  is  characterized  by  continuous  movement  of  the 
fingers  and  the  toes,  and  by  the  impossibility  of  keeping  them  at  rest ;  it 
is  a  variety  of  post-hemiplegic  hemichorea. 

Hysterical  chorea  must  claim  our  attention  for  a  moment,  because  the 
association  of  chorea  and  hysteria  may  take  place  in  various  ways.  Some- 
times a  patient  with  ordinary  chorea  is  clearly  hysterical ;  at  other  times 
the  hysteria  is  less  manifest,  but  undeniable  stigmata  are  found,  such  as 
painful  hysterogenous  points,  constriction  of  the  field  of  vision,  and  hemi- 
ansesthesia (Marie).  In  these  various  cases  the  morbid  association  takes 
place  between  hysteria  and  ordinary  chorea,  and  the  patient  is  attacked  by 
arrhythmic  chorea,  with  contradictory  and  illogical  movements.  "  But  in 
opposition  to  this  variety  of  chorea,  complicated  by  hysteria,  we  must  place 
another  variety  of  hysterical  chorea  in  which  hysteria  has  the  largest  part, 
because  it  gives  to  the  choreic  movements  their  signification.  This  variety, 
also  called  hysterical  rhythmic  chorea,  is  characterized  by  systematic, 
rhythmical  movements.  One  patient  shows  movements  of  the  shoulder, 
movements  of  flexion  and  extension  of  the  trunk.  We  must  speak  of  it 
as  a  deep  and  repeated  salutation,  rendered  ridiculous  by  its  very  repetition 
and  by  its  exaggeration  "  (Charcot).  This  form  of  chorea  may  last  for 
months  and  years  ;  m  some  cases,  on  the  contrary,  it  ceases  suddenly. 

Under  the  name  of  electrical  chorea,  Dubini  has  described  an  afiection, 
characterized  by  rapid  shocks,  accompanied  by  acceleration  of  the  pulse  and 
rise  in  temperature,  and  generally  ending  in  an  attack  of  apoplexy.  "  It 
may  be  asked  whether  it  is  a  special  form  of  cerebro-spinal  typhus,  or  an 
abnormal  meningitis,  but  it  certainly  is  not  chorea  "  (Jaccoiid). 

The  name  of  electrical  chorea  has  also  been  given  to  a  rhythmical 
convulsive  neurosis,  differing  from  chorea,  and  especially  freqaent  In 
children. 


NEUROSES  1529 

Several  times  a  ininute  the  litilf  sufferer  is  seized  with  sudden  and  rapid 
rausoular  spusnis,  like  an  electrical  discharge  ;  the  head  is  suddenly  jerl<cd 
forwards  or  ba(^kwards.  In  another  patient  the  spasm  consists  in  a  suddi-n 
elevation  of  the  shoulders,  or  in  a  jerking  forward  of  an  arm.  Tartar 
emetic  sometinios  causes  the  ininiediate  disappearance  of  the  choreiform 
movements. 

Under  the  name  of  variable  chorea  (Brissaud)  a  kind  of  chorea  has  been 
described,  which  in  its  initial  period  resembles  true  chorea,  and  which  later 
becomes  modified,  and  is  accompanied  by  complex,  polymorphous  move- 
ments. After  remissions  and  sudden  recurrences,  the  movements  become 
more  rare,  more  sudden,  and  more  limited,  reappearing  almost  always  under 
the  same  form,  and  resembling  a  tic.  Variable  chorea  is  essentially  degenera- 
tive ;  it  appears  in  moat  cases  at  the  age  of  puberty. 

Chorea  must  be  distinguished  from  cramps,  tics,  and  "  systematic  loco- 
motor impulses  "  (Jaccoud),  which  have  nothing  in  common  with  true 
chorea.  Most  of  these  morbid  conditions,  chorea  saltatoria  ei  festinans 
and  chorea  rotatrix,  differ  from  true  chorea,  in  that  the  abnormal  move- 
ments are  not  continuous  ;  they  may  even  be  suspended  by  an  energetic 
effort  of  the  will.  Volition  never  suspends  the  movements  of  chorea  ;  on 
the  contrary,  it  increases  them. 

The  convulsive  condition  described  by  Friedrich  under  the  name  of 
paramyoclonus  mvltiflex  must  be  distinguished  from  Sydenham's  chorea. 
This  disease  is  characterized  by  sudden  involuntary  clonic  convulsions, 
generally  without  displacement  of  the  affected  limb.  The  convulsions  are 
repeated  at  unequal  intervals,  and  generally  affect  a  certain  number  of 
symmetrical  muscles  of  the  limbs.  The  movements  may  be  diminished  by 
an  effort  of  will.  Psychical,  secretory,  and  vaso-motor  troubles  are  gener- 
ally absent.  The  disease  may  appear  suddenly,  last  for  months  or  years, 
and  then  recover. 

Various  methods  of  treatment  have  been  praised  in  chorea.  The  ether 
spray  to  the  vertebral  column,  arsenical  preparations,  bromide  of  potassium, 
chloral,  cold  douches,  sulphur  baths,  gymnastic  exercises,  have  all  given 
some  results.  Antipyrin  gives  remarkable  results  ;  salicylate  of  soda  may 
be  given  with  it.  In  hypnotizable  subjects  suggestion  has  sometimes  cut 
short  the  attacks  of  chorea. 

The  pathological  anatomy  of  chorea  is  still  obscure,  and  side  by  side 
with  absolutely  negative  post-mortem  examinations  various  lesions  of  the 
nerve  centres  have  been  found,  but  they  have  no  pathogenic  value.  I 
shall  return  to  this  subject  in  the  following  section. 


1530  TEXT-BOOK  OF  MEDICINE 

XTI.  CHOREA  GRAVIS— CHOREIC  PSYCHOSES. 

Althougli  chorea  is  generally  a  benign  disease,  especially  in  children, 
there  are,  nevertheless,  cases  in  which  it  is  followed  by  death.  The  relative 
gravity  of  chorea  is  shown  by  the  following  statistics  :  In  158  cases  of 
Sydenham's  chorea  See  quotes  nine  deaths.  In  235  cases  in  children 
Bonnaud  quotes  only  one  death.  In  327  cases  of  chorea  in  childhood 
Triboulet  collected  eight  fatal  cases.  After  adding  up  these  various  statis- 
tical tables,  we  find  that  chorea  is  fatal  on  an  average  in  2  to  3  per  cent,  ot 
the  cases.  These  statistics  agree  with  Trousseau's  assertion  :  "  Although 
St.  Vitus's  dance  generally  ends  in  recovery,  this  disease  may  be  fatal. 
Rare  though  these  cases  may  be,  they  are  none  the  less  too  frequent." 

The  point,  however,  is  to  know  why  and  how  chorea  is  fatal,  because 
the  prognosis  is  especially  affected  by  the  answer.  I  shall  follow  Leudet, 
Sturges,  and  Charcot,  and  divide  the  cases  of  fatal  chorea  into  two  classes. 
The  first  group  includes  those  cases  of  chorea  in  which  death  results  from 
the  complications  ;  the  second  group  includes  those  cases  of  chorea  which 
are  fatal  per  se. 

Death  irom  Complications. — Let  me  mention  fijst  the  cardiac  lesions — 
endocarditis,  especially  vegetative  endocarditis,  which  is  a  frequent  compli- 
cation of  chorea  in  the  adult.  The  choreic  patient  may  die  during  an 
attack  of  chorea,  from  endopericarditis  or  myocarditis,  but  he  is  more 
likely  to  die  later,  when  he  is  no  longer  choreic,  the  cardiac  lesion  giving  rise 
to  cerebral  embolism,  apoplexy,  or  softening. 

Amongst  the  complications  which  may  cause  death  in  the  choreic  patient 
cerebral  haemorrhage  has  been  noticed. 

In  Buchanan-Baxter's  case — a  young  girl,  eight  years  of  age,  who  suffered  from 
recurrent  chorea,  and  who  died  fi'om  apoplexy — the  post-mortem  examination  showed 
a  cerebral  haemorrhage,  which  had  invaded  the  left  ventricle. 

Chorea  is  sometimes  fatal,  in  consequence  of  purulent  infection.  In  Thompson's 
case  a  child  nine  years  of  age  suffered  during  the  decline  of  its  chorea  from  pustules 
on  the  index-finger,  on  the  sacrum,  on  the  occiput,  with  abscesses  in  the  scapular 
region,  and  consecutive  gangrene.  At  the  post-mortem  examination  lobular  pneumonia 
was  found.  Trousseau  speaks  of  a  young  girl  who,  during  an  attack  of  chorea,  suffered 
from  a  whitlow,  with  ceUuhtis  of  the  hand,  wrist,  and  forearm.  CeUuUtis  soon  appeared 
in  the  lower  hmbs,  and  the  patient  succumbed.  Guinon  has  pubhshed  a  case  of  chorea 
which  proved  fatal  in  consequence  of  comphcations  of  a  similar  nature.  The  patient 
had  a  diffuse  celluhtis  of  the  left  arm,  purulent  infiltration  of  the  right  arm,  foci  of 
lobular  pneumonia  in  both  lungs,  and,  further,  the  patient  was  four  months  pregnant. 
Pregnancy  generally  makes  the  prognosis  of  chorea  worse  ;  the  pregnant  condition, 
when  associated  with  chorea,  aggravates  the  latter  (Jaccoud). 

We  have,  then,  in  the  first  group  a  certain  number  of  dissimilar  cases, 
which  prove  that  cardiac  lesions,  cerebral  lesions,  purulent  infection,  broncho- 
pneumonia, and  pregnancy  may,  for  various  reasons,  render  the  prognosis 
of  chorea  more  grave,  and  may  cause  death. 


NETTRORR.S  ^r>?,\ 

Death  In  Consequence  of  Chorea.  In  i,he  other  <(roii|),  liow-.-vcr 
the  (tliorea  is  fatal  per  tit'..  Tho  follnwiii;^  case  is  taken  frnm  urn;  of  mv 
clinical  lecturos  :* 

A  yoiing  man,  nineteen  years  of  age,  was  admitted  for  Sydenham's  chorea.  Th^ 
diagnosis  presented  no  difficulty.  From  the  firHt  I  was  struck  with  the  severity  of  the 
attack,  which  was  only  five  days  old.  Tlie  movements  never  Htop[H>d  day  nor  night ; 
ho  performed  thousand.-^  of  involuntary  gesticulations.  He  sat  down  on  his  bod,  as  if 
moved  by  a  spring.  Ho  turned  round  suddenly,  and  would  have  hurt  himself  had  it 
not  been  for  the  attendants  who  wore  looking  after  him.  His  head  beat  the  pillows  ; 
his  face  made  the  most  various  grimaces.  The  muscles  of  the  tongue  and  of  the 
pharynx  participated  in  these  disorderly  movements,  so  that  deglutition  was  extremely 
difficult,  and  speech  was  reduced  to  an  unintelligible  mumbling.  The  skin  over  the 
elbows,  the  hips,  and  the  heels  was  erythematous. 

As  the  patient  was  incapable  of  giving  any  information,  we  questioned  his  parents. 
They  told  us  that  the  chorea  had  commenced  five  days  previously  on  the  left  side 
of  the  body,  and  had  speedily  become  general.  They  also  told  us  (and  this  is  of  the 
utmost  importance)  that  about  ten  days  prior  to  the  appearance  of  the  chorea  their 
son  had  shown  some  intellectual  disorder.  He  commenced  to  make  incoherent  speeches, 
talking  to  himself,  rambling  in  his  speech,  and  showing  extreme  irritation.  He  suddenly 
broke  the  thread  of  his  conversation,  and  turned  to  another  subject.  He  complained 
bitterly  of  imaginary  wrongs.  Several  times  he  was  seized  with  hallucinations  of  sight 
and  hearing.  He  came  home  one  day  looking  very  worried,  and  saying  that  he  had 
just  seen  his  father  fighting  with  several  strange  men.  As  he  was  telUng  his  tale,  his 
father  arrived,  and  he  had  the  greatest  difficulty  in  convincing  the  boy  that  the  fight 
existed  only  in  his  imagination.  This  mental  condition  lasted  four  or  five  days,  and 
then  gave  place  to  stupor  and  to  profound  melanchoUa.  The  chorea  then  made  its 
.appearance.  Whilst  in  this  state  the  patient  was  admitted.  He  had  a  dull  look,  and 
was  incapable  of  making  any  intellectual  effort.  The  pulse  was  quick,  the  insomnia  was 
complete ;  there  was  incontinence  of  faeces.  The  urine  contained  neither  albumin  nor 
sugar.  The  patient  had  not  had  rheumatism,  and  the  heart  was  healthy.  I  gave  a 
very  bad  prognosis,  stating  that  I  feared  the  youth  would  only  Uve  a  few  days.  I  did 
not  take  this  view  because  of  the  severity  of  the  choreic  movements,  because  the  most 
violent  chorea  may  recover ;  but  it  was  suggested  to  me  by  the  association  of  the 
mental  condition  with  the  chorea,  an  association  which  is  nearly  always  of  fatal  augury. 
I  recalled  to  my  mind  a  young  girl  who  suffered  from  chorea,  associated  with  acute 
mania,  and  whom  I  had  seen  die  in  about  a  fortnight  in  Trousseau's  ward.  I  pre- 
scribed cold  douches,  wet  packs,  bromides,  and  antipyrin — treatment  which  succeeds 
well  in  cases  of  simple  chorea.  The  treatment  proved  futile.  In  a  few  days  grave 
complications  appeared :  the  temperature  rose,  the  pulse-rate  was  150,  the  heart 
was  irregular,  and,  as  it  were,  dehrious.  The  choreic  movements  were  followed 
by  a  relative  calm.  The  patient  lay  stupefied,  and  uttering  inarticulate  cries.  The 
loss  of  flesh  was  so  rapid  that  the  muscles  seemed  to  melt  away  before  oiir  eyes ;  an 
ecthymatous  eruption  appeared  on  the  face,  the  tnmk,  and  the  hmbs.  The  temperature 
rose  to  104°  F.,  and  the  patient  died  six  days  after  his  admission  into  my  ward,  and 
twenty-one  days  after  the  commencement  of  the  Ulness.  The  family  refused  a  post- 
mortem examination. 

Charcot :  A  youth  of  eighteen  had  been  suffering  for  three  weeks  with  Sydenham's 
chorea.  On  his  admission  to  the  Salpetriere  the  choreic  movements  had  reached  their 
maximum,  being  present  day  and  night  without  intermission.  The  patient,  whether 
in  bed  or  in  an  arm-chair,  was  a  prey  to  the  most  extensive  movements.     The  elbows 

*  "Un  Cas  de  Choree  mortelle"  (Cliniqw  Medicate  de  V Hotel-Dieu,  1897,  S""  le5on). 


1532  TEXT-BOOK  OF  MEDICINE 

and  the  bony  points  became  red,  in  consequence  of  the  violent  and  incessant  rubbing. 
Immediately  after  his  admission  he  created  a  scene,  saying  that  he  could  not  stand  the 
smell  in  the  ward,  and  that  he  could  not  remain  with  such  common  persons  as  his  fellow- 
patients.  Next  day  he  complained  that  he  was  being  persecuted  by  the  nurses.  He 
said  that  they  accused  him  of  suffering  from  syphilis.  He  maintained  that  his  scrotum 
had  been  removed.  During  the  following  days  the  chorea  and  the  mental  condition 
remained  the  same.     He  had  complete  insomnia  and  involuntary  emission  of  urine. 

The  patient,  who  had  lost  much  flesh,  did  not  recognize  the  people  around  him. 
The  pulse  was  irregular,  and  the  rate  was  140  a  minute,  and  the  temperature  was 
over  104°  F.  His  hands  and  nose  became  cyanosed ;  his  face  was  expressionless. 
Subsultus  appeared,  and  death  supervened  on  the  twenty-seventh  day  of  the  disease. 
The  autopsy  only  revealed  some  scattered  adhesions  between  the  pia  mater  and  the 
cerebral  cortex.  The  results  of  the  post-mortem  examination  were,  says  Charcot, 
purely  negative.  The  complications  causing  death  were  evidently  not  due  to  an 
appreciable  organic  lesion,  and  the  comparison  made  by  Charcot  between  the  status 
epilepticus  and  the  status  choreicus  is  perfectly  justified.  Some  old  vegetations  were 
present  on  the  mitral  valve.     The  patient  had  not  suffered  from  rheumatism. 

De  Beauvais  :  A  httle  girl,  fourteen  years  of  age,  was  taken  ill  with  Sydenham's 
chorea,  and  almost  at  the  same  time  with  cerebral  disorder.  When  the  chorea  appeared, 
she  experienced  a  sudden  distaste  for  study  and  for  music,  of  which  she  was  fond.  She 
almost  lost  her  memory ;  her  character  became  capricious  and  violent  without  any 
reason.  She  struck  her  Httle  sister,  aged  eighteen  months.  She  had  gloomy  fore- 
bodings, and  on  seeing  a  hearse,  she  cried  excitedly :  "  That  is  the  carriage  which  is 
soon  going  to  take  me  away."  In  a  few  days  her  condition  became  most  grave.  The 
spasm  of  the  laryngeal  and  thoracic  muscles  brought  on  fits  of  suffocation  ;  deglutition 
was  almost  impossible.  The  patient  seemed  to  be  suffering  from  aphasia.  The  fever 
was  high  ;  the  pulse  was  120.  There  was  continual  insomnia  and  incontinence  of  urine. 
The  restlessness  became  extreme.  The  elbows  became  excoriated ;  the  ears,  the  nape 
of  the  neck,  the  sacrum,  and  the  heels  were  raw  from  the  incessant  rubbing  of  the  skin 
on  the  sheets.  During  the  next  few  days  the  fever  increased ;  the  pulse-rate  rose  to 
150.  The  patient  fell  into  a  state  of  coma,  and  died  about  twenty  days  after  the  com- 
mencement of  the  chorea. 

Mitchinson  :  A  woman,  twenty-one  years  of  age,  who  had  had  four  previous  attacks 
of  chorea  of  increasing  gravity,  was  admitted  into  hospital  for  a  severe  attack  of  chorea. 
The  temperature  was  104°  F.  The  patient  was  very  noisy  and  restless.  During  the 
next  few  days  the  insomnia  was  absolute.  The  mental  phase  became  complete ; 
delirium  set  in.  The  pulse-rate  was  144,  and  the  temperature  ran  up  to  107°  F.  The 
face  was  Hvid,  the  respiration  irregular.  The  pulse  became  almost  imperceptible 
and  the  extremities  grew  cyanosed.  The  patient  died  on  the  twelfth  day.  At  the 
post-mortem  examination  the  cerebral  lesions  were  unimportant ;  the  brain  was 
hypersemic.  Vegetations  were  found  on  the  mitral  valve.  The  patient  had  not 
had  rheumatism. 

Another  case  of  Mitchinson  refers  to  a  youth  of  sixteen  years  of  age  with  chorea 
consequent  on  an  attack  of  rheumatism.  The  mental  phase  soon  appeared.  The 
patient  became  noisy,  calhng  out  and  throwing  himself  in  every  direction.  No  treat- 
ment succeeded  in  calming  him.  The  choreic  movements  continued.  The  pulse-rate 
rose  to  130 ;  the  respiration  became  quick ;  the  temperature  reached  105°  F.  ;  and  the 
patient  died.  At  the  post-mortem  examination  cerebral  hypersemia  was  found.  There 
were  a  few  vegetations  on  the  mitral  valve. 

Donkin  and  Hebb  :  A  young  girl,  twenty  years  of  age,  was  admitted  into  the  West- 
minster Hospital  for  generaUzed  chorea.  The  patient  was  also  suffering  from  violent 
mania.  She  struck  the  attendants,  and  rushed  about  the  staircases,  uttering  pierciag 
shrieks.     The  insomnia  was  absolute;  the  delirium  continued  night  aaid  day.     She 


NRU  ROSES  1M3 

Bufferod  from  liiillinin.it ions,  tliinkiiig  that  her  mothr-r  was  di-ad,  and  tliat  sho  saw 
her  in  tho  next  ward.  L'ndor  tlio  inlluonco  of  morjihia  tho  pati(;tit  went  to  sloop  for  a 
short  time,  but  on  awakening,  it  was  imposHiltle  to  keep  hor  quiot.  She  drovo  tho  nnrwo 
out  of  the  ward,  locked  herself  in.  and  broke  tho  furniture.  She  was  at  last  over- 
come, but  only  with  mueh  difliculty.  Tho  patient  gradually  wore  herself  out.  She 
began  to  got  drowsy  ;  tho  respiration  became  halting,  and  she  dird.  Nothing  was 
discovered  at  the  post-mortem  examination. 

Powell  has  reported  two  similar  cases.  A  youth,  nineteen  years  of  ape,  was  taken  ill 
with  generalized  chorea  six  weeks  after  rheumatism.  At  tho  time  tho  chorea  was  most 
violent ;  the  pulso-ratc  was  170.  Deglutition  was  almost  impossible.  Thr*  patient, 
who  was  violent  and  suspicious,  had  delusions  of  persecution,  and  believed  that  his 
food  was  poisoned.  The  restlessness  and  delirium  gave  place  to  a  phase  of  calm.  The 
appetite  and  thirst  were  so  excessive  that  the  patient  gained  22  pounds  in  less  than  a 
fortnight.  The  disease  then  resumed  its  course.  The  choreic  and  delirious  symptoms 
reappeared,  and  would  not  yield  either  to  chloral  or  to  other  sedatives.  Tho  patient 
became  comatose,  and  died  six  weeks  after  the  onset  of  his  illness.  Hypersemia  of  the 
brain  and  of  the  meninges  was  foimd  at  the  autopsy.  A  few  vegetations  were  present 
on  the  mitral  valve. 

In  another  case  of  Powell  a  woman  of  twenty  years  of  age  had  violent  generalized 
chorea.  A  fortnight  after  the  commencement  of  the  chorea,  the  patient  showed 
symptoms  of  mental  alienation,  with  hallucinations  of  sight  and  hearing.  The 
pulse-rate  was  140 ;  there  was  nystagmus  of  both  eyes  ;  the  temperature  rose  above 
120°  P.  After  alternating  amelioration  and  aggravation,  the  patient  fell  into  a  con- 
dition of  exhaustion,  which  giadually  became  more  marked.  The  choreic  movements 
ceased  almost  completely,  and  the  mental  faculties  grew  clear.  Coma  then  set  in,  and 
the  patient  died.  The  autopsy  revealed  acute  congestion  of  the  meninges  and  of  the 
brain. 

Cook  and  Cliflford  have  reported  a  case  in  which  a  little  girl  of  nine  years  of  age  was 
taken  ill  with  hemichorea  on  the  right  side.  It  soon  became  generahzed,  and  was 
compUcated  with  delirium.  On  her  admission  into  hospital,  violent  choreic  movements 
were  present.  The  pulse  stood  at  160  pulsations  a  minute.  The  face  expressed  terror. 
During  the  following  days  the  httle  sufferer  uttered  cries,  and  passed  her  motions  and 
her  urine  under  her.  The  heart  beat  quickly,  and  the  pulse  grew  imperceptible.  The 
respiration  was  irregular  and  jerky,  and  the  patient  died  on  the  sixth  day.  The  post- 
mortem examination  showed  that  the  brain  and  the  upper  part  of  the  spinal  cord  were 
healthy.     There  were  a  few  vegetations  on  the  mitral  valve. 

Rousseau  :  A  youth,  nineteen  years  of  age,  was  taken  ill  on  the  third  day  of  an 
attack  of  chorea  with  furious  dehrium.  He  was  taken  to  Beaujon  Hospital,  where 
they  had  the  greatest  difficulty  in  putting  him  to  bed.  His  agitation  increased ;  his 
eyes  were  haggard  ;  he  talked  incessantly  ;  and  deglutition  was  most  difficult.  Hydro- 
therapy did  not  quiet  the  patient.  He  suffered  from  paroxysms,  in  which  the  choreic 
movements  and  the  maniacal  condition  became  more  severe.  He  also  had  hallucina- 
tions of  sight  and  hearing.  He  refused  his  draught,  saying  it  was  poisoned.  He  died, 
and  at  the  autopsy  no  especial  lesion  was  discovered. 

Discussion. — These  cases  give  us  an  exact  idea  of  fatal  chorea.  In 
the  first  place,  I  would  point  out  that  all  the  cases  of  fatal  chorea  which  I 
have  just  described  (cases  of  chorea  fatal  of  themselves)  refer  to  young 
people  or  to  adults.  One  single  case,  that  of  Cook  and  ClifEord,  refers  to  a 
Httle  girl  of  nine  years  of  age.  The  other  patients  were  at  least  fourteen 
years  of  age. 

It  is,  therefore,  very  rare  for  this  variety  of  chorea  to  be  fatal  before  the 


1534  TEXT-BOOK  OF  MEDICINE 

age  of  fourteen,  which,  explains  the  absence  of  fatal  cases  in  the  statistics 
referring  to  young  children.  The  gravity  of  the  disease  coincides  especially 
with  the  age  of  puberty.  Thus,  as  Charcot  has  pointed  out,  under  the  age 
of  twelve  to  fourteen  years,  although  the  choreic  convulsions  may  be  most 
severe,  a  fatal  issue  is  not  to  be  expected  as  long  as  there  is  no  rheumatic, 
cardiac,  pulmonary,  or  other  complication.  "But  after  this  a  remarkable 
change  takes  place  in  the  clinical  history  of  chorea  ;  and  we  may  then 
witness,  contrary  to  the  rule  in  the  previous  periods  of  life,  the  onset  of 
grave  symptoms,  whether  the  disease  remains  in  the  chronic  condition,  oi 
whether  it  takes  the  more  or  less  rapid  form,  and,  without  the  aid  of  any 
visceral  complication,  leads  to  a  fatal  termination  "  (Charcot). 

If  we  look  carefully  for  danger-signals,  we  shall  find  them  in  the  mental 
condition  of  the  patients.  We  have  seen  in  the  previous  chapter  that 
chorea  is  almost  always  accompanied  by  some  intellectual  troubles.  They 
are  so  frequent  that  they  may  be  considered  as  epiphenomena.  They  are 
more  or  less  lasting  and  more  or  less  marked,  but  they  do  not  afEect 
the  prognosis.  The  symptoms  which  constitute  the  mental  condition 
present  in  each  of  the  preceding  cases  are  very  different.  These  symptoms — 
hallucination  of  sight  and  of  hearing,  acute  delirium,  delusions  of  persecu- 
tion, melancholia — comprise  the  mental  troubles,  or  choreic  psychoses, 
which,  when  associated  with  chorea,  point  to  a  fatal  issue.  If  we  take  these 
cases  separately,  we  find  in  each  one  similar  cerebral  troubles. 

In  my  patient  at  the  Hotel-Dieu  the  mental  phase  appeared  a  fortnight  before  the 
choreic  phase,  with  hallucinations  of  sight  and  heariag,  incoherent  speech,  great  rest- 
lessness, stupor,  and  melancholia.  In  Charcot's  patient  the  choreic  phase  preceded  the 
mental  phase,  and  the  principal  symptoms  of  the  latter  were  maniacal  excitement, 
delusions  of  persecution,  and  melanchoha.  In  Beauvais'  patient  the  choreic  phase  and 
the  cerebral  condition  appeared  at  the  same  time.  The  principal  symptoms  of  the 
latter  were  violent  delirium  and  lipemania.  In  the  two  patients  of  Mitchinson  the 
choreic  phase  preceded  the  onset  of  delirium.  In  the  patient  of  Donkin  and  Hebb 
the  choreic  phase  was  immediately  followed  by  a  mental  phase,  characterized  by  most 
violent  delirium,  with  hallucinations  of  sight  and  hearing.  One  of  Powell's  patients 
suffered  during  the  course  of  the  chorea  from  dehritim  of  persecution.  In  the  other 
patient  the  choreic  phase  preceded  the  phase  of  mental  alienation  by  a  fortnight.  In 
Rousseau's  patient  the  choreic  phase  preceded  the  mental  phase  by  three  days.  It  was 
characterized  by  most  violent  dehrium,  with  haUucinationa  of  sight  and  of  hearing. 

I  shaU  not  attempt  to  discuss  the  pathogenesis  of  choreic  psychosis, 
because  it  is  still  a  matter  of  theory.  That  it  may  be  a  question  of  heredity, 
of  predisposed  subjects,  of  degenerates,  and  of  a  soil  being  favourable  to 
the  production  of  psychoses,  is  absolutely  true.  This,  however,  does  not 
prevent  our  seeing  cases  in  which  heredity  is  not  in  evidence,  and  the 
patient  is  not  a  degenerate,  but  yet  the  mental  condition  associated  with 
chorea  appears  in  a  most  marked  degree. 

Whenever  we  find  grave  mental  troubles  (hallucinations  of  sigi^t  and  of 


NEUROSES  l.-3'5 

hearing,  raania,  and  dt^Iiriuin)  in  n  young  adult,  especially  if  there  is  also  any 
hereditary  taint,  we  must  be  on  our  guard.  T  do  not  say  that  the  prognosis 
must  necessarily  he  fatal,  but  in  any  case  it  is  most  serious.  The  imminent 
gra\nty  of  the  prognosis  rests  on  certain  signs  which  Charcot  has  described  : 
rise  of  temperature,  cardiac  arrhythmia,  unusual  acceleratiotj  of  the  pulse, 
paralysis  of  the  sphincters,  cyanosis,  rapid  loss  of  flesh,  diminution  or 
cessation  of  the  choreic  movements,  which  are  replaced  by  subsultus  ten- 
dinum,  fictitious  improvement,  and  sudden  disappearance  of  the  delirium, 
replaced  by  stupor.  These  signs,  which  point  to  death  within  a  short  time, 
were  all  present  in  the  case  of  Charcot's  patient,  and  I  found  them  in  my 
patient. 

Such  is  the  picture  of  chorea  gravis.  The  mental  condition  dominates 
the  situation  and  regulates  the  gravity  of  the  prognosis,  and  the  patient 
dies,  according  to  Charcot's  comparison,  in  a  status  choreicus,  resembling 
the  status  epilepticus,  without  our  being  able  to  find  the  reason  of  this 
excessive  gravity  at  the  post-mortem  examination. 

Unfortimately,  treatment  is  very  unsuccessful  in  this  variety  of  chorea. 
It  would  seem  at  first  sight  that  we  might  obtain  good  results  from  chloro- 
form, administered  in  large  doses  ;  but  in  one  of  Mitchinson's  patients,  who 
took  so  much  chloroform  that  he  slept  for  nearly  forty-eight  hours,  the 
symptoms  reappeared,  and  terminated  in  death.  Another  of  Mitchinson's 
patients  was  treated  with  large  injections  of  morphia,  but  neither  the  injec- 
tions of  morphia  nor  the  inhalations  of  chloroform  which  were  also  given 
afEected  the  disease.  I  may  say  the  same  for  the  administration  of  chloral 
and  of  bromides,  which  Charcot  employed  without  result.  Hydrotherapy 
has  been  recommended.  While  a  douche  can  be  given,  baths  are  abso- 
lutely impracticable.  It  might,  perhaps,  be  rational  in  such  a  case 
to  use  the  ether  spray  along  the  vertebral  column,  to  apply  leeches  behind 
the  ears,  and  to  blister  the  scalp  ;  but  I  am  afraid  that  these  remedies  would 
have  no  more  success  than  the  others. 

Xm.  TETANY. 

Description.  —  Tetany,  described  by  Dance  under  the  name  of 
"  intermittent  tetanus,"  is  generally  announced  by  a  sensation  of  tingling 
and  of  numbness  in  the  parts  which  are  about  to  be  afiected  by  spasms. 
Rigidity  then  appears,  followed  by  painful  contraction  analogous  to  cramp. 
The  cramps  occur  in  a  constant  order,  first  affecting  the  upper  limbs.  The 
thumb  is  adducted,  the  fingers  are  pressed  against  one  another,  slightly  bent 
on  the  metacarpus,  and  the  hand  has  been  compared  with  the  hand  of  a 
beggar  asking  for  alms,  or  with  the  hand  of  the  accoucheur  which  he  is 
about  to  insert  into  the  vagina  (Trousseau).     Flexion  and  extension  of  the 


1536  TEXT-BOOK  OF  MEDICINE 

fingers  are  less  common.  In  a  case  reported  by  Herard  the  flexion  of  the 
fingers  was  so  great  that  the  nails  penetrated  the  flesh.  The  wrist  is  nearly 
always  in  the  position  of  flexion.  When  the  contraction  reaches  the  lower 
limbs,  the  toes  are  flexed  and  pressed  together,  the  heel  is  drawn  upwards, 
and  the  foot  is  strongly  arched.  The  contracted  muscles  are  painful,  and 
resist  attempts  to  alter  the  position  of  the  tetanized  parts. 

The  contraction  may  last  for  several  hours  in  the  shape  of  a  fit.  It 
disappears,  and  then  returns  during  the  day,  or  during  the  following  day, 
and  the  series  of  fits  constitutes  the  attack,  which  lasts  for  several  weeks. 
It  is  easy  to  reproduce  the  fit  artificially.  It  is  sufl&cient  "  to  exercise  a 
compression  on  the  affected  limbs,  either  along  the  nerve  trunks  or  on  the 
bloodvessels  "  (Trousseau), 

The  tetany  just  described  is  the  benign  form  of  the  disease.  It  is  some- 
times accompanied  by  anaesthesia,  paresis,  and  oedema  of  the  invaded  parts. 
It  is  generally  bilateral,  affects  the  upper  extremities  more  often  than  the 
lower  ones,  and  recovers  without  other  complications.  More  severe  forms, 
however,  occur.  The  contraction,  instead  of  remaining  limited  to  the 
extremities,  attacks  the  muscles  of  the  trunk  and  of  the  face.  It  causes 
spasms  of  the  muscles  of  the  eyes,  of  the  pharynx,  and  of  the  larynx  (spasms 
of  the  glottis),  and  it  may  attack  the  muscles  of  respiration,  causing  attacks 
of  dyspnoea  similar  to  those  of  tetanus  and  threatening  the  life  of  the 
patient. 

etiology. — The  disease  is  most  frequent  about  the  age  of  twenty,  and 
from  the  first  to  the  third  year  (Rilliet  and  Barthez).  We  find  a  primary 
form,  provoked  by  cold,  and  more  or  less  associated  with  rheumatism,  and 
a  secondary  form,  determined  by  typhoid  fever,  cholera,  dentition,  diarrhoea. 
Pregnancy  and  lactation  are  such  frequent  causes  that  the  disease  was 
called  "  rheumatic  contracture  of  wet-nurses."  Tetany  is  met  with  in 
hysteria,  and  imitation  provokes  it.  An  epidemic  form  has  been  described 
(Simon). 

Albarran  and  Caussade  are  of  opinion  that  the  same  origin  may  be 
ascribed  to  tetany  and  to  tetanus  when  it  is  consequent  on  lesions  and  on 
intestinal  troubles.  Clinically,  it  is  difficult  to  define  the  absolute  limit 
between  tetanus  and  tetany,  and  in  some  cases  doubt  has  persisted 
(Guinon,  Bouveret,  and  Devic).  Experimentally,  Albarran  and  Caussade 
have  been  able  to  provoke  convulsions  and  transitory  contractions  in  the 
hind-legs  of  a  dog  by  injecting  Nicolaiev's  bacillus  into  the  intestine  after 
having  ligatured  it.  Furthermore,  these  authors,  by  causing  acute  intestinal 
obstruction,  found  in  the  intestines  of  dogs  which  had  died  with  more  or  less 
localized  convulsions  a  drum- stick-like  bacillus,  that  differed  from  Bien- 
stock's  bacillus.  These  facts  would  seem  to  indicate  that  tetany  may  be 
due  to  Nicolaiev's  baciUus. 


NKUROSKS  ir,:;7 

XIW  OCCUPATION  NEUR08KS. 

'V\\v  iiiimodtiraic  use  of  f(!r(ain  muscles  ends  by  causing  sufli  an  irrita- 
Lilitv  in  those  muscles  that  they  j)ass  into  a  condition  of  contracture. 
Cramps  and  spasms  are  the  result.  These  spasms  are  met  with  in  many 
professions — writers  (writer's  cramp  is  the  most  common),  pianists,  cora- 
])ositors,  etc.,  are  liable  to  this  neurosis,  and  it  must  be  rcmari<cd  that  a 
special  predisposition  of  the  patient  is  also  present  in  most  instances. 

In  writers  the  cramp  appears  as  soon  as  the  individual  tries  to  write. 
It  attacks  the  flexor  and  extensor  muscles  of  the  fingers,  and  may  extend 
to  the  muscles  of  the  forearm.  Before  arriving  so  far  the  troubles  have 
been  transient  and  gradual.  The  subject  at  first  has  a  feeling  of  stillness 
and  of  numbness  in  the  fingers.  This  sensation  is  produced  after  writing 
for  some  considerable  time,  and  the  disease  gradually  declares  itself.  The 
very  idea  of  holding  a  pen  then  brings  on  the  functional  spasm,  and  if 
the  patient  learns  to  write  with  his  left  hand,  the  spasm  sometimes  appears 
in  it.     The  spasm  may  be  replaced  by  choreiform  movements. 

Duchenne  has  quoted  many  cases  of  occupation  neuroses.  In  a  tailor  the  hand 
turned  inwards  as  soon  as  ho  tried  to  make  a  few  stitches.  In  a  fencing-master  the 
sword-arm  turned  inwards  as  soon  as  he  stood  on  guard.  A  turner  could  not  work 
his  lathe  without  the  flexor  muscles  of  his  foot  becoming  contracted.  In  a  pavior  the 
sterno-cleido-mastoid  muscles  were  contracted.  In  a  country  parson  who  played  the 
serpent  the  inspiratory  muscles  on  the  right  side  became  contracted  at  each  violent 
inspiration. 

Cramps  have  been  noted  in  the  left  hand  of  violinists,  in  the  right  hand 
of  telegraph  operators  who  used  the  Morse  instrument  (Onimus) ;  in  the 
fingers  of  milkers  (Eulenberg) ;  in  the  legs  of  dancers,  etc. 

These  various  spasms  have  an  indefinite  duration,  and  are  rebellious  to 
ail  forms  of  treatment. 


CHAPTER   VII 
NEURALGIA 

I.  MIGRAINE. 

Description.  —  Migraine  is  a  disease  of  attacks.  "  Every  person  who 
suffers  from  continuous  Headache  is  therefore  exchided."  The  fits  recur 
every  week  or  every  month,  or  at  more  distant  intervals,  and  it  is  exceptional 
for  a  patient  to  have  two  fits  in  one  week.  The  attack  of  migraine  lasts 
at  least  six  hours,  and  not  more  than  forty-eight  hours. 

The  initial  or  prodromal  period  is  characterized  by  symptoms  of  depres- 
sion— inaptitude  for  work  and  loss  of  appetite  ;  or  by  symptoms  of  excita- 
tion— alacrity  and  intellectual  vivacity.  The  disease  then  pursues  its 
incubation,  and  after  a  night  of  heavy  and  prolonged  sleep  the  fit  appears. 

In  the  second  period  the  headache  appears.  There  is  at  first  a  sensation 
of  pressure,  which  is  most  severe  in  the  orbital,  supra-orbital,  or  temporal 
regions,  and  the  pain  then  makes  its  appearance.  It  becomes  diffuse, 
without  limiting  itself,  like  neuralgia,  to  the  course  of  a  nerve  trunk,  and 
without  encroaching  on  the  suborbital  region.  The  pain  of  migraine  may 
be  unbearable  (sensation  of  crushing,  of  perforation,  or  of  dislocation  of 
the  bones  of  the  skull).  It  is  rather  dull  than  lancinating,  and  is  increased 
by  walking  and  by  movement.  The  face  is  pale  or  injected  ;  the  temporal 
artery  is  hard  and  prominent,  and  beats  forcibly  on  the  side  of  the  hemi- 
crania.  The  bloodvessels  of  the  retina  are  dilated.  The  senses  become 
very  acute,  the  least  noise  or  the  least  ray  of  light  increasing  the  pains. 
Sudden  displacement  of  the  pain  during  the  attack  is  a  curious  fact,  hemi- 
crania  of  the  right  side  passing  to  the  left  side,  and  vice  versa.  From  the 
commencement  of  the  attack  the  patient  suffers  from  nausea,  which  increases 
as  the  day  wears  on.  The  fits  of  yawning,  the  attacks  of  nausea,  the  eruc- 
tations and  the  vomiting,  are  not  accompanied  by  pain  in  the  stomach  or 
by  diarrhoea.  Constipation  is  the  rule.  Vomiting  in  the  first  period  is  not 
an  index  of  recovery.  In  the  second  period  it  sometimes  shortens  the 
attack.  During  the  period  of  decline  the  headache  and  the  nausea  become 
less  severe,  but  the  sufferer  remains  in  a  condition  of  mental  torpor,  which 
only  disappears  with  sleep.     The  sufferer  is  not  cured  until  he  has  eaten. 

1538 


NKIIKAF/JIA  1539 

Ophthalmic  Migraine.  Tho  [ncdfmiinance  of  oculur  troubloK  has  led 
to  llio  desi-iiptioii  of  an  ophthalmic  form  of  mij^raiiie.  Fii  tho  simple  forms, 
eye  symptoms  of  a  nervous  character  form  tho  most  important  part  of  tho 
attack.  The  patient  experiences  a  kind  of  obnubilation,  of  monocular  or 
binocular  hcmiopia,  or  of  scintillatinfT  scotoma.  He  sees  a  sheaf  of  stars, 
balls  of  lire,  or  fortification  figures.  Frontal  headache,  nausea,  and  vomiting 
then  appear.  In  the  severe  forms  ophthalmic  migraine  is  a(;companied 
by  transient  aphasia,  and  by  numbness,  formication,  jerks,  and  paresis  of 
one  side  of  the  body.  Epileptiform  convulsions  have  been  noted.  Although 
ophthalmic  migraine  is  not  grave,  we  must  remember  that  in  some  cases  it 
has  been  the  precursor  of  locomotor  ataxy  and  of  general  paralysis  (Charcot). 

etiology — Diagnosis. — WTiether  considered  as  a  neurosis  or  as  a 
neuralgia,  migraine  is  rarely  an  isolated  disease.  It  is  almost  always 
associated  with  the  gouty  diathesis,  oi  which  it  is  only  a  manifestation.  It 
is  hereditary,  like  the  diathetic  diseases.  An  individual  who  in  his  youth 
suffers  from  migraine  will  later  be  liable  to  eczema,  asthma,  gravel,  or 
gout  (Trousseau).  Rheumatism,  chorea,  and  migraine  are  closely  related. 
Migraine  generaUy  makes  its  appearance  at  an  early  age.  If  a  person  has 
not  had  migraine  at  the  age  of  twenty-five  years,  he  is  almost  certain  to 
escape  it.  The  attacks  of  migraine  often  return  without  appreciable  cause. 
At  other  times  they  are  brought  on  by  late  hours,  digestive  disorders, 
certain  odours,  bright  lights,  menstruation,  excess  of  work,  or  change  of 
weather. 

The  anatomical  cause  of  migraine  has  been  variously  interpreted.  It 
has  been  attributed  to  excitation  (Dubois-Raymond),  or  to  paralysis  of  the 
sympathetic  nerves  (Mollendorff),  and  to  neuralgia  of  the  meningeal  branches 
of  the  trifacial  nerve. 

The  characteristics  of  migraine  are  so  clearly  defined  that  it  is  impossible 
to  confound  the  headache  of  migraine  with  any  other  headache  (headache 
due  to  cerebral  tumours,  growing  headache,  syphilitic  and  hysterical  head- 
ache, pains  of  meningitis).  Errors  of  diagnosis  are,  however,  made  for 
want  of  sufficient  attention.  Headache  is  too  readily  called  migraine  when 
it  does  not  possess  the  true  character  of  migraine.  Mistakes  are  often  made 
in  the  case  of  growing  headaches  and  of  paroxysmal  headaches,  caused  in 
children  or  m.  youths  by  late  hereditary  syphilis.  The  headache  of  ursemia 
is  often  incorrectly  called  migraine. 

The  methods  of  treatment  advised  in  migraine  are  numerous.  During 
the  attack  subcutaneous  injections  of  morphia,  antipyriu  in  solution  or  in 
cachets,  pyramidon  (5  grains),  spraying  with  ether  and  with  chloride  of 
ethyl  to  the  cilio-spinal  region,  the  application  of  electricity  to  the  forehead, 
massage,  etc.,  have  been  recommended. 

As  a  general  treatment,  hydrotherapy  and  the  bromides  constitute  the 


1540  TEXT-BOOK  OF  MEDICINE 

most  efficacious  means.  To  these  may  be  added  alkalis,  arsenic,  and  iron. 
In  certain  cases  (gouty  alternation)  tlie  salicylic  preparations  give  good 
results. 

II.  NEURALGIA  OF  THE  TRIFACIAL  NERVE- 
TIC  DOULOUREUX. 

Tlie  trifacial  nerve  emerges  from  tlie  Gasserian  ganglion,  which  is  situated 
on  the  internal  portion  of  the  anterior  surface  of  the  petrous  bone.  From 
the  ganglion  which  has  received  the  root  of  the  trifacial  nerve  three  branches 
arise — the  ophthalmic,  the  superior  maxillary,  and  the  inferior  maxillary 
nerves. 

Description. — Neuralgia  of  the  trifacial  nerve  (facial  neuralgia) 
rarely  attacks  all  three  branches  of  the  nerve  at  the  same  time.  The 
ophthalmic  branch  is  more  often  affected  than  the  superior  and  inferior 
maxillary  branches.  In  some  cases  the  neuralgia  confines  itself  to  a  single 
filament,  to  the  dental  nerve,  or  to  the  lingual  nerve. 

The  neuralgia  reveals  itseK  (1)  by  continuous  pains  ;  (2)  by  paroxysmal 
pains.  The  continuous  pains  are  not  acute.  There  is  a  kind  of 
numbness  in  the  invaded  region.  The  paroxysmal  pains  constitute  the 
attack,  which  arises  as  the  result  of  a  slight  stimulus,  and  the  subject  experi- 
ences a  series  of  painful  shocks,  which  increase  in  intensity  until  the  attack 
reaches  its  maximum.  The  painful  shocks,  which  may  be  very  acute, 
recur  at  more  or  less  close  intervals.  They  sorhetimes  run  along  a  nerve 
branch,  like  a  flash  of  lightning  ;  at  other  times  they  arise  at  various  points, 
and  rush  in  various  directions.  The  attack  may  last  for  an  hour,  or  even 
longer,  if  the  neuralgia  is  of  long  standing.  It  recurs  every  day,  or  several 
times  a  day,  and  often  at  a  fixed  hour,  with  a  periodicity  which  is  also  met 
with  in  almost  every  case  of  idiopathic  or  symptomatic  neuralgia.  Pulsa- 
tion of  the  arteries,  redness  of  the  face,  and  rise  of  temperature  often 
accompany  the  neuralgia. 

Apart  from  the  attack,  the  skin  of  the  face  preserves  a  hypereesthesia 
which  may  later  give  place  to  anaesthesia.  The  teeth,  the  lingual  and  buccal 
mucosae,  and  the  hair,  are  also  hypersesthetic.  Pressure  on  the  skin  is  par- 
ticularly painful :  (1)  at  the  exit  of  the  nerve  trunks  ;  (2)  at  the  points  where 
a  nerve  filament  leaves  a  muscle  to  enter  the  skin ;  (3)  at  the  expansion 
of  the  nerve  in  the  skin.  Those  are  VaUeix's  painful  points,  which  present 
the  same  characteristics  in  most  cases  of  peripheral  neuralgia.  To  these 
painful  points  the  apophysial  point  must  be  added  (Trousseau).  It  is 
seated  over  the  external  occipital  protuberance  and  the  second  and  third 
cervical  spines.  Such  are  the  general  characteristics  of  facial  neuralgia, 
but,  according  to  the  branches  invaded,  the  neuralgia  reveals  itself  by  the 
following  symptoms  : 


NEURALfJIA  mil 

1.  Ntur(t!(jia  of  tlie  OphfluUmic  Nerve. — The  <i|tlithiiltnic  nerve  enters 
tlio  orbit  bv  the  s{)henoidcil  Hssure,  and  hreak^  u[>  into  three  nerves  :  tho 
hichrvMial,  which  emerges  at  the  outer  side  of  the  U|»i)<!r  eyelid  (pal{)eljral 
point)  ;  tlie  frontal,  the  external  branch  of  which  leaves  the  orbit  by  the 
supra-orbital  foramen  (supra-orbital  point)  ;  the  nasal,  the  external  branch 
of  which  leaves  the  orbit  near  the  nose,  below  the  inner  canthus  of  the 
eye  (nasal  point),  and  the  internal  branch  of  which  enters  the  nasal  fossse, 
and  furnishes  a  filament,  which  traverses  the  lateral  cartilage  of  the  nose, 
and  spreads  over  the  lobule  of  the  nose  (naso-lobar  point).  Accordiiig  to 
the  anatomical  distribution  of  this  nerve,  we  see  which  are  the  regions 
invaded  by  the  neuralgia.  During  the  attack  the  eye  is  red,  injected,  and 
painful,  and  cannot  bear  the  light.  Lachrymation  is  profuse.  Chemosis, 
mydriasis,  and  transitory  amaurosis  have  been  met  with  (Notta). 

2.  Neuralgia  of  the  Superior  Maxillary  Nerve. — The  superior  maxillary 
nerve,  after  having  traversed  the  supra-orbital  canal,  emerges  through  the 
supra-orbital  foramen  (supra- orbital  point).  Amongst  the  number  of  its 
numerous  branches  are  :  the  orbital  nerve,  a  filament  of  which — the  temporo- 
malar — traverses  the  cheek-bone,  and  spreads  over  the  cheek  (malar  point) ; 
the  dental  nerves,  each  dental  root  possibly  becoming  a  centre  of  pain 
(dental  points).  The  spheno-palatine  ganglion,  which  is  connected  to  this 
branch,  perhaps  explains  the  secretion  from  the  nasal  mucosa  during  the 
attack  (Vulpian). 

3.  Neuralgia  of  the  Inferior  Maxillary  Nerve. — From  the  inferior  maxil- 
lary nerve  arise  the  branches  frequently  afiected  by  neuralgia.  These 
are  :  the  auriculo-temporal  nerve,  which  passes  through  the  parotid  gland, 
winds  round  the  neck  of  the  condyle,  and  distributes  itseK  to  the  temple 
and  the  auricle  (auriculo-temporal  point) ;  the  lingual  nerve,  which  supplies 
the  edges  of  the  tongue  (lingual  point)  ;  the  inferior  dental  nerve,  which 
supplies  the  teeth  in  the  lower  jaw  (dental  points),  and  which  makes  its 
exit  through  the  mental  foramen  (mental  point).  At  the  time  of  the  attack 
the  movements  of  the  tongue,  speech,  mastication,  and  deglutition  are 
excessively  painful,  and  the  saliva,  secreted  in  abundance  (reflex  action  of 
the  lingual  nerve  on  the  chorda  tympani),  flows  from  the  mouth. 

Trophic  Troubles. — Consequent  on  violent  or  inveterate  facial  neuralgia, 
the  nerve  being  probably  attacked  by  neuritis,  we  see  various  trophic 
troubles. 

Herpes  is  frequent  on  the  skin  and  on  the  mucosae.  It  afiects,  accord- 
ing to  circumstances,  the  lips,  the  tongue,  the  forehead,  and  the  face.  Herpes 
of  the  eye,  or  ophthalmic  zona,  has  been  specially  described.  It  may  invade 
the  eyelids,  the  conjunctiva,  and  the  cornea. 

Atrophy,  induration  (sclcrodermia),  and  hypertrophy  of  the  skin  have 
been  noted.  The  hair  and  the  beard  are  sometimes  attacked.  The  hair 
iL  98 


1542  TEXT-BOOK  OF  MEDICINE 

falls  out  and  loses  its  colour,  becoming  white  throughout  its  entire  length, 
or  only  wanting  in  pigment  in  sections,  this  alternation  coinciding  with 
the  paroxysms  of  neuralgia.  It  was  at  first  supposed  that  the  trophic 
troubles  only  existed  when  the  Gasserian  ganglion  was  involved.  This 
interpretation,  though  true  in  many  cases,  is  not  absolute,  because  similar 
troubles  may  be  produced  when  the  lesion  goes  beyond  the  ganglion  to  the 
bulbar  root  of  the  trifacial  nerve  (Duval). 

Tic  Douloureux  of  the  Face — Epileptiform  Neuralgia. — In  certain  indi- 
viduals facial  neuralgia  assumes  special  characters.  The  patient  is  suddenly 
seized  with  acute  pain  ;  he  presses  his  face  in  his  hands  or  rubs  it  \'iolently, 
hoping  thereby  to  lessen  the  pain,  and  after  a  few  seconds — a  minute  at 
the  most— the  attack  ends.  Most  frequently  at  the  moment  of  the  attack 
the  muscles  of  the  face,  especially  on  the  side  of  the  neuralgia,  show  rapid 
convulsive  movements,  which  produce  the  most  varied  grimaces,  so  that 


Fig.  76. — Beakches  of  thk  TRiGEMrN-AL  Nebvb. 
I,   Ophthalmic  branch  ;  ii,  superior  maxillary  branch ;  in,  inferior  maxiUary  branch ; 
a,  supra-orbital  point ;  6,  nasal  point ;  c,   inlra-orbital  point ;  d,  mental  point ; 
e,  auriculo-temporal  point. 

the  disease  has  been  called  tie  douloureux  of  the  face.  These  two  forms 
of  facial  neuralgia— the  one  non-convulsive,  the  other  convulsive — were 
called  epileptiform  by  Trousseau,  because  they  resembled  the  vertigo  and 
the  aura  of  epilepsy.  They  have  its  suddenness  and  its  duration.  Never- 
theless, says  Trousseau,  they  are  merely  analogous,  and  not  identical  with 
epilepsy. 

Tic  douloureux  does  not  always  establish  itself  from  the  outset,  but  is 
at  times  the  transformation  of  a  non-convulsive  facial  neuralgia.  In  certain 
patients  the  attacks  follow  one  another  almost  without  respite.  In  others 
there  is  a  longer  interval  between  the  attacks.  The  attack  is  sometimes 
produced  without  apparent  cause ;  at  other  times  it  is  produced  by  the 
most  varied  and  trifling  causes.  A  simple  scratch,  the  act  of  mastica- 
tion, the  contact  of  food  and  drink,  the  movements  undertaken  for 
the  purpose  of  speaking  or  of  expectorating,  may  bring  on  the  spasm, 
so  that  the  patient  sufiers  agony.     The  question  is  thoroughly  discussed  in 


NKURAI.dIA  I'.rj 

the  h'ft lire  pji veil  by  Troussciiu.     From  this  lecture   I   liorrow  the  following 
case  : 

"  An  old  lady,"  bhvh  Troiisscuii,  "  inrno  iitKif-r  my  earn  in  IH4'>.  She  had  U'on 
.siitTt  fillip  fruni  cpiloptiform  noiiralf^ia  of  thu  faco  for  tli«  pawt  t«n  youiu.  'I'ho  ulta<kn 
la.st<-d  from  a  few  seiondH  to  thrcti  miniitfs.  Thoy  sumotimi-a  commoncod  in  the  huIj- 
orbital  norve,  sometimes  in  tho  mental,  and  at  other  times  in  tho  supra-orbital  nervo. 
The  troublo  rapidly  spread  to  the  three  branches,  and  when  the  jtaroxysm  waa  at  it« 
height  the  museles  of  tho  face  worked  convulsively.  Tho  [)oor  woman  had  aomotimeH 
twenty  attacks  in  an  hour  ;  they  roturnod  on  the  least  movement.  She  could  not 
speak,  cough,  eat,  or  drink  without  having  a  most  severe  paroxysm.  To  moderat* 
the  pain,  she  rapidly  carried  her  hand  to  her  face,  which  she  pressed  violently,  making 
tho  skin  move  over  the  bones.  When  the  pain  was  more  acute,  she  started  up  and 
walked  about  the  room,  stamping  her.  foot  and  uttering  dull  groans.  At  times  the 
attac:k8  did  not  appear  for  a  week,  a  fortnight,  a  month,  or  even  longer.  They  then 
returned  with  renewed  vigour. 

"  Tho  most  remarkable  thing  was  that  the  pain  disappeared  completely  after  each 
paroxysm,  except  for  a  feehng  of  numbness.  I  ordered  morphia  internally,  commencing 
with  fairly  large  doses  of  3  to  5  grains  a  day,  and  being  resolved  to  increase  the  doses 
if  tho  drug  was  well  borne.  In  less  than  a  fortnight  I  was  giving  60  grains  each  day. 
The  improvement  was  great.  During  the  course  of  the  day  she  had  only  slight  shocks 
of  dull  pain  in  the  branches  of  the  trifacial  nerve.  The  digestive  functions  were  but 
httle  disturbed,  and  the  intellectual  faculties  were  in  good  condition  ;  but  the  patient 
havuit;  a  Hmited  fortune,  the  enormous  price  of  morphia  almost  ruined  her.  I  therefore 
had  recourse  to  opium.  She  began  to  suffer  as  soon  as  she  ceased  using  the  remedy.  I 
found  a  chemist  who  consented  to  sell  her  raw  opium  at  the  market-price,  and  she  was 
able  to  obtain  raw  opium,  which  she  made  up  into  15-grain  pills,  and  took  five,  ten,  or 
twenty  a  day,  as  occasion  arose. 

"  It  is  remarkable  that  these  enormous  doses  of  opium  did  not  notably  disturb  her 
digestion.  There  was  no  somnolence,  and  she  obtained  her  usual  rest  at  night.  For 
six  years  I  saw  the  patient  from  time  to  time,  and  I  was  able  to  notice  the  following 
therapeutic  effects  :  She  sometimes  had  no  attack  for  two  or  three  months.  She  then 
suspended  the  use  of  the  opium,  after  having  gradually  diminished  the  quantity  in 
proportion  as  the  pains  diminished.  The  epileptiform  neuralgia  then  returned  suddenly 
with  renewed  violence.  She  took  from  the  first  about  ^  ounce  of  raw  opium,  and 
kept  up  this  dose  until  the  attack  had  calmed  down.  The  opium,  therefore,  gave  her 
immense  rehef,  but  did  not  completely  cure  her,  and  I  repeat,  especially  since  my 
attention  has  been  especially  called  to  this  kind  of  neuralgia,  I  have  never  met  with  a 
case  that  was  curable." 

iEtiology. — Every  neuralgia  presupposes  a  change  in  a  sensory  nerve 

at  some  point  of  its  origin,  course,  or  termination.     The  change  in  the  nerve 

may  betray  itself  by  more  or  less  gross  lesions,  by  neuritis,  congestion, 

oedema,  or  abnormal  condition  of  the  blood ;  or  the  change  may  be  purely 

dynamic,  then  escaping  our  means  of  investigation.     Dynamic  troubles  are 

met  with  in  all  the  manifestations  of  the  nervous  system,  whether  we  have 

to  deal  with  the  nerve  centres  (neuroses)  or  with  the  sensory  or  motor  nerves. 

The  nervous  organ  the  functions  of  which  are  disturbed  is  evidently  in  an 

abnormal  condition,   but  this  abnormal  condition  may  reveal  itself   by 

material  lesions,  or  by  a  purely  d}Tiamic  change,  without  alteration  of 

structure  or  of  texture. 

98—2 


1544  TEXT-BOOK  OF  MEDICINE 

With  regard  to  this  subject  certain  correct  comparisons  have  been 
made.  A  Leyden  jar  charged  with  electricity  and  one  not  so  charged,  a 
piece  of  soft  iron  which  is  magnetized  and  a  piece  which  is  not  magnetized 
differ  in  their  properties,  and  yet  there  is  no  change  in  the  texture  or  in  the 
structure  of  the  anatomical  elements  ;  there  is  only  a  modification  in  the 
transmission  of  the  forces.  Analogous  comparisons  are  applicable  to  the 
disorders  of  the  nervous  system. 

Facial  neuralgia  is  often  the  result  of  an  infection  (malaria,  syphilis). 
It  is  associated  with  rheumatism  and  with  gout.  The  local  causes  act  at 
some  point  of  the  nerve  :  at  its  periphery  (trauma,  foreign  bodies,  dental 
caries,  coryza)  ;  along  its  course  (lesions  of  the  bone  and  of  the  periosteum, 
tumours,  aneurysm  of  the  internal  carotid  artery) ;  in  the  Gasserian  ganglion 
(cancer,  exostosis  of  the  petrous  bone) ;  at  the  bulbar  origin  (locomotor 
afcasy).  Cold,  a  frequent  cause  of  facial  neuralgia,  attacks  the  terminal 
expansion  of  the  nerves,  or  causes  swelling  of  the  nerve-trunk  and  its  strangu- 
lation in  the  bony  canal  of  the  petrous  bone.  Neuralgia  is  sometimes 
the  result  of  a  reflex  action  (intestinal  worms). 

Amongst  these  causes  malaria  is  frequent,  and  deserves  to  arrest  our 
attention.  The  malarial  infection  has  a  predilection  for  the  ophthalmic 
nerve.  Many  people  infected  with  malaria  one  or  two  years  previously 
are  seized,  without  warning  and  without  fever,  with  facial  neuralgia,  which 
is  really  an  attack  of  larval  malaria.  The  neuralgia  reappears  every  day 
or  every  other  day.  It  may  be  very  severe,  and  accompanied  by  intolerable 
pains,  vomiting,  prostration,  and  sweating. 

The  diagnosis  of  facial  neuralgia  is  simple.  Its  pathogenic  diagnosis 
is  important,  because  it  decides  the  treatment.  The  duration  of  the 
disease,  its  course,  and  its  gravity  are  dependent  on  the  cause.  We  see 
benign  cases  which  readily  yield  to  therapeutic  means,  and  obstinate  cases 
which  resist  aU  remedies. 

The  treatment  differs  according  to  the  cause  of  the  neuralgia.  Quinine 
is  absolutely  indicated  in  cases  of  malarial  origin.  It  must  be  given  in  large 
doses,  15  grains  in  two  doses,  repeated  every  day  for  a  week.  From  this 
period  a  longer  interval  is  allowed  between  the  doses  of  quinine.  In  the 
other  varieties  of  facial  neuralgia  we  may  employ  the  following  remedies  : 
Opium  in.  large  doses  ;  aconitine,  in  doses  of  ^  milligramme  daily,  and 
gradually  increased  to  4  to  5  milligrammes,  has  been  praised  by  Gubler, 

Subcutaneous  injections  of  morphia  diminish  the  attacks,  and  may 
be  curative.  We  may  inject  daily  a  grain  of  hydrochlorate  of  morphia,  and 
in  certam  individuals  the  toleration  is  such  that  we  may  use  enormous 
doses.  I  have  several  times  had  a  patient  suffering  from  epileptiform  facial 
neuralgia,  which  I  could  only  relieve  by  injecting  daily  from  10  to  15  grains 
of  hydrochlorate  of  morphia. 


NEURAT/JTA  If,  15 

The  ia<'lhyl  chluiidi'  sjiray  (])t'l)<»vo)  has  hfon  advisod.  Anf  ij)\Tin  mav  ho 
given  in  doses  of  30  to  60  grains  a  day.  Broinidn  of  potassium  in  large 
doses  gives  good  results.  The  application  of  oleetrieity  miLst  he  tried 
(Lacaille).  A  continuous  current  of  from  ten  to  twelve  units  is  pa8.s«;d  for 
a  few  minutes,  the  negative  pole  being  placed  at  the  exit  of  the  nerve,  and 
the  positive  pole  at  the  periphery  of  the  nerve  (Onimus).  We  mu.st  never 
forget  that  s}'^ihilis,  as  we  shall  see  in  the  next  .section,  may  in  variou-s 
wa^'s  cause  facial  neuralgia. 

Surgical  treatment  has  given  good  results.  The  first  measure  is  resection 
of  the  aflFected  branch.  If  this  is  not  sufficient,  the  Gasserian  ganglion  may 
be  removed. 


III.  SYPHILITIC  NEURALGIA  OF  THE  TRIFACIAL  NERVE. 

Let  me  first  quote  a  case  from  a  clinical  lecture  which  I  gave  on  this 
subject  :* 

A  man,  forty-one  years  of  age,  came  to  me  "  as  a  last  resource,"  being  unable  to 
bear  the  terrible  pains  which  "  had  tortured  him  for  the  last  fourteen  years."  He 
had  facial  neuralgia  of  the  right  side,  the  three  branches  of  the  trifacial  being  affected, 
but  to  an  unequal  degree.  As  regards  the  ophthalmic  nerve,  the  frontal  branch  was 
chiefly  affected,  the  lachrymal  branch  to  a  sUght  extent,  and  the  nasal  branch  hardly 
at  all.  The  orbital  and  suborbital  branches  of  the  superior  maxillary  nerve  were 
affected,  the  dental  nerves  to  a  shght  degree.  The  inferior  maxillary  nerve  was  chiefly 
affected  in  its  amiculo-temporal  and  mental  branches  ;  the  dental  branch  was  sUghtly 
involved,  and  the  hngual  branch  was  unaffected.  The  patient  was  admitted  into  my 
wards  during  an  attack.  The  pains  were  especially  severe  at  night.  During  the  day 
the  pain  was  bearable.  The  pain  at  night  prevented  any  rest,  and  led  him  to  thiok  of 
suicide. 

The  course  of  the  disease  had  been  as  follows  :  The  facial  neuralgia  had  commenced, 
without  any  apparent  cause  fourteen  years  before,  in  the  year  1884.  At  this  period  the 
patient  felt  some  pain  in  the  right  side  of  his  face.  From  the  outset  the  ophthalmic 
nerve  was  most  affected,  whilst  the  other  branches  of  the  trifacial  nerve  were  hardlj' 
involved.  From  the  commencement  of  the  disease  the  nature  of  the  attacks  had  varied 
but  httle.  The  acute  stage  of  the  attack  lasted  from  a  fortnight  to  a  month.  During 
this  period  the  pains,  which  were  paroxysmal  at  night,  were  accompanied  by  lachr}'- 
mation.  The  patient  compared  them  "  with  grinding  of  the  bones  and  tearing  of  the 
flesh."  There  was  not  in  this  case,  as  in  tic  douloiireux,  any  complete  remission,  and 
the  pain  lasted  for  hours  at  a  stretch  without  diminishing. 

After  a  period  of  suffering,  extending  over  a  fortnight  or  three  weeks,  the  patient 
experienced  relative  rehef.  The  sharp  pains  ceased,  and  sleep  returned,  but  the  region 
remained  painful,  and  slight  shooting -pains  proved  that  the  disease  was  always  ready 
to  be  awakened.  In  fact,  after  a  few  days  or  weeks  of  comparative  rest,  the  attacks 
reappeared. 

The  patient  had  consulted  physicians,  surgeons,  pharmacists,  herbalists,  and  quacks, 
begging  for  a  rehef  from  his  pains,  without  result. 

*  "  Nevi-algie  Syphilitique  du  Nerf  Trijumeau,"  (Clinique  Medicale  de  VHotd-Dieu, 
1899,  15""=  lecon). 


1546  TEXT-BOOK  OF  MEDICINE 

Feeling  tliat  an  operation  might  help,  he  went  into  a  private  hospital  under  the  care 
of  Schwartz.  The  pains  at  this  time  were  so  severe  and  so  obstinate  that  morphia  was 
given  in  increasing  doses.  The  pains  were  reUeved.  for  the  time  being,  but  if  the  doses 
of  morphia  were  insufficient,  they  reappeared.  The  result  was  that  the  patient  left 
the  hospital  a  morphomaniac,  and  continued  the  injections  of  morphia  at  home.  For 
some  time  the  facial  neuralgia  was  kept  in  check  by  injecting  large  doses  of  morphia. 
As  soon  as  the  doses  of  morphia  became  insufficient,  the  pains  reappeared. 

The  time  came,  however,  when  the  injections  of  morphia  had  to  be  abandoned,  the 
punctures  having  caused  numerous  abscesses.  In  1895 — that  is  to  say,  after  treatment 
with  morphia  for  over  two  years — he  entered  the  Saint-Louis  Hospital,  in  order  to  be 
treated  for  morphinomania.  The  morphia  was  suppressed,  but  the  facial  neuralgia 
reappeared,  and  the  patient,  on  the  advice  of  a  physician,  had  recourse  to  opium.  He 
obtained  some  rehef  by  increasing  the  doses  progressively. 

It  was  under  these  conditions  that  the  unfortunate  man  came  into  my  wards  in 
the  hope  that  I  would  advise  an  operation.  Whilst  I  was  examining  the  patient,  my 
attention  was  directed  to  the  deformity  of  his  nose  and  to  the  foetid  odour  of  his  breath. 
His  nose  had  the  appearance  of  one  deformed  by  syphihs.  The  rhinoscopic  examination 
proved  the  existence  of  tertiary  syphiUtic  rhinitis,  with  exostoses  in  both  nostrils,  and 
almost  complete  destruction  of  the  septum  and  of  the  inferior  meatus.  The  patient 
told  us  that  the  rhinitis  had  made  its  appearance  some  httle  time  after  the  facial 
neuralgia.  In  1885  he  had  symptoms  of  syphihtic  coryza — swelling  of  the  nose,  muco- 
purulent discharge,  thick  crusts,  and  foetor  of  the  breath.  The  rhinitis  did  not  recede, 
sequestra  came  out  from  the  nose,  and  the  ozsena  was  most  distressing. 

As  the  rhinitis  had  run  a  parallel  course  with  the  facial  neuralgia,  was  it  not  likely 
that  the  neuralgia  was  also  syphilitic  ?  Ahd  this  hypothesis  granted,  was  there  an 
exostosis  compressing  the  trifacial  nerve  at  its  exit  from  the  Gasserian  ganglion,  or  was 
there  a  sclero-gummatous  neuritis  ?  I  cannot  answer  this  question,  because  the 
examination  gave  no  help  in  the  matter.  The  point  was  to  decide  whether  the  neuralgia 
was  or  was  not  syphilitic. 

The  fact  that  the  facial  neuralgia  had  persisted  for  fourteen  years  without  other 
symptoms  was  no  reason  for  eliminating  the  hypothesis  of  syphilis.  I  have  quoted 
elsewhere  (Syphilis  of  the  Palate,  Syphilitic  Sciatica)  examples  in  which  syphilis  had 
been  hmited  for  ten  or  twelve  years  to  a  special  point.  An  injection  of  the  oily  solution 
of  biniodide  was  administered  daily,  and  I  permitted  the  patient  to  continue  for  the 
time  being  the  daily  dose  of  ©pium  (3  grains)  to  which  he  had  been  accustomed  for  a 
long  time. 

After  the  eighth  injection  the  rehef  was  so  marked  that  he  abandoned  the  opium. 
At  the  same  time  the  rhinitis  improved.  The  ozasna  diminished.  After  fourteen 
injections  the  patient  slept  well,  ate  with  a  good  appetite,  and  had  put  on  flesh.  The 
nasal  syphilis  improved,  nasal  respiration  was  almost  free,  the  muco-purulent  secretion 
was  slight,  and  the  ozsena  had  disappeared.  Examination  of  the  nose  showed  that  the 
lesions  were  rapidly  healing. 

After  the  eighteenth  injection  the  patient  left  the  hospital  on  urgent  business.  He 
returned  twelve  days  later,  still  quite  satisfied  with  his  condition,  the  pains  being  slight 
and  of  short  duration.  I  gave  five  injections,  and  he  left  the  hospital  cured.  He  was 
now  able  to  work  from  three  o'clock  in  the  morning  till  six  o'clock  in  the  evening.  To 
sum  up :  By  means  of  twenty-six  injections  of  biniodide  of  mercury  we  were  able  to 
cure  one  of  the  most  painful  diseases  which  it  is  possible  to  see — a  disease  which  had 
lasted  for  fourteen  years,  and  which  had  resisted  all  remedies.  Mercury  alone,  without 
the  addition  of  iodide  of  potassium,  brought  about  this  result. 

I  had  a  woman  in  the  Hotel-Dieu  under  my  care  for  severe  syphilitic 
neuralgia  of  the  trifacial  nerve  and  syphilitic  retinitis.    Injections  of  mer- 


NEURALGIA  1^47 

cwry  ciirfd  tli«^  nfMiral'^Ia,  mid  at  the  Hanift  time  oonsidf^rahly  r<^lievpil  the 
retinitis. 

Although  avphilitic  neuralgia  of  the  trifacial  m^rvf  has  not  been  tin.' 
object  of  a  monograph,  it  has  still  received  attention.  Fournier  ("  Traite 
de  la  Syphilis  ")  devotes  a  cha]>ter  to  syphilitic  neuralgia.  He  looks  upon 
secondary'  facial  neuralgia  as  fairly  common.  ''  This  secondary'  facial 
neuralgia,"  says  he,  "  is  peculiar,  in  that  it  does  not  affect,  save  in  excep- 
tional cases,  the  inferior  branch  of  the  trifacial  nerve  and  the  middle  branch 
in  rare  cases  ;  while  the  supra-orbital  branches  are  often  attacked.  Supra- 
orbital neuralgia  certainly  occupies  the  front  rank  as  regards  frequency  of 
appearance."  Fournier,  with  regard  to  this  subject,  quotes  the  following 
case  : 

"  I  was  called  some  years  ago  to  see  a  young  married  woman  who  had  siifferr-d  for 
four  or  five  months  from  acute  facial  neuralgia.  All  imaginable  treatment  (sulphate 
of  quinine,  opium,  belladonna,  chloral,  bromide,  hypodermic  injections,  bhsters,  etc.) 
had  been  tried,  and  had  httle  or  no  result.  This  want  of  success  with  the  most  rational 
and  most  energetic  remedies  in  a  young  woman  whose  general  health  was  good,  and 
who  had  so  far  been  free  from  any  nervous  affection,  seemed  to  me  somewhat  sus- 
picious. 

"  I  sought  for  the  cause  of  the  neuralgia  for  a  long  time,  and  I  did  not  find  it.  1  then 
examined  the  patient  for  any  sign  of  sypliihs,  and  discovered  nothing  suspicious.  I 
questioned  her  in  this  respect,  and  only  obtained  a  formal  denial.  As  the  colleagues 
who  had  preceded  me  had  left  me  nothing  to  do  if  it  were  a  case  of  ordinary  neuralgia, 
I  decided  to  prescribe  mercury.  The  result  was  dramatic.  After  two  days  the 
patient,  who  had  not  slept  for  several  months,  was  able  to  rest  a  little.  A  week 
later  she  was  cured.  I  had,  therefore,  hit  the  nail  on  the  head."  The  patient  subse- 
quentlj-  confessed  that  she  had  had  syphihs. 


IV.  CERVICO-OCCIPITAL  AND  CERVICO-BRACHIAL 
NEURALGIA. 

Description.  —  1.  Cervico  -  occipital  neuralgia  affects  the  posterior 
branches  of  the  first  four  cervical  nerves  (cer^-ical  plexus),  and  especially 
the  suboccipital  nerve,  which  arises  from  the  second  cervical  pair.  The 
pains  are  analogous  to  those  of  facial  neuralgia,  being  continuous  or  par- 
oxysmal. The  pains  are  seated  in  the  occipital  and  in  the  posterior  cervical 
regions.  Certain  painful  points  are  found.  The  most  frequent  one  is  the 
occipital  point,  at  the  exit  of  the  occipital  nerve,  about  midway  between 
the  mastoid  process  and  the  first  cervical  vertebra.  Apart  from  the  usual 
causes  of  neuralgia  (cold  must  be  placed  in  the  front  rank),  there  are  local 
causes,  such  as  Pott's  disease,  periostitis,  and  caries  of  the  cervical  vertebrae, 
h}'pertTophic  cervical  pachymeningitis,  adenitis,  and  cancer  of  the  spine. 
These  lesions  give  rise  to  neuralgia,  which  is  almost  always  bilateral,  thus 
differing  from  primary  cervico-occipital  neuralgia,  which  is  unilateral. 


1548  TEXT-BOOK  OF  MEDICtN'E 

2.  Cerrico-braciial  neuralgia  attacks  most  of  the  sensory  branclics  of 
the  brachial  plexns,  and  especially  the  ulnar  nerve.  Neuralgia  of  the 
circumflex  nerve  is  sometimes  complicated  by  paresis  and  atrophy  of  the 
deltoid  muscle.  In  neuralgia  of  the  ulnar  nerve  several  painful  points  are 
found  :  the  epitrochlear  point,  where  the  nerve  lies  in  the  epitrochlear 
groove  ;  and  the  ulno-carpal  point,  where  the  nerve  grooves  the  carpus 
before  reaching  the  palm  of  the  hand.  Hypertrophy  of  the  heart  has  been 
met  with  in  cases  of  this  kind  of  neuralgia  (Potain). 

Injury  has  a  large  share  in  the  setiology  of  this  form  of  neuralgia  (dis- 
locations, fractures,  burns).  I  must  also  mention  syphihs.  I  have  seen  a 
case  of  ulnar  neuralgia  of  syphilitic  origin,  where  the  intense  pain  ceased 
after  a  few  days  of  treatment.  The  treatment  of  these  neuralgias  is  analo- 
gous with  that  of  facial  neuralgia.  Do  not  let  us  forget  that  syphilis  may 
be  a  cause,  in  which  case  specific  treatment  must  be  at  once  given. 

V.  NEUEALOIA  OF  THE  PHEENIC  NERVE. 

Although  the  phrenic  nerve  is  more  motor  than  sensorv,  its  sensory 
filaments  acquire  in  the  pathological  condition  an  exquisite  sensibility.  The 
phrenic  nerve  arises  from  the  third,  fourth,  and  fifth  pairs  of  cer\dcal  nerves. 
It  is  one  of  the  most  important  branches  of  the  cervical  plexus.  It  runs 
along  the  front  of  the  scalene  muscle,  enters  into  the  thorax,  and  spreads 
out  over  the  diaphragm.  The  left  phrenic  nerve  passes  between  the  pleura 
and  the  pericardium.     It  may  therefore  be  affected  in  pericarditis. 

Description. — The  causes  of  phrenic  neuralgia  are  those  of  aU  forms  of 
neuralgia  (cold,  rheumatism),  to  which  must  be  added  the  causes  peculiar 
to  this  nerve — diaphragmatic  pleurisy,  lesions  of  the  organs  in  the  neigh- 
bourhood of  the  diaphragm  (liver,  spleen),  pericarditis,  and  lesions  of  the 
aorta,  which  act  through  the  pericardium  (Peter). 

The  pain  is  seated  at  the  base  of  the  thorax,  on  a  level  with  the  insertion 
of  the  diaphragm,  and  by  pressure  we  can  determine  painful  points  over 
the  lower  ribs  at  the  points  of  insertion  of  the  diaphragm,  and  over  the 
lateral  part  of  the  neck,  in  front  of  the  scalenus  anticus.  The  pains  often 
radiate  to  the  branches  of  the  cervical  and  brachial  plexuses  and  to  the  cir- 
cumflex nerve,  which  explains  the  pain  in  the  shoulder  and  the  formication 
and  numbness  in  the  hand.  The  pain  in  the  diaphragm  makes  the  act  of 
respiration  painful.  It  is  increased  by  any  movement  of  the  diaphragm,  by 
cough,  by  yawning,  by  sighing,  and  by  sneeziag.  Neuralgia  of  the  phrenic 
nerve  is  associated  with  certain  forms  of  angiaa  pectoris,  and  forms  a  part 
of  the  symptom-complex  in  diaphragmatic  pleurisy. 


NKURALCIA  1540 


VI.  INTERCOSTAL  NEURALGIA— ZONA. 

The  twelve  dorsiil  nerves  give  off  posterior  and  anterior  branches.  Tlie 
postorior  branchos  jiorforato  tlio  muscles  along  the  eoato-v^ertebral  groove, 
and  spread  out  over  the  skin  as  the  posterior  perforating  nerves.  The 
anterior  branches  form  the  intercostal  nerves.  Each  intercostal  nerve  is 
placed  in  the  groove  of  the  rib ;  ])etween  the  muscles  and  at  about  the  middle 
of  its  course  it  gives  off  the  lateral  perforating  branch.  The  lateral  branch 
of  the  first  two  intercostal  nerves  supplies  the  skin  of  the  arm  ;  the  others 
supplv  the  skin  of  the  thorax  and  of  the  abdomen.  Tlie  intercostal  nerve 
continues  its  course,  becomes  superficial,  and  makes  its  exit  just  external 
to  the  sternum  and  to  the  rectus  abdominis  as  the  anterior  perforating 
branch. 

Description. — Intercostal  neuralgia  is  most  frequent  on  the  left  side, 
and  more  common  in  women.  Chlorosis  and  hysteria  are  the  most  common 
causes.  As  regards  local  causes  I  may  mention  pulmonary  tuberculosis, 
caries,  necrosis  of  the  ribs  and  of  the  veitebrae,  Pott's  disease,  and  aneurysm 
of  the  aorta.  The  pain  in  the  side  which  accompanies  pneumonia  and 
pleurisy  has  been  variously  interpreted,  but  it  is  generally  attributed  to 
neuritis  or  to  intercostal  neuralgia. 

The  neuralgia  generally  attacks  several  nerves  at  the  same  time,  and  the 
attacks  are  not  as  clearly  defined  as  those  of  facial  neuralgia.  The  pain, 
which  is  more  or  less  continuous,  is  increased  by  pressure,  by  the  contact 
of  the  clothes,  and  by  deep  inspirations.  The  most  constant  painful  points 
are  the  spinal  point  (Trousseau)  and  the  anterior  perforating  point.  Hyper- 
sesthesia  is  constant.  It  is  easy  to  provoke  h}'per3esthesia  by  gently  rubbing 
the  sldn,  and  thus  to  define  the  limit  of  the  neuralgia,  which  stops  just  on 
the  median  line. 

The  pains  of  intercostal  neuralgia  often  cause  patients  much  alarm. 
Some  patients  attribute  the  thoracic  pains  to  an  affection  of  the  chest ; 
others  fear  a  lesion  of  the  heart,  because  the  prgecordial  pains  are  brought 
on  by  the  palpitation  that  accompanies  chlorosis.  One  patient  will  speak  of 
gastralgia,  when  the  condition  is  really  epigastralgia  (pressure  of  the  corset) ; 
another  talks  about  disease  of  the  liver,  when  the  skin  of  the  hypo- 
chondrium  is  affected  by  the  neuralgia. 

Treatment  must  include  both  the  general  and  the  local  condition  of  the 
subject.  Antipyrin,  tonics,  iron,  quinine,  and  hydrotherapy,  are  of  use  in 
the  former  condition.  Locally,  injections  of  pure  water  or  injections  of 
morphia  may  be  given  (Potain  and  Dieulafoy).  An  ointment  of  methyl 
salicylate,  one  or  two  leeches,  wet-cupping  the  actual  cautery,  or  a  small 
blister,  may  be  used  over  the  painful  area. 


1550  TEXT-BOOK  OF  MEDICINE 


Zona — Herpes  Zoster. 

Zona  belongs  to  the  trophic  troubles  of  intercostal  neuralgia.  The 
name  "  zona  "  (herpes  zoster)  is  given  to  the  groups  of  vesicles  of  herpes 
which  develop  along  the  track  of  one  or  more  intercostal  nerves,  and  form 
a  half -circle  around  the  trunk  {^covv,  girdle).  This  name  "  zona,"  originally 
reserved  for  the  eruptions  of  herpes  in  intercostal  neuralgia,  is  now  applied 
to  similar  eruptions  in  the  other  forms  of  neuralgia,  and  we  speak  of 
ophthalmic  (neuralgia  of  the  trifacial  nerve),  cervical,  brachial,  sciatic, 
lumbo-abdominal,  and  plantar  zona.  The  vesicular  eruption  which 
characterizes  zona  shows  itself  in  two  different  conditions.  Zona  exists 
as  a  primary  disease  ;  zoster  fever,  analogous  to  the  eruptive  fevers, 
is  sometimes  epidemic,  and  was  considered  by  Trousseau  as  being  con- 
tagious. It  has  been  placed  among  the  infectious  diseases  by  Landouzy. 
On  the  other  hand,  we  fiijd  zosteroid  eruptions,  symptomatic  of  grave 
lesions  of  the  nerve  centres  or  of  the  peripheral  nerves.  Such  is  the  zosteroid 
eruption  accompanying  the  lightning  pains  of  tabes  and  the  zosteroid 
eruption  of  syphilis.     I  shall  here  deal  with  zona. 

Symptoms. — Every  case  of  zona  is  generally  composed  of  two  elements — 
pa,in  and  eruption.  The  eruption  may  be  limited  to  one  or  two  small  groups 
of  vesicles  ;  at  other  times  large  areas  are  invaded,  the  vesicles  appearing 
along  the  track  of  the  pain.  A  characteristic  eruption  may,  however, 
exist  without  any  pain  being  present.  The  description  of  zona  applies  to 
aU  the  localizations  of  the  disease,  but  I  shall  here  confine  my  description 
chiefly  to  intercostal  zona,  which  is  the  most  frequent  form.  The  neuralgia 
precedes  the  eruption,  and  often  persists  after  the  eruption  has  disappeared. 
The  eruption  appears  at  first  in  the  form  of  erythematous  patches,  separated 
by  intervals  of  healthy  skin.  Transparent  vesicles  of  herpes  appear  on  these 
patches.  In  three  or  four  days  the  development  of  these  vesicles  is  com- 
plete, and  the  erythematous  patch  extends  about  an  inch  beyond  the  vesicles. 
After  five  or  six  days  the  fluid  in  the  vesicles  becomes  turbid,  the  vesicle 
shrivels  and  becomes  covered  with  a  dark  crust,  and  about  the  twelfth 
day  the  eruption  ends.  The  vesicles  may  unite  and  form  bullae.  The 
eruption  may  be  accompanied  by  fever  and  by  enlargement  of  the  glands 
(Barthelemy).  The  existence  of  aberrant  vesicles  (Tenneson,  Jeanselme, 
Leredde,  Giraudeau)  is  a  further  plea  in  favour  of  the  infectious  nature 
of  zona. 

The  intensity  of  the  eruption  is  not  in  proportion  with  the  severity  of 
the  pains,  because  pain  may  be  almost  absent.  Furthermore,  the  eruption 
does  not  always  follow  the  anatomical  course  of  a  nerve.  Thus,  in  the 
thorax  the  half-circle  formed  by  the  eruption  is  almost  perpendicular  to 


NEURALPrlA  inr,i 

fclie  axis  of  tlir  ImxIw  uliilst  the  rihs  mid  IIm-  intorrostal  nerve  run  .111  ob]if|uf' 
course  from  above  downwards.  The  same  remark  appli«'s  to  Ihe  otln-r 
varieties  of  zona. 

Zona  is  often  followed  hy  paiiifid  neiiriilyia.  wliicli  may  last  for  month" 
and  years.  Painful  facial  paralysis  is  sometimes  accompar)ied  by  zona.  I 
shall  discuss  this  question  under  Facial  Paralysis.  Raymond,  Klip|)el,  and 
Aynaiid  have  quoted  some  exaInpl(^s.  Zona  presents  special  features, 
according  to  the  age  of  the  patient.  Thus  in  children  at  the  breast  zona  is 
generally  benign  and  painless.  In  old  people,  o!i  the  contrarv,  the  pain  is 
very  severe  and  obstinate.  In  some  cases  zona  is  chronic,  and  mav  persist 
for  many  months,  whether  it  recurs  in  situ  or  in  a  neighbouring  region,  or 
whether  the  vesicles  give  place  to  ulcerations,  which  sometimes  end  in 
keloid  (Leudet). 

Pathogenesis — Metamerism. — Zona  was  formerly  considered  as  a  trophic 
trouble  due  to  changes  in  the  sensory  nerves,  and  has  been  explained 
in  an  ingenious  manner  by  Brissaud.  He  has  emphasized  the  discord 
between  the  topography  of  zona  and  the  nerve  supply  of  the  peripheral 
nerves,  the  vesicles  not  corresponding  in  all  cases  to  the  sensory  distribution 
of  these  nerves.  He  considers  that  zona  has  a  spinal  origin.  The  topo- 
graphy of  zona  can  be  explained  by  the  embryological  relation  between 
each  segment  of  the  skin  and  a  metameric  segment  of  the  spinal  cord. 
These  segments  comprise  a  series  of  superposed  metameres.  The  metameres 
are  readily  seen  in  the  embryo  of  the  chicken  from  the  sixty-eighth  hour, 
and  even  in  the  human  embryo  in  the  shape  of  lateral  protuberances  of  the 
primitive  nerve  axis — Houssay's  neurotomes.  The  limbs  are  composed 
of  metameric  stages  of  the  second  order.  This  metameric  disposition 
accounts  for  certain  facts  which  are  apparently  inexplicable,  such  as  the 
girdles  of  anaesthesia  in  s}T:ingomyelia,  the  symmetrical  disposition  of  the 
tropho-neuroses,  the  strange  colouring  of  the  coat  in  certain  mammals— in 
the  Belgian  hare,  for  example.  The  metameric  segmentation  of  the  spinal 
cord,  which  supervenes  in  the  embryonic  period,  is  alone  capable  of  explaining 
zona  (Brissaud). 

The  examination  of  the  cerebro -spinal  fluid  often  shows  lymphocytosis, 
pointuig  to  meningeal  irritation.  In  some  cases  the  fluid  contains  micro- 
organisms (infective  zona). 

Pathological  Anatomy. — Zona  (atrophic  trouble)  recognizes  as  its 
anatomical  origin  either  a  lesion  of  the  intervertebral  ganglia  or  of  the 
Gasserian  ganglia,  or  a  lesion  of  the  nerves  or  of  their  peripheral  branches. 
This  aetiology  includes  all  the  local  or  general  causes  capable  of  provoldng 
neuritis  and  peripheral  neuritis— tuberculosis,  tabes,  syphilis,  chills,  certain 
forms  of  poisoning  (carbonic  oxide)' ;  but  the  condition  is  generally  one  of 
zosteroid  eruption  rather  than  of  true  zona. 


1552  TEXT-BOOK  OF  MEDICINE 

Treatment. — The  pain  may  be  relieved  by  injections  of  morpliia  or  by 
the  application  of  compresses  soaked  in  a  solution  of  cocaine,  1  in  100.  The 
following  powder  is  applied  locally  : 

Powdered  starch    . .  . .         . .  . .     40  parts. 

^  Oxide  of  zinc  18     „ 

This  powder  is  kept  in  place  by  means  of  a  layer  of  oil  (Hardy). 

VII.  LUMBAE  NEUEALGIA. 

The  lumbar  nerves  are  the  analogues  of  the  dorsal  nerves.  They  give  off 
the  sensory  posterior  branches  which  perforate  the  muscles  of  the  vertebral 
groove,  in  order  to  spread  out  in  the  skin  and  the  anterior  branches  which 
form  the  lumbar  plexus.  The  lumbar  plexus  furnishes  collateral  branches, 
the  seat  of  lumbo-abdominal  neuralgia,  and  terminal  branches,  the  most 
important  of  which— the  crural  nerve — is  the  seat  of  crural  neuralgia. 

1.  In  lumbo-abdominal  neuralgia  the  collateral  branches  of  the  lumbar 
plexus  are  affected.  Shooting-pains,  pain  on  pressure,  and  hyperaesthesia 
are  met  with  here,  as  in  all  forms  of  neuralgia.  Neuralgia  of  the  ilio- 
scrotal  branch  has  its  painful  points  about  the  middle  of  the  iliac  crest 
(iliac  point),  at  the  exit  of  the  inguinal  canal  (inguinal  point),  and  at  the 
termination  of  the  nerve  in  the  scrotum  or  in  the  labia  majora.  Neuralgia 
of  this  nerve  comprises  the  affection  described  under  the  name  of  "  irritable 
testicle  "  (Cooper),  or  testicular  neuralgia,  often  accompanied  by  a  sensa- 
tion of  sjTicope,  which  might  lead  us  to  suppose  the  participation  of  the 
great  sympathetic  nerve. 

In  neuralgia  of  the  femoro-cutaneous  nerve  we  find  a  painful  point  near 
the  antero-superior  iliac  spine. 

2.  Crural  neuralgia  affects  the  antero-internal  part  of  the  thigh  and  of 
the  knee  and  the  inner  side  of  the  leg  and  of  the  foot.  The  principal  painful 
points  are  the  inguinal  point,  where  the  nerve  leaves  the  Fallopian  ligament, 
outside  the  crural  ring,  the  points  where  the  branches  of  the  musculo- 
cutaneous nerve  perforate  the  fascia,  and  a  point  on  the  level  of  the  internal 
condyle.     In  crural  neuralgia  walking  is  often  painful. 


VIII.  SCIATIC  NEURALGIA— SCOLIOSIS. 

Sciatic  neuralgia,  which  is  more  common  than  facial  and  intercostal  neuralgia,  is 
most  important.  The  sciatic  nerve  is  the  only  terminal  branch  of  the  sacral  plexus. 
It  leaves  the  pelvis  by  the  great  sciatic  notch,  and  the  gluteal  point  which  corresponds 
to  this  level  is  affected  in  neuralgia  of  the  small  sciatic  nerve,  which  is  often  associated 
with  sciatica.  The  great  sciatic  nerve  passes  between  the  ischium  and  the  great  tro- 
chanter (trochanteric  point),  and  reaches  the  popliteal  space.  It  then  divides  (pophteal 
point)  into  the  internal  and  external  popliteal,  the  latter  passing  round  the  head  of  the 


NEUKAi.GlA  ir,-;; 

fibula  (pcronoal  j)niiit).  Tho  tonnin.il  cutuiicuus  bninclica  of  tlm  Hi-iatic  t4ii|i|iiv  tho 
bkin  of  tho  lug  aiul  of  tho  foot,  excopUng  tho  iniior  sido  (o.vlcni.il  malleolar  and  plantar 
points). 

Description.  The  pain  of  sciatic  neuralgia  is  botii  continuous  and 
parux\  snial.  It  breaks  out  in  the  form  of  attacks,  wliich  are  caused  by 
walking,  or  by  the  heat  of  the  bed.  Shooting-pains  start  from  various 
points,  and  run  through  the  limb  in  various  places  (foot,  leg,  knee,  thigh, 
and  buttock).  During  the  attack  radiation  of  the  pain  is  freciuent.  It 
follows  the  collateral  branches  of  the  sacral  plexus,  the  branches  of  the 
lumbar  plexus,  and  the  intercostal  nerves.  Apart  from  the  attack,  the 
patient  experiences  a  sensation  of  pain,  numbness,  formication,  or  burning. 
There  is  cutaneous  hyperesthesia,  or  anaesthesia  if  the  neuralgia  is  of  long 
standing.  The  pain  may  be  provoked  by  pressure  on  the  points  already 
indicated,  or  in  the  course  of  the  nerve  along  the  posterior  portion  of  the 
thigh.  If  the  leg,  in  a  case  of  sciatica,  is  lifted  and  bent  at  the  same  time, 
the  patient  only  experiences  slight  pain  ;  but  if  the  leg  is  lifted  while  in  the 
extended  position,  he  utters  a  cry  of  pain  (Lasegue). 

The  patient  often  complains  of  cramps  or  of  painful  shocks  in  the  muscles 
of  the  leg  and  of  the  thigh.  Some  patients  have  zona ;  others  suffer  from 
muscular  weakness  in  the  same  regions. 

Atrophic  lesions  are  sometimes  seen  in  the  limb  affected  with  sciatica. 
It  is  not  a  simple  loss  of  flesh,  due  to  the  inertia  of  the  muscles,  but  a  mus- 
cular atrophy,  which  may  be  masked  by  h}^ertrophy  of  the  skin  and  by 
development  of  the  subcutaneous  tissue.  These  trophic  troubles  are  said 
to  depend  on  the  anatomical  condition  of  the  nerve.  They  are  absent  or 
only  slight  in  the  case  of  simple  neuralgia,  and  very  marked  in  the  case  of 
neuritis.  The  gradual  increase  of  the  pain,  the  numbness  and  formication 
preceding  the  acute  attacks,  the  pain  spreading  along  the  trmik  of  the 
nerve  itself,  are  said  to  be  symptoms  in  favour  of  neuritis. 

Scoliosis. — In  the  case  of  severe  or  inveterate  sciatica  the  attitude  of 
the  patient  when  stripped  and  in  the  erect  position  is  characteristic.  We 
often  meet  vnth.  crossed  scoliosis,  and  sometimes  with  homologous  scoliosis. 
In  crossed  scoliosis,  which  is  the  more  frequent,  the  lateral  curvatiue  of 
the  spine  and  of  the  trunk  and  the  lowering  of  the  shoulder  occur  on  the 
side  opposite  to  the  sciatica.  Let  us  take  a  patient  suffering  from  sciatica 
on  the  left  side.  The  body  is  bent  to  the  right ;  the  lumbar  column  describes 
a  curve,  with  its  couca\dty  towards  the  right ;  the  right  hand  is  lower  than 
the  left  one  ;  the  left  leg  is  semiflexed,  and  the  fold  of  the  left  buttock  is 
pulled  upwards. 

It  is  "  the  position  which  the  patient  suffering  from  sciatica  instinctively 
takes  to  relieve  the  painful  limb.  He  takes  the  weight  off  it  by  displacing 
the  centre  of  gravity,  and  the  hip  of  the  diseased  side  stands  out  "  (Phuipiu). 


1554  TEXT-BOOK  OF  MEDICINE 

When  the  scoliosis  is  very  marked,  the  costal  margin  comes  in  contact  with 
the  pelvis.  Furthermore,  the  degree  of  the  scoliosis  is  generally  in  pro- 
portion to  the  severity  of  the  pain.  In  the  long  run  this  crossed  scoliosis, 
which  at  the  commencement  is  an  instinctive  attitude  assumed  to  relieve 
the  pain,  becomes  a  permanent  attitude,  and  may  persist  for  weeks  and 
for  months  after  the  disappearance  of  the  sciatica,  as  though  the  muscles 
had  acquired  the  habit  of  remaining  contracted. 

In  some  cases  the  scoliosis  is  homologous — -homologous  meaning  that 
the  scoliosis  is  on  the  same  side  as  the  sciatica.  In  a  case  of  syphilitic 
sciatica  of  the  right  side,  with  homologous  scoliosis,  we  see  flexion  of  the 
diseased  leg,  lowering  of  the  fold  of  the  buttock,  bending  of  the  spine  and 
of  the  body  to  the  right,  while  the  left  hip  stands  out. 

At  first  sight  this  fact  seems  paradoxical,  because  in  such  a  case  the 
weight  of  the  body  rests  on  the  painful  limb.  It  is  true  that  the  patient 
partially  remedies  this  by  bending  the  healthy  hip  out  by  means  of  a  com- 
pensatory curvature.  "  In  such  a  case,"  says  Brissaud,  "  the  patient  has 
the  attitude  of  a  person  who  is  carrying  a  paU  of  water  at  the  end  of  his 
arm,  and  who  is  trying  to  avoid  wetting  himself." 

In  order  that  a  patient  with  sciatica  should  not  allow  himself  to  assume 
the  instinctive  attitude  of  crossed  scoliosis,  and  in  order  that,  in  spite  of 
himself,  he  should  adopt  the  paradoxical  attitude  of  homologous  scoliosis, 
there  must  be  a  reason,  because  homologous  scoliosis,  the  compensatory 
curvature  notwithstanding,  makes  walking  more  difficult  and  more  painful. 
What,  then,  is  the  cause  of  homologous  scoliosis  ?  According  to  Brissaud, 
the  reason  is  :  "  Whilst  crossed  scoliosis  is  produced  by  the  contraction  of 
the  muscles  of  the  healthy  side,  homologous  scoliosis  is  produced  by  the 
contraction  of  the  muscles  of  the  diseased  side.  The  contraction  is  not 
limited  to  the  muscles  supplied  by  the  sciatic  nerve,  but  extends  in  the 
lateral  region  of  the  trunk  to  the  muscles  supplied  by  the  branches  of  the 
lumbar  plexus."  It  is  therefore  a  lumbo-sacral  neuralgia,  with  contrac- 
tion and  painful  points  in  the  flank  and  along  the  course  of  the  crural  nerve, 
with  exaggeration  of  the  patellar  reflex  and  epileptoid  tremor.  Brissaud 
in  one  of  his  cases  which  is  identical  with  one  of  mine — a  case  labelled 
"  sciatic  neuritis  " — speaks  of  a  patient  who  had  sciatica  of  the  left  side, 
with  homologous  scoliosis,  exaggeration  of  the  patellar  reflexes  on  both 
sides,  and  epileptoid  tremor  as  soon  as  the  foot  was  straightened.  Lumbo- 
sacral neuralgia,  with  homologous  scoliosis,  or  Brissaud's  spasmodic  sciatica, 
with  painful  contraction  and  epileptcid  tremor,  has  also  been  studied  by 
Lami,  who  has  published  two  cases.  In  some  cases  the  leg  of  the  healthy 
side  is  attacked  by  paresis  or  by  spasmodic  symptoms.  I  shall  describe 
in  the  next  section  (Syphilitic  Sciatica)  a  remarkable  example  of  this 
condition. 


^Etiology.  —Cold  and  rheumatiHiii  ani  friMjiumt  causes  of  sciatic  neuralgia. 
Many  people  have  got  sciatica  in  consequoncc  of  liaviiipj  gone  to  siftctt  on 
the  grass,  or  of  having  had  their  foot  in  cold  water.  Sciatica  is  brought  on 
by  injury,  by  lesions  of  the  vertebral  column,  of  the  meninges,  and  of  the 
spinal  cord,  and  by  compression  of  the  nerve  ([)olvic  tumours,  exostoses,  or 
cancer),  whence  the  necessity  of  rectal  and  vaginal  examination,  when  it 
becomes  necessary  to  establish  the  pathogenic  diagnosis  of  sciatica.  Gout 
and  gonorrha?a  deserve,  as  regards  tetiology,  Hj)ecial  mention.  Syphilitic 
sciatica  will  be  dealt  with  in  the  following  section.  Double  sciatica  is  often 
dependent  on  diabetes  (Worms). 

The  sciatic  nerve,  like  all  the  nerves,  may  be  attacked  by  neuralgia 
during  the  course  of  tuberculosis.  According  to  Peter,  sciatica  is  sometimes 
the  initial  sign  of  tuberculosis.  We  have  seen,  as  a  matter  of  fact,  imder 
Pulmonary  Phthisis  that  sensory  troubles  of  all  kinds  are  very  frec^uent  in 
patients  suffering  from  tuberculosis,  and  are  often  due  to  peripheral  neuritis. 

The  diagnosis  of  sciatica  is  easy.  It  is  not,  however,  sufficient  to  diagnose 
sciatica  ;  we  must  also  find  its  cause,  because  the  treatment  must  be  varied 
according  to  this  cause.  The  sciatica  of  diabetes  and  of  syphilis  requires 
the  treatment  for  diabetes  and  syphilis.  Sciatica  associated  with  tumour 
in  the  neighbourhood  demands  surgical  treatment. 

Certain  remedies  are  of  service  in  sciatica.  Prolonged  baths  (Krishaber) 
give  excellent  results.  The  patient  must  remain  in  his  bath  for  several 
hours.  Antipyrin  may  be  prescribed  in  doses  of  from  15  to  45  grains. 
Injections  of  morphia  and  inunction  of  an  ointment  of  methyl  salicylate 
may  give  relief.  Blisters,  the  actual  cautery,  injections  of  sterilized  water 
(Potain  and  Dieulafoy),  injections  of  air,  and  epidural  injections  by  the  sacro- 
coccygeal route,  have  their  indications.  Bleeding,  leeches,  and  cupping  are 
useful.  Local  freezing  gives  good  results.  A  spray  of  ethyl  chloride  is 
played  over  the  painful  area,  so  as  to  reduce  the  temperature  to  76°  F.  The 
spray  is  directed  by  means  of  a  special  siphon  (Debove).  Electricity  has 
achieved  many  successes.  Superheated  air  has  given  remarkable  results ; 
a  full  description  will  be  found  in  the  Appendix  on  Therapeutics. 


IX.  SYPHILITIC  SCIATICA-HOMOLOGOUS  SCOLIOSIS. 

Description. — A  young  man  was  admitted  one  day  into  my  wards  in  great  distress. 
The  left  hip  stood  out,  the  body  Avas  bent  to  the  right  side.  He  took  short  steps, 
supported  by  an  attendant,  leaning  to  the  right  side  on  a  stick,  dragging  his  bent  right 
leg,  and  seeking  by  means  of  this  position  to  lessen  liis  sufferings.  I  had  him  put  to 
bed,  and  then  examined  him.  The  right  leg,  buttock,  hip,  and  lumbar  region  showed 
marks  of  blisters  and  scars,  with  cicatrices,  due  to  spraying  with  ethyl  chloride.  Ho 
gave  us  the  folio  wing  history  of  his  case : 


1556  TEXT-BOOK  OF  MEDICINE 

Three  years  ago,  without  apparent  cause,  he  felt  mcreasLng  pain  in  the  right  buttock, 
the  thigh,  and  the  leg.  In  spite  of  his  sufferings,  he  continued,  his  -work  as  a  carter  as 
well  as  he  could.  This  condition  continued  to  grow  worse  all  the  time  until  the  month 
of  November.  At  this  period,  six  months  before  his  admission  to  the  hospital,  the 
pains  became  extreme.  They  were  most  marked  in  the  thigh  or  in  the  calf,  and  some- 
times radiated  into  the  groin,  the  front  of  the  thigh,  the  penis,  and  the  scrotum,  after 
the  manner  of  lumbo-sacral  nem-algia.  At  night  the  suffering  was  much  increased, 
and  he  was  imable  to  he  do-mi  and  sleep.  In  six  months  he  had  lost  18  pounds  in 
weight. 

During  these  three  years  of  suffering,  and  especially  dui'ing  the  last  six  months,  he 
had  consulted  several  physicians,  and  had  taken  many  forms  of  treatment,  without 
obtaining  the  shghtest  rehef. 

He  obtained  admission  into  the  annexe  of  the  Hotel-Dieu,  where  sciatica  wa-s 
diagnosed,  and  the  ethyl  chloride  spray  was  used  without  success.  He  was  discharged 
unreheved.  He  then  came  to  the  out-patients'  department  at  the  Hotel-Dieu,  ajid 
was  at  once  admitted  under  my  care. 

Questioned  as  to  the  nature  of  his  pains,  he  told  us  that  they  never  ceased.  He 
described  them  as  dragging  and  crushing.  He  could  bear  them  during  the  day-time 
when  at  rest,  but  at  night  they  were  terrible,  no  matter  what  position  he  assumed. 
Sometimes  he  felt  himself  becoming  "  as  stiff  as  a  poker."  The  leg  was  affected  by  a 
painful  contraction,  in  which  the  lumbar  region  participated.  On  pressture,  we  found 
the  painful  points  of  sciatic  neuralgia — over  the  right  buttock,  the  sciatic  notch,  along 
the  ischio-trochanteric  groove,  in  the  popliteal  space,  in  the  antero- external  region  of 
the  leg,  and  on  the  dorsal  surface  of  the  foot.  Furthermore,  the  pain  ascended  into 
the  lumbar  region,  and  extended  to  the  gluteal  muscles.  The  patient  even  stated  that 
in  severe  attacks  the  pain  radiated  into  the  scrotum  (geni to -crural  sphere)  and  into  the 
left  leg. 

Lasegue's  sign  was  present.  When  the  right  leg  was  hfted  and  bent,  the  patient 
felt  but  shght  pain  ;  but  when  the  extended  leg  was  hfted,  he  uttered  a  cry  of  pain.  In 
short,  there  was  no  doubt  that  the  patient  was  suffering  from  sciatica,  but  from  a 
somewhat  special  form. 

When  in  bed,  the  patient  kftpt  his  leg  shghtly  flexed.  He  could  only  sit  on  a  chair 
at  the  cost  of  great  suffering.  Even  then  he  sat  down  in  a  peculiar  manner,  resting  the 
left  buttock  on  the  edge  of  the  chair,  and  keeping  the  right  buttock  fi'om  it.  As  soon 
as  he  sat  down,  he  was  seized  with  the  epileptoid  tremors  in  the  right  leg  and  shooting 
pains,  which  made  him  get  up.  T\Tien  he  wished  to  unlace  his  boots,  he  did  not  lean 
forward,  as  any  other  person  would  do,  but,  standing  up,  he  hfted  his  foot  backwards, 
bent  his  body  sideways,  and  with  his  extended  arm  reached  his  boot,  without  having 
bent  his  leg.  At  meal-times  he  assumed  the  most  varied  positions,  standing  with 
one  knee  on  a  chair,  or  with  his  body  bent. 

The  right  leg  had  got  thinner  and  less  firm  than  the  left  leg,  but  the  sensation  waa 
normal,  and  the  electrical  examination  did  not  show  any  degeneration.  The  cremas- 
teric and  plantar  cutaneous  reflexes  were  intact.  The  pateUar  reflexes  were  exagge- 
rated, especially  on  the  right.  Both  legs  showed  the  epileptoid  tremor,  although  it 
was  very  shght  in  the  healthy  leg. 

In  view  of  these  latter  sjmiptoms,  which  had  a  tendency  to  be  bilateral,  it  might 
be  asked  whether  the  chagnosis  of  sciatic  neuralgia  was  sufficient,  and  vvhether  the 
lesion  ought  not  to  be  placed  higher,  and  meningo-mjehtis  thought  of. 

The  patient  on  admission  had  the  appearance  of  a  man  suffering  from  sciatica  with 
homologous  scoliosis.  The  trimk  was  bent,  forming  a  concavity  towards  the  affected 
bide.  The  left  hip  st<jod  out ;  the  right  shoulder  was  inchned  to  the  right ;  the  interval 
between  the  costal  margin  and  the  ihac  crest  was  much  diminished ;  and  the  fold  of 
he  buttock  was  lowered.     In  an  individual  with  sciatica,  homologous  scohosis — that 


NKUiJAi.ciA  ir,r,7 

is  to  say,  scoliosis  on  Uio  siuno  Kido  as  Lho  siijitira  is  niii\  Tho  HfolioKJH  i«  almost 
alwa^'s  oroHHocl ;  in  other  wohIh,  tho  lateral  curve  of  tho  baiikhoiio  and  of  tho  trunk  and 
tho  lowering  of  tho  .shouklor  aro  on  tho  sido  opfiowito  to  tin;  miatica.  ThiH  ••roMwod 
scoliosis  "is  tho  position  itistinctivcly  taken  hy  tho  patient  t<)  reliove  tho  painful 
limb.  Ho  does  this  by  displaciuf^  tho  contro  of  gravity,  and  the  hij)  on  tho  disoased 
side  stands  out."  (I  refer  tho  reader  to  tho  preceding  section  for  the  description  of 
scoliosis  in  sciatica.)  Tho  patient,  therefore,  had  spasmodic  sciatica,  with  homologous 
scoliosis. 

We  had  next  to  think  of  the  treatment,  but  seeing  that  attempts  as  numerous  as 
they  had  been  unsuccessful  had  been  made  for  the  past  three  years,  the  task  was  not  an 
cfisy  one  ;  and  yet,  in  order  to  succeed,  it  was  only  necessary  to  go  back  to  the  cause 
of  tho  disease. 

My  first  care,  after  ha\'ing  made  the  diagnosis,  was  to  seek  for  the  cause  of  this 
severe  sciatica.  The  patient  was  not  suffering  from  malaria,  tuberculosis,  dial)ote8, 
or  rheumatism  ;  he  was  syphilitic.  In  1889,  ten  years  previously,  he  had  had  a  chancre, 
roseola,  and  headache.  It  Avas,  therefore,  logical  to  think  that  the  sciatica  was  of 
syphilitic  origin.  I  could  not  say  whether  the  nerve  itself  was  affected  (sclero-gum- 
matous  neuritis),  or  whether  it  suffered  from  the  contact  of  a  neighbouring  lesion 
(gumma  or  exostosis).  I  ordered  a  daily  injection  of  1  gramme  of  oily  solution  of 
biniodide  of  mercury,  which  represents  4  miUigrammes  of  the  active  principle.  I  pur- 
poseh^  did  not  order  any  other  remedy,  so  as  to  note  the  effect  produced  by  the  mercury. 
For  about  a  week  the  effect  of  the  treatment  was  unnoticeable,  but  from  that  time  for- 
ward it  -was  possible  to  follow  day  by  day  the  rapid  improvement.  After  the  twelfth 
injection  the  patient  passed  a  better  night  than  he  had  done  for  the  past  six  months. 
After  the  fourteenth  injection  he  slept  the  whole  night  through.  He  sat  down  on  his 
bed,  got  up,  and  took  a  few  steps  without  much  difficulty. 

In  the  next  few  days  the  patient  walked  from  one  end  of  the  ward  to  the  other 
without  a  stick.  He  walked  almost  erect.  The  scohosis  had  considerably  chminished. 
The  left  hip  was  much  less  prominent.  The  fold  in  the  right  buttock  was  not  so  low. 
The  right  leg  was  hardly  flexed,  and  movements  impossible  a  fortnight  ago  on  accoimt 
of  the  pain  were  now  performed  by  the  patient,  who  seemed  quite  surprised.  His 
appetite  was  good,  and  he  regained  his  strength.  He  was  now  able  to  "  run  Uke  a 
hare,"  as  he  expressed  it.  This  marvellous  result  was  obtained  after  eighteen  mercurial 
injections.  From  this  date  all  the  symptoms  disappeared.  The  patient  could  sit  down 
without  difficulty.  The  reflexes  were  normal,  and  the  sudden  straightening  of  the  foot 
no  longer  provoked  an  epUeptoid  tremor.  The  muscular  contraction  causing  the 
homologous  scohosis  had,  however,  not  completely  disappeared,  the  trunk  being 
shghtly  bent  towards  the  right  side.  A  few  days  later  I  ordered  a  new  series  of  injec- 
tions to  be  commenced,  and  the  cure  was  definite.  In  this  case,  as  in  many  others,  I 
obtained  a  cure  of  the  syphihtic  mischief  by  means  of  mercury  alone.  Iodide  of 
potassium  was  not  associated  with  it. 

I  quote  other  cases  of  syphilitic  sciatica.  De  Lavarenne  communicated 
the  following  case  to  me  : 

A  man,  forty-six  years  of  age,  was  taken  ill  ■with  sciatica,  and  sent  to  him  at 
Luchon  in  July,  1888.  The  pains  had  commenced  sixteen  months  previously  in  the 
left  lumbar  region.  They  then  attacked  the  left  leg  in  the  form  of  sciatica.  A 
noteworthy  feature  was  that  the  pains  were  more  severe  at  night,  and  the  patient, 
blaming  the  heat  of  the  bedclothes,  always  slept  with  his  left  leg  outside  the  bed. 
In  the  past  eight  months  the  sciatica  had  become  much  worse.  De  Lavarenne  noticed 
that  the  patient  bent  over  to  the  left  side,  the  side  of  the  sciatica  (homologous  scoliosis). 
The  left  leg  was  soft,  and  commenced  to  atrophy.  The  measurement  through  the  middle 
of  the  thighs  showed  that  the  left  side  was  2  inches  smaller  than  the  right  side. 

II.  99 


1558  TEXT-BOOK  OF  MEDICINE 

The  patient  had  so  far  been  treated  for  rheumatic  sciatica.  As  sulphate  of  quinine 
in  large  doses,  saUcylate  of  soda,  injections  of  morphia,  the  cautery,  bhsters,  and 
inimctions  had  failed,  it  was  proposed  to  stretch  the  nerve — an  operation  to  which  the 
patient  would  only  consent  after  having  tried  the  thermal  cure.  The  sulphur  treat- 
ment was  then  prescribed  :  baths  and  sitz  baths  at  a  temperature  of  110°  F.  In  spite 
of  the  sulphur  baths,  the  pains  became  still  more  severe.  Injections  of  morphia  were 
given. 

On  account  of  certain  indications,  De  Lavarenne  got  an  idea  that  the  patient 
might  be  syphilitic.  He  ordered  inunctions  of  mercurial  ointment.  The  result  was 
surprising.  After  the  third  inimction  the  disease  began  to  \-ield.  In  a  week  the  pains 
had  diminished,  so  that  the  patient  could  sleep  without  the  aid  of  morphia.  He  walked 
without  a  stick,  and  could  put  on  his  boots.  The  mercurial  inunctions,  and  then  iodide 
of  potassium,  were  continued  for  a  month,  and  the  patient  left  Luchon  perfectly  cured. 
A  year  later  he  was  in  good  health. 

The  following  cases  are  taken  from  Dubois's  paper  : 

A  lady,  twenty-three  years  of  age,  suffered  intense  pains  in  the  left  thigh.  The 
painful  points  extended  along  the  sciatic  nerve,  and  descended  as  far  as  the  foot. 
Several  methods  of  treatment  had  been  tried  without  success,  when  Gerard  found 
gumma,  flat  pustules,  and  vegetations.  Antisyphiht^c  treatment  cured  the  sciatica  in 
a  fortnight. 

Zambacco  speaks  of  a  man  who  had  had  syphilis  eighteen  months  previously.  He 
came  to  the  Hopital  du  jNIidi  for  syphilitic  sciatica.  The  painful  points  were  situated 
over  the  sacrum,  the  left  buttock,  and  the  posterior  portion  of  the  thigh  and  of  the  leg. 
Walking  caused  intense  pain.  Pills  of  proto-iodide  of  mercury  were  prescribed.  Ten 
days  later  the  patient  left,  completely  cured. 

Another  case  of  Zambacco  referred  to  a  syphilitic  patient.  Two  years  after  the 
chancre  he  was  taken  ill  with  sciatica  on  the  left  side,  thought  to  be  rheumatic.  The 
pains,  which  were  very  severe  at  night,  were,  for  the  time  being,  reheved  by  cold 
compresses,  but  they  reappeared  as  soon  as  the  compresses  got  warm.  The  patient 
came  to  Paris  and  consulted  Zambacco,  who  found  sciatica  on  the  left  side.  The  pains 
were  intense,  especially  at  night.  Pressure  over  the  left  sciatic  nerve  from  the  lower 
portion  of  the  buttock  as  far  as  the  pophteal  space  caused  extreme  pain.  The  most 
careful  exploration  revealed  no  tumour  along  the  sciatic  nerve.  As  the  patient  had  the 
stigmata  of  syphihs  on  his  legs,  mercury  and  iodide  of  potassium  were  immediately 
prescribed.  By  the  fourth  day  the  improvement  was  noticeable,  and  six  weeks  later 
the  patient  returned  to  London,  completely  rid  of  his  pains. 

Taylor  quotes  the  case  of  a  man  who  contracted  syphihs,  and  was  several  months 
later  seized  with  intense  neuralgic  pains  in  the  sciatic  and  crui'al  nerves  on  the  right 
side.  The  sciatic  pain  extended  fi'om  the  ischium  to  the  knee.  It  was  continuous, 
■R-ith  violent  exacerbations  at  night.  It  was  at  first  thought  to  be  a  case  of  malarial 
neui-algia,  and  sulphate  of  quinine  was  prescribed  in  large  doses.  The  result  was  nil. 
Taylor  then  suspected  the  sypMlitiG  origin  of  the  neuralgia,  and  ordered  inunctions  of 
mercury  and  iodide  of  potassium.  The  pains  quickly  subsided.  Next  summer  a  shght 
relapse  was  cured  by  similar  means,  and  the  sciatica  did  not  reappear. 

I  win  conclude  with,  a  case  of  Oettinger  : 

A  young  woman,  twenty-one  years  of  age,  who  had  had  syphihs  the  year  before, 
came  to  the  hospital  in  188.3  for  extremely  acute  sciatica  on  the  left  side.  The  pains 
were  particularly  severe  at  night.  The  warmth  of  the  bed  and  pressure  of  the  bed- 
clothes were  so  painful  that  the  patient  got  up  and  vainly  tried  to  get  some  rehef  by 
moving  about.  When  she  did  succeed  in  getting  a  few  moments'  rest,  she  woke  up 
with  a  start,  thinking  of  the  pain.     On  pressure,  the  sciatic  nerve  was  painful  from  the 


NKURALaiA  l.o59 

Ihiuh  to  tlio  log.  Near  tlio  big  loo  llio  picsHurt)  iiuulo  tho  paliotit  ary  out.  Iiijoi-fionH 
of  morphia  gHvo  hut  little  roliof.  An  injeotiua  of  amiuonio  luoroury  |)«pt«Jiia(<!  wo-h 
given  every  oth»-r  day  (1  centigramme).  After  tho  lirst  injocitioriH  tho  p/ilimL  filt  a 
marivod  improvement.  A  few  {lays  later  aho  was  aliio  to  get  up  and  fo  put  ln-r  foot  on 
to  tho  ground.  Tlie  treatment  was  eontinuod  for  six  weekw,  and  nhe  left  tho  hf)Hpitiil 
completely  euicd. 

Discussion.  —  The  foregoing  casus  give  a  fair  picjtiirc.  of  sypliilitic 
sciatica.  The  sciatic  nerve,  as  well  as  the  trifacial,  facial,  oculo- 
motor, ulnar,  and  other  nerves,  may  be  attacked  by  syphilis.  Whether 
syphilis  is  localized  directly  in  the  sciatic  nerve  in  tho  form  of  sclorf»-gum- 
matous  neuritis,  or  whether  the  neuralgia  is  provoked  by  a  neighbouring 
syphilitic  lesion,  such  as  gumma,  osteo-periostitis,  etc.,  matters  little. 
The  result  is  the  existence  of  sciatica,  which  may  be  most  severe,  and  which 
resists  all  therapeutic  remedies  other  than  antisyphilitic  treatment. 

Syphilitic  sciatica  in  nowise  differs  from  the  other  kinds  of  sciatica. 
Continuous  and  paroxysmal  pains,  localization  of  the  painfid  points,  Lasegue's 
sign,  zones  of  anaesthesia,  wasting  of  the  limb,  exaggeration  of  the  reflexes, 
spasm  of  the  muscles,  epileptoid  tremor,  and  crossed  or  homologous  scoliosis, 
may  be  met  with  in  any  of  the  varieties  of  sciatica. 

As  regards  the  evolution  of  the  sciatica,  there  is  no  sign  or  symptom 
which  allows  us  to  say  that  the  sciatica  is  or  is  not  syphilitic.  A  point  in 
favour  of  syphilis  is  the  nocturnal  recrudescence  of  the  pains.  My  patient 
dreaded  the  approach  of  night-time,  because  it  was  during  the  night  that 
the  pains  were  so  severe.  Zambacco's  patient  suft'ered  more  at  night  than 
in  the  day ;  Oettinger's  patient  also  had  the  most  severe  pains  during  the 
night.  The  nocturnal  exaggeration  of  the  pains  is  here,  as  in  all  cases  of 
pain  with  nocturnal  recrudescence,  an  index  in  favour  of  syphilis.  In 
deciding  the  pathogenic  diagnosis,  we  have  particularly  the  information 
which  the  patient  is  able  to  give,  and  the  presence  of  stigmata  (cicatrices) 
or  of  syphilitic  lesions  (eruption,  gummata,  periostitis,  etc.)  contemporary 
with  the  sciatica. 

Sciatica  may  appear  in  the  early  secondary  stage  as  well  as  in  the  tertiary 
stage.  "  Sciatica,"  says  Fournier,  "  is  not  a  rare  symptom  of  secondary 
syphilis.  If  it  appears  to  be  less  frequent  than  it  really  is,  it  hi  because  its 
real  cause  remains  unlaiown."  I  am  quite  disposed  to  consider  it  at  least 
as  frequent  as  in  the  tertiary  stage.  It  is  our  duty  to  find  it  out.  In  a  ca.-se 
of  severe  sciatica,  which  is  worse  at  night,  and  which  has  resisted  all  treat- 
ment, we  must  think  of  syphilis.  Let  us  inquire  into  the  previous  history  : 
question  your  patient ;  search  his  past  life,  and  examine  for  old  or  recent 
marks  of  syphilis  (cicatrices,  nodes  on  the  tibia) ;  and  if  it  is  certain  that  the 
patient  has  had  syphilis,  let  us  prescribe  immediate  treatment.  Give 
mercury,  which  may  be  combined  with  iodide  of  potassium.  Of  all  the 
mercurial  preparations,  I  know  of  none  which  acts  with  greater  eflicacy  than 

9'J— 2 


1560  TEXT-BOOK  OF  MEDICINE 

the  aqueous  injection  of  biniodide  of  mercury,  which  is  described  in 
detail  in  the  Appendix  on  Therapeutics.  If  the  sciatica  is  syphilitic,  we 
shall  soon  know  the  result.  After  eight  or  ten  injections  the  patient 
experiences  considerable  relief,  and  the  progress  is  then  rapid.  The  future 
will  tell  whether  salvarsan  will  replace  mercury. 


X.  PAE^STHETIC    MERALGIA—NEURITIS  OF  THE  EXTERNAL 
CUTANEOUS  NERVE. 

Description. — This  affection  is  constituted  by  "  disturbance  of  the 
cutaneous  sensibility  of  the  thigh,  due  to  a  change  in  the  superficial  nerves, 
and,  in  particular,  to  the  crural  branch  of  the  external  cutaneous  nerve  " 
(Claisse). 

The  first  symptom  is  numbness,  soon  followed  by  formication  in  the 
antero-external  region  of  the  thigh.  The  pains  are  frequent.  They  have 
the  rapidity  and  the  severity  of  lightning  pains  (Dopter).  They  have  been 
compared  to  the  stabs  of  a  knife  (Lop),  or  to  pinchings.  The  skin  is 
red,  cyanotic,  hot,  and  stiff.  Anaesthesia  is  the  rule,  and  takes  the  shape 
of  a  racket,  with  the  handle  uppermost.  Pricks  are  not  felt.  Sensibility 
to  cold  is  much  decreased,  and  a  difference  of  several  degrees  of  tempera- 
ture cannot  be  felt.  The  reflexes  are  never  abolished.  Walking  is  diflficult, 
sometimes  impos  ible. 

The  course  of  parsesthetic  meralgia  is  very  slow.  Recurrences  are  not 
rare.  It  may  disappear  after  some  years,  or  may  persist  for  a  lifetime. 
The  prognosis  is  not  serious.  The  diagnosis  is  based  on  the  symptoms 
above  described. 

The  aetiology  of  paisesthetic  meralgia  is  very  obscure.  It  occurs  in 
adults,  and  in  men  more  often  than  in  women.  Injury  seems  to  have  some 
action  by  reason  of  the  superficial  course  of  the  nerve  filaments.  It  has 
been  attributed  to  the  infectious  diseases,  to  alcoholism,  to  lead-poisoning, 
to  arthritism,  and  to  obesity  (the  parsesthetic  troubles  disappear  during  a 
cure  for  obesity)  (Florand).  Cold  may  play  some  part  (Dopter).  The 
pathogenesis  is  still  in  doubt.  A  varicose  condition  of  the  limbs  has  been 
blamed,  because  meralgia  has  some  analogy  with  varicose  sciatica  (Dopter) ; 
but,  after  all,  we  have  probably  to  deal  with  peripheral  neuritis,  which  owes 
to  the  composition  of  the  nerve  a  clinical  physiognomy  exempt  from  motor 
and  trophic  troubles.  The  local  treatment  by  massage,  rubbing  with 
alcohol  or  turpentine,  gives  good  results.  Iii  fat  or  gouty  persons  strict 
hygiene  is  imperative.  I  would  recommend  the  use  of  superheated  air. 
In  the  obese  and  in  the  gouty  rigid  hygienic  measures  are  indicated. 


NEURAT/UA  ir,(;i 

Xr.   liADKJULITIS. 

The  aiil(M  iof  and  posU'rior  roots  of  the  spinal  nerves  innervate,  in  the 
one  case,  a  definite  gronp  of  muscles;  in  the  other,  a  definite  area  of  the 
skin.  These  areas  are  given  in  treatises  on  Anatomy  and  IMiysiology.  The 
symptoms  caused  by  traumatic  lesions  of  the  roots  have  long  been  known. 
The  inflammatory  lesions  have  not  been  described  until  recently;  Camus 
and  Sezary  were  tlie  first  to  do  so  under  the  name  of  Radiculitis. 

These  inflammatory  lesions  are  usually  limited  to  a  group  of  roots  ;  in 
most  cases  they  affect  the  lumbo-sacral  plexus,  being  then  spoken  of  as 
radicular  sciatica;  they  may  affect  the  lumbar  roots  alone  and  also  those 
of  the  upper  limb. 

Eadiculitis  is  ushered  in  by  progressively  increasing  pain,  similar  to 
the  pain  of  neuritis,  but  having  a  localization  independent  of  the  course  of 
the  peripheral  nerves.  Fits  of  coughing  or  of  sneezing  cause  a  sharp 
exacerbation  of  the  pain.  The  objective  sensory  disturbances  may  occur  in 
the  form  of  hypersesthesia  or  of  afc?esthesia,  having  a  radicular  disposition, 
that  is  to  say,  longitudinal  bands  in  the  case  of  the  limbs,  transverse  in 
the  case  of  the  thorax.     This  feature  is  most  important  in  diagnosis. 

Eadiculitis  may  be  merely  sensory,  or  sensori-motor ;  it  is  accom- 
panied by  paresis  or  by  paralysis  with  altered  electrical  reactions  similar 
to  those  of  neuritis ;  but,  an  important  point,  the  muscles  are  affected  in 
complete  or  incomplete  radicular  groups  ;  for  instance,  when  the  upper 
roots  of  the  brachial  plexus  are  affected,  we  find  paralysis  of  the  deltoid 
(circumflex  nerve),  of  the  biceps  (musculo-cutaueous),  and  of  the  supinator 
longus  (musculo-spinal). 

Eadiculitis  is  usually  secondary  to  a  lesion  of  the  meninges  surround- 
ing the  nerve -roots.  Hence,  in  the  majority  of  cases,  lumbar  puncture 
shows  lymphocytosis  of  the  cerebro-spinal  fluid. 

Eadiculitis  of  the  lower  cervical  roots  is  accompanied  by  oculo-papillary 
disturbances  (myosis,  retraction  of  the  eyeball,  narrowing  of  the  palpebral 
aperture)  just  as  occurs  in  traumatic  radicular  palsies  of  the  brachial  plexus. 
These  symptoms  were  very  evident  in  a  case  of  alcoholic  polyneuritis, 
associated  with  syphilitic  radiculitis,  noted  in  one  of  my  patients  by  Le 
Play  and  Sezary. 

In  short,  a  radicular  distribution  of  the  motor  and  sensory  troubles  and 
lymphocytosis  of  the  cerebro-spinal  fluid  are  the  diagnostic  signs  of 
radiculitis.  But  the  lesions  of  the  grey  matter  of  the  spinal  cord  (anterior 
and  posterior  cornua)  also  show  themselves  by  disturbances  having  a 
radicular  distribution.  After  we  have  found  an  absence  of  medullary 
signs  (disturbances  in  the  reflexes,  bladder  and  rectum  troubles,  Babinski's 
sicn,  thermo-analgesic  dissociation  of  sensibility,  absence  of  lymphocytosis 


1562  TEXT-BOOK  OF  MEDICINE 

in  the  cerebro-spinal  fluid),  we  may,  then,  interpret  the  symptoms  in  favour 
of  a  radicular  lesion. 

Eadiculitis  is  at  times  symptomatic  of  Pott's  disease,  of  cancer  of  the 
vertebrae,  or  of  a  meningeal  tumour,  compressing  the  nerve-roots  before 
reaching  the  spinal  cord ;  radiculitis  is  then  an  advance  sign  of  spinal 
compression.  When  it  is  isolated,  it  is  usually  dependent  upon  syphilis, 
more  rarely  upon  tuberculosis  or  gonorrhoea.  The  specific  naiure  of  many 
cases  of  radiculitis  is  to  be  noted,  because  treatment  (injections  of  biniodide 
of  mercury)  is  marvellously  effective.  In  an  obscure  case  of  radiculitis,  it 
is  essential  to  search  most  systematically  for  some  history  or  signs  of 
syphilis. 


CHAPTER  VIII 
PARALYSES 

I.  FACIAL  PARALYSIS. 

Paralysis  of  the  facial  nerve  does  not  lend  itself  to  a  general  description, 

because  the  symptoms  vary  according  to  the  part  of  the  nerve  affected. 

It  is  therefore  customary  to  describe  central  and  peripheral  paralysis.     As 

this  di\asion  is,  in  my  opinion,  insufficient,  I  shall  describe  the  following 

varieties :    (1)    Paralysis    of    peripheral    origin ;    (2)    paralysis    of     intra- 

temporal  origin  ;  (3)  paralysis  of  bulbar  origin ;  (4)  paralysis  of  cerebral 

origin . 

1.  Paralysis  of  Peripheral  Origin. — This  variety  is  the  most  common.  It  attacks 
the  terminal  branches  of  the  nerve  after  its  exit  from  the  Fallopian  aqueduct.  The 
facial  nerve  emerges  from  the  Fallopian  aqueduct  through  the  stylo  -  mastoid 
foramen,  traverses  the  parotid  gland,  and  suppUes  two  branches — temporo- facial  and 
cervico-facial.  These  two  branches  anastomose  to  form  the  subparotid  plexus.  From 
this  plexus  branches  are  distributed  to  the  muscles  of  the  skin,  of  the  neck,  of  the  face, 
and  of  the  anterior  portion  of  the  scalp.  The  facial  nerve,  therefore,  sujipUes  all  the 
muscles  of  the  face,  with  the  exception  of  the  muscles  of  the  eyeball  (third,  fourth,  sixth 
nerves),  of  the  upper  eyelid  (third  pair),  and  of  the  lower  jaw  (the  motor  portion  of  the 
fifth  pair).  Below  the  stylo-mastoid  foramen  the  facial  nerve  gives  off  the  posterior 
auricular  nerve  to  the  occipitalis  muscle,  and  to  the  posterior  and  superior  auricular 
muscles. 

Cold  is  the  most  common  cause  of  this  paralysis,  especially  in  subjects 
with  the  gouty  diathesis.  A  draught  of  air,  an  open  window  in  a  train, 
cold  rain,  and  livuig  in  a  damp  locality,  are  responsible  in  many  cases.  In 
a  patient  of  Trousseau  facial  hemiplegia  showed  itself  after  a  severe  fright. 
Injury,  parotid  tumours,  compression  of  the  nerve  by  the  forceps  during 
delivery,  are  less  common  causes. 

Syphilis  often  causes  facial  paralysis.  I  shall  devote  a  special  section 
to  it  later. 

Facial  paralysis  appears  suddenly  or  gradually,  according  to  the  pro« 
voking  cause.     It  is  almost  always  unilateral  (facial  hemiplegia). 

The  paralysis  is  often  preceded  or  accompanied  by  pains  in  or  behind 
the  ear,  in  the  cheek,  and  in  the  temporal  and  frontal  regions.  According 
to  Weber,  these  pains  are  present  in  more  than  half  the  cases  of  facial 
paralysis.     I  have  met  with  them  several  times,  and  I  have  had  in  my  wards 

1563 


1564  TEXT-BOOK  OF  ]\IEDICINE 

a  young  patient  in  whom  painful  paralysis  of  the  facial  nerve  was  accom- 
panied by  zona,  while  in  another  patient  very  severe  pain  preceded  the 
onset  of  paralysis  by  several  days.  The  pathogenesis  of  these  pains  (painful 
facial  paralysis)  will  be  discussed  in  the  following  section  on  Syphilitic 
Facial  Paralysis. 

The  paralysis  reveals  itself  by  signs  which  become  more  marked  if  the 
patient  is  made  to  laugh  or  to  speak,  because  the  contraction  of  the  muscles 
on  the  healthy  side  pulls  the  paralyzed  muscles  over.  As  the  facial  nerve 
presides  over  the  facial  mimicry,  all  expression  on  the  paralyzed  side  is 
abolished.  The  result  is  deviation  of  the  features  and  deformity  of  the  face. 
When  we  look  straight  at  a  person  with  facial  hemiplegia,  the  paralyzed 
side  looks  as  if  it  were  pushed  forwards  by  the  healthy  side,  which  hides 
itself  behind  it.  The  paralyzed  side  is  immobile,  and  presents  a  strange 
contrast  with  the  animation  of  the  other  side  of  the  face.  The  muscles  no 
longer  contract,  the  skin  of  the  forehead  is  smooth,  and  the  wrinkles  are 
efiaced  on  the  paralyzed  side.  Facial  hemiplegia  is  accompanied  by 
paralysis  of  the  muscles  which  co-operate  in  the  working  of  the  sense  organs. 

(1)  Organ  of  Vision. — The  eye  of  the  paralyzed  side  appears  larger 
and  more  widely  open,  on  account  of  the  paralysis  of  the  orbicularis  muscle. 
Two  muscles  govern  the  movements  of  the  eyelids.  The  one  serving  to 
close  them  is  the  orbicularis  muscle,  supplied  by  the  facial  nerve  ;  the  other, 
serving  to  open  them,  is  the  levator  palpebree  superioris,  supplied  by  the 
third  nerve.  When  the  orbicularis  is  paralyzed,  complete  closing  of  the 
eye  is  impossible,  and  the  elevator  then  keeps  the  upper  eyelid  raised  ;  wink- 
ing is  imperfect,  and  the  eyeball  remains  partially  uncovered,  even  during 
sleep.  The  lower  eyelid  undergoes  commencing  ectropion  ;  the  palpebral 
aperture  is  deformed  ;  the  inner  canthus  of  the  eye  becomes  narrow  ;  the 
tears  do  not  flow  uniEormly,  and  the  conjunctiva  becomes  injected,  dry,  and 
inflamed. 

Paralysis  of  the  facial  nerve  gives  rise  to  epiphora,  or  flowing  of  the  tears 
on  to  the  cheek,  from  paralysis  of  Homer's  muscle,  which  makes  the  punctse 
lachrymales  stand  out,  by  carrying  them  towards  the  lachrjTiial  gland, 
whence  they  draw  the  tears. 

BeU,  in  1823,  first  drew  attention  to  the  upward  and  outward  dis- 
placement of  the  eyeball  when  a  person  with  peripheral  facial  paralysis 
attempts  to  close  his  eye.  Palpebral  occlusion  and  elevation  of  the  eyeball 
are  two  associated  phenomena.  ^\Tien  vertigo,  syncope,  or  sleep  suppresses 
the  oculo-motor  act  which  presides  over  the  function  of  looking,  the  eyeball 
is  raised  upwards  and  outwards.  If  we  prevent  the  occlusion  of  the  eyelid 
with  the  finger,  or  when  the  want  of  occlusion  is  due  to  peripheral  facial 
paralysis,  the  second  part  of  the  synergic  action  takes  place  of  its  own 
accord — that  is  to  say,  the  eye  is  raised  as  though  the  eyelid  reaUy  closed. 


PARALYSES  1505 

Til  is  ])lionomonon,  variously  interpreted  by  Romberg,  Erb,  Bonnier,  is,  after 
all,  normal.  Bonnier  has  shown  that  in  cases  where  the  facial  paralysis  is 
accompanied  by  labyrinthine  irritation  the  movement  of  the  eye  may 
assume  the  spasmodic  character  of  an  "  eye  on  springs,"  as  in  one  of  my 
patients  suffering  from  facial  paralysis  of  otitic  origin.  This  fact  is  due 
to  the  action  of  the  labyrinthine  apparatus  on  the  nuclei  of  the  oculo- 
motor nerve. 

(2)  Organ  of  S)nell. — The  facial  nerve  moves  the  nostrils.  Accordingly, 
in  facial  hemiplegia  the  tip  of  the  nose  is  slightly  turned  to  the  healthy 
side,  the  nostril  is  constricted,  the  ala  nasi  is  no  longer  uplifted  at  each 
inspiration,  and  the  sense  of  smell  is  less  acute,  on  account  of  the  constric- 
tion of  the  nostril.  In  man,  whose  nostrils  are  rigid,  facial  paralysis  has 
little  influence  on  respiration;  but  in  the  horse,  in  the  case  of  double  paralysis 
of  the  facial  nerve,  the  nostrils  fall  in  at  each  inspiration,  and  as  the  larynx 
is  drawn  up  to  the  posterior  nares,  grave  respiratory  troubles  result. 

(3)  Speech  and  Mastication. — The  movements  of  the  lips  are  abolished 
on  the  paralyzed  side.  The  patient  can  neither  whistle  nor  blow,  and  the 
pronunciation  of  the  labial  letters  is  almost  impossible.  The  mouth  is 
twisted.  The  angle  on  the  healthy  side  is  drawn  upwards,  the  deformity 
being  increased  when  the  patient  laughs  or  speaks.  The  occlusion  of  the 
lips  being  incomplete,  the  saliva  sometimes  flows  from  the  mouth.  The 
paralyzed  cheek  is  flaccid  on  account  of  the  inertia  of  the  buccinator  muscle, 
and  the  food  accumulates  between  the  dental  arch  and  the  paralyzed  cheek. 
Mastication  is  imperfect.  The  cheek,  having  become  flaccid,  presents  no 
resistance  to  the  expired  air.  It  is  raised  like  a  sail  at  each  expiration,  and 
the  patient  is  said  to  be  "  smoking  a  pipe." 

(4)  The  Disorders  of  Taste  and  Hearing  will  be  described  under  Intra- 
temporal  Paralysis. 

In  facial  paralysis  a  frigore  the  electrical  contractility  undergoes  notable 
modifications.  When  the  paralysis  is  slight,  the  contractility  is  almost 
normal  (Erb).  In  this  benign  form  recovery  follows  in  two  to  three  weeks, 
but  in  the  grave  forms  the  galvanic  and  faradic  excitability  of  the  nerves 
is  lost,  as  well  as  the  faradic  excitability  of  the  muscles — an  indication  that 
the  paralysis  will  last  for  some  months.  It  is  not  uncommon  for  the  move 
ments  to  remain  affected  for  several  years,  and  certain  muscles  may  become 
contracted. 

Injections  of  pUocarpin  on  the  healthy  side  and  on  the  paralyzed  side 
show  a  delay  of  one  to  three  minutes  in  the  appearance  of  the  perspiration 
on  the  paralyzed  side.  This  phenomenon  is  peculiar  to  peripheral  facial 
paralysis  of  a  grave  type.  It  does  not  exist  in  facial  paralysis  of  cerebral 
origin.  In  the  latter  case  "  the  sweating  reaction  "  to  pilocarpin  is  ecjual 
on  both  sides  of  the  face  (Strauss). 


1566  TEXT-BOOK  OF  MEDICINE 

2.  Paralysis  of  Intiatemporal  Origin. — The  facial  nerve,  after  entering  the  internal 
auditory  canal,  with  the  auditory  nerve  and  Wrisberg's  nerve,  takes  a  long  course 
through  the  temporal  bone.  It  enters  the  Fallopian  aqueduct,  where  it  presents  the 
geniculate  ganghon,  in  which  Wrisberg's  nerve  loses  itself.  From  the  ganghon  there 
arise  the  large  and  small  superficial  petrosal  nerves.  The  facial  nerve  continues  its 
course,  gives  off  the  nerve  to  the  stapedius,  the  chorda  tjonpani,  and  a  few  nervous 
branches,  and  leaves  the  aqueduct  by  the  stylo-mastoid  foramen. 

Paralysis  of  intratemporal  or  petrous  origin  reveals  itself  by  tlie  symptoms 
already  mentioned  under  Periplieral  Paralysis,  to  whicli  are  added  symptoms 
dependent  on  tlie  paralysis  of  tlie  various  branches  just  enumerated.  These 
symptoms  are  : 

(1)  Organ  of  Taste. — (a)  In  certain  patients  the  sense  of  taste  is  per- 
verted. If  we  place  a  sapid  substance  alternately  on  the  healthy  and  on 
the  paralyzed  side  of  the  tongue,  the  sensation  is  obscure,  and  is  slow  in 
being  produced  on  the  paralyzed  side.  The  sensation  of  taste  in  the  pos- 
terior third  of  the  tongue,  due  to  the  glosso-pharjmgeal  nerve,  remains 
intact,  and  the  general  sensibility,  due  to  the  trifacial  nerve,  also  remains 
intact  throughout  the  whole  extent  of  the  tongue,  but  the  sensation  of  taste 
is  absent  in  the  anterior  two-thirds  of  the  paralyzed  half.  This  loss  of  taste 
is  due  to  the  paralysis  of  the  chorda  tympani,  paralysis  of  this  nerve  being 
said  to  produce  the  loss,  either  by  modifying  the  circulation  of  the  lingual 
mucosa  (Brown-Sequard),  or  by  producing  in  the  contractile  elements  of 
the  papillse  certain  changes  which  affect  their  relations  with  sapid  substances 
(Bernard). 

(&)  The  deviation  of  the  tongue  met  with  in  some  cases  and  the  difl&- 
culty  of  turning  the  tip  of  the  tongue  upwards  are  due  to  the  paralysis  of 
the  nerves  supplying  the  digastric  and  stylo- glossus  muscles.  It  is  not  un- 
common to  meet  with  deviation  of  the  uvula  and  with  slight  dysphagia, 
because  the  palatine  nerves  come  from  the  spheno-palatine  ganglion. 

(c)  Dryness  of  the  mouth  and  diminished  secretion  of  saliva  are  some- 
times observed.  These  symptoms  are  caused  by  paralysis  of  the  chorda 
tympani,  which  governs  the  secretion  of  the  parotid  gland  (Bernard), 
and  by  paralysis  of  the  small  petrosal  nerve,  which  regulates  the  secretion 
of  the  submaxillary  gland. 

(2)  Organ  of  Hearing. — The  facial  nerve  supplies  the  pinna  of  the 
ear.  In  long-eared  animals,  such  as  the  rabbit,  the  ear  falls  as  soon  as  the 
nerve  is  cut.  Certain  persons  with  facial  paralysis  show  increased  power 
of  hearing  on  the  paralyzed  side.  This  phenomenon  may  be  thus  ex- 
plained :  The  tensor  tympani  supplied  by  the  small  superficial  petrosal  nerve 
and  the  stapedius  muscle,  which  also  receives  a  twig  from  the  facial  nerve, 
constitute  the  motor  apparatus  of  the  chain  of  ossicles.  The  tensor  tympani 
has  as  its  function  the  stretching  of  the  membrana  tympani — that  is  to  say, 
to  diminish  the  amplitude  of  the  vibrations,  and  consequently  to  moderate 


PARALVRKS  1507 

the  intenslt;^  of  liie  soiiiul-vvavcs.  Tlioso  coMdilioiis  arc  no  longer  fulfilled 
when  tiio  niusule  is  paralyzed  and  the  sense  of  hearing  becomes  more  acute 
(Landouzy). 

Facial  paralysis  of  intrali-nijioral  ori;j;iii  is  produced  by  many  lesions — 
fractures,  otitis,  syphilitic  lesions,  tubercular  caries  of  the  petrous  bone. 
Cold,  which  so  often  causes  peripheral  paralysis,  may  also  cause  this  variety. 
The  nerve  affected  by  cold  undergoes  an  inllammatory  swelling  (Berard, 
Erb),  and  is  then  compressed  in  different  points  of  its  course  or  at  its  exit 
from  the  Fallojiian  aqueduct.  This  explanation  of  paralysis  a  frigore, 
which  has  also  been  given  for  peripheral  paralysis,  must  not  be  applied  to 
all  cases  of  paralysis  from  cold. 

3.  Paralysis  of  Bulbar  Origin. — The  facial  nerve  has  two  nuclei  in  the  bulb  :  (1)  an 
upper  nucleus,  in  couimon  with  the  sixth  nerve,  and  situated  in  the  floor  of  the  fourth 
ventricle,  at  the  lower  border  of  the  pons  ;  (2)  an  inferior  nucleus,  in  connnon  with  the 
motor-root  of  the  fifth  nerve  (Pierrot),  and  situated  between  the  nucleus  of  the  hypo- 
glossal and  spinal  accessory  nerves.  It  is  easy  to  follow  the  fibres  of  the  facial  nerve, 
which  start  from  these  nuclei,  in  order  to  go  from  the  bulb  to  the  pei-iphery.  The 
cerebral  fibres  of  the  inferior  facial  nerve  arise  at  the  foot  of  the  ascending  frontal  con- 
volution, descend  with  the  geniculate  bundle,  and,  after  passing  through  the  lower 
part  of  the  cerebral  jjcduncle,  enter  the  pons,  where  they  cross,  in  order  to  join  lower 
down  the  fibres  arising  from  tlie  bulbar  nuclei.  This  intercrossing  of  the  fibres  of  the 
facial  nerve  takes  place  about  the  middle  of  the  pons. 

The  region  wliich  extends  from  the  crossing  of  the  cerebral  fibres  of  the  facial  nerve 
to  the  bulbar  nuclei  comprises  the  inferior  half  of  the  pons,  a  region  which  also  com- 
prises the  tract  of  the  motor  fibres  destined  for  the  limbs,  with  this  difference — that 
these  fibres  cross  lower  at  the  decussation  of  the  pyramids.  The  resxUt  is  that  a  lesion 
(tumour,  haemorrhage,  softening)  in  this  part  of  the  pons  may  attack  both  the  fibres 
which  have  crossed  and  the  motor  fibres  of  the  limbs  prior  to  their  crossing.  In  this 
way  a  crossed  paralysis  results  (Gubler).  The  paralysis,  as  far  as  the  face  is  concerned, 
is  on  the  same  side  as  the  lesion,  whilst  it  is  on  the  opposite  side  as  far  as  the  limbs  are 
concerned. 

Facial  hemiplegia  of  bulbar  origin  is,  therefore,  associated  with  crossed 
hemiplegia  of  the  limbs.  Furthermore,  it  is  complete — ^that  is  to  say,  it 
attacks  the  orbicularis  palpebrarum,  as  well  as  the  orbicularis  oris — and 
the  muscles  lose  their  electrical  contractility,  as  in  the  peripheral  paralysis, 
previously  described. 

4.  Paralysis  of  Cerebral  Origin. — Facial  paralysis  of  cerebral  origin 
must  be  divided  into  two  varieties,  according  as  the  cerebral  lesion  is  central 
or  cortical. 

(1)  The  central  lesions  of  the  brain  (haemorrhage,  softening,  tumour) 
are  accompanied  by  ordinary  hemiplegia,  whether  the  lesion  occupies  the 
opto-striate  nuclei,  the  internal  capsule,  or  the  fronto- parietal  bundles  of 
the  centrum  ovale.  The  facial  hemiplegia  is  on  the  same  side  as  the  hemi- 
plegia of  the  limbs,  and  presents  the  following  characters  :  The  face  is 
paralyzed  in  the  lower  portion  only ;  the  orbicularis  palpebrarum  is  almost 


1568  TEXT-BOOK  OF  MEDICINE 

always  spared  ;  the  paralysis  is  rarely  as  marked  as  in  cases  of  peripheral 
origin  ;  the  faradic  contractility  is  preserved,  and  the  sweating  reaction  to 
pUocarpin  is  equal  on  both  sides  (Strauss). 

The  absence  of  paralysis  in  the  orbicularis  palpebrarum  in  facial  hemi- 
plegia of  cerebral  origin  has  been  variously  interpreted.  In  the  first  place, 
the  integrity  of  the  muscle  is  not  always  absolute  ;  it  is  latent,  and  requires 
to  be  sought  for.  In  order  to  explain  the  majority  of  the  cases — that  is  to 
say,  the  apparent  integrity  of  the  orbicularis  palpebrarum — we  might  adopt 
Broadbent's  opinion.  In  hemiplegia  of  cerebral  origin  the  immunity  is  not 
limited  to  the  orbicularis,  but  is  common  to  all  the  muscles  performing 
associated  movements.  Such  are  the  muscles  of  the  eyes,  of  the  trunk, 
and  of  the  larynx.  It  is  probable  that  the  nuclei  of  the  nerves  of  these 
muscles  are  united  together  by  commissures,  which  allow  the  healthy 
nucleus,  in  a  certain  measure,  to  supplement  the  destroyed  nucleus. 

Three  cases  of  hemiplegia  have  been  collected  (Huguenin,  Chwostek, 
Hallopeau)  in  which,  contrary  to  the  general  rule,  there  was  complete 
paralysis  of  the  orbicularis.  In  these  cases  a  haemorrhage  involved  the 
lenticular  nucleus.  It  is,  therefore,  probable  that  the  upper  fibres  of  the 
facial  nerve,  arising  in  a  part  of  the  cerebral  cortex  as  yet  undefined,  traverse 
the  lenticular  nucleus,  and  continue  their  course  to  the  internal  part  of  the 
cerebral  peduncle.  In  order  to  go  from  the  lenticular  nucleus  to  the  cerebral 
peduncle,  they  certainly  do  not  follow  the  internal  capsule,  because  the 
lesions  of  this  tract  do  not  paralyze  the  orbicularis.  It  is  probable  that  they 
follow  the  ansa  lenticularis.  In  the  cerebral  peduncle  they  meet  with  the 
lower  fibres  of  the  facial  nerve,  which  passes  down  in  the  geniculate  bundle 
of  the  internal  capsule,  and  the  two  united  bundles  cross  in  the  middle  of 
the  pons,  and  continue  their  course  through  the  bulb.  An  objection  has 
been  raised  to  the  hypothesis  that  a  lesion  of  the  lenticular  nucleus  had  been 
in  these  cases  the  cause  of  the  paralysis  of  the  superior  facial  nerve.  If  it 
were  so,  it  has  been  argued,  we  ought  to  find  paralysis  of  the  orbicularis  in 
cases  of  obliteration  of  the  Sylvian  artery,  because  the  arteries  of  the  corpus 
striatum  come  exclusively  from  the  Sylvian  artery  (Duret),  and  the  superior 
facial  nerve  might  well  have  its  origin,  not  in  the  lenticular  nucleus,  but  in 
the  ansa  lenticularis  (Mathias  Duval).  The  answer  is  (Hallopeau)  that  the 
distribution  of  the  Sylvian  artery  varies,  that  in  many  cases  other  arterioles 
from  the  anterior  cerebral  artery  or  from  the  anterior  choroidal  artery 
enter  the  lenticular  nucleus,  and  that,  consequently,  obliteration  of  the 
Sylvian  artery  does  not  necessarily  cause  softening  of  the  lenticular  nucleus. 

(2)  Cerebral  lesions  of  cortical  origin  may  cause  facial  hemiplegia 
similar  to  the  facial  hemiplegia  of  central  origin.  The  inferior  facial  nerve 
alone  is  paralyzed.  The  electro-muscular  contractility  is  preserved,  and 
the  facial  paralysis  is  associated  with  hemiplegia  of  the  limbs  on  the  same 


r.VRALYSES  l.Oii'.i 

side.  Ncvertlicless,  this  association  is  less  comiilote  than  in  the  central 
lesions.  The  f.iciiil  juinilysis  is  the  cliief  feature,  and  to  it  is  addfid  tuoiio- 
plegia  or  iii)liasia,  according  to  the  site  and  to  the  extent  of  the  cortical 
focus. 

Atheroma,  softening,  meningitis,  and  tumours  are  the  most  commrm 
causes  of  facial  paralysis  of  cortical  origin.  The  lesion  is  situated  at  the 
base  of  the  ascending  frontal  convolution,  the  supposed  origin  of  the  inferior 
facial  nerve,  and  when  hemiplegia  of  the  limbs  is  also  present,  the  lesion 
occupies  the  upper  two-thirds  of  the  ascending  frontal  and  parietal  con- 
volutions or  the  paracentral  lobule. 

Prognosis  —  Termination. — According  to  Erb,  three  forms  of  facial 
paralysis  must  be  distinguished— slight,  grave,  and  moderate,  the  symptoms 
of  which  are  summed  up  by  Grasset  in  the  following  manner  : 

1.  In  the  slight  form  there  is  no  change  in  galvanic  or  faradic  reactions 
in  the  muscles  or  in  the  nerves.  In  these  cases  the  prognosis  is  very  favour- 
able.    Recovery  generally  takes  place  in  two  to  three  weeks. 

2.  In  the  grave  form  we  find  complete  reaction  of  degeneration  ;  diminu- 
tion and,  later,  abolition  of  the  galvanic  and  faradic  excitability  of  the 
nerves  ;  loss  of  the  faradic  excitability  of  the  muscles  ;  quantitative  increase 
and  qualitative  alteration  of  the  galvanic  excitability  of  the  muscles  ; 
increase  of  their  mechanical  excitability.  The  prognosis  is  essentially 
unfavourable.  The  duration  varies  from  three  to  six  months.  Contractures 
often  appear. 

3.  Between  these  two  extreme  types  every  intermediate  t)^e  exists. 
Contracture  is  the  worst  complication  of  facial  hemiplegia,  and  must  be 

studied  in  detail.  When  the  facial  paralysis  forms  part  of  an  ordinary 
hemiplegia  (cerebral  lesions),  the  secondary  contracture,  so  frequent  in 
the  muscles  of  the  limbs,  is  very  rare,  and  is  but  little  marked  in  the  muscles 
of  the  face.  When  the  facial  hemiplegia  is  of  peripheral  origin,  permanent 
contractures  of  the  muscles  of  the  face  are  to  be  feared.  These  contractures 
were  most  accurately  described  by  Duchenne  in  his  "  Traite  de  1' Electri- 
sation Localisee."  They  may  attack  aU  the  paralyzed  muscles  or  only 
some  of  them.  They  appear  three  or  four  months,  or  even  longer,  after 
the  onset  of  the  paralysis.  They  are  often  announced  by  premonitory 
signs  :  spasms  supervening  in  the  paralyzed  muscles  under  the  miluence 
of  their  natural  excitability,  too  rapid  return  of  the  tonic  force  in  the  para- 
l}'zed  muscles  (Duchenne),  and  spontaneous  shocks  analogous  to  the  con- 
vulsive tic  of  the  face,  are  the  precursory  signs  of  contracture. 

''  The  return  of  the  tonicity  to  the  normal  condition  usually  takes  place 
in  a  certain  order.  It  generally  requires  two  or  three  weeks  in  paralysis 
of  the  facial  nerves  of  the  second  degree  for  the  first  tonic  movement  to 
become  manifest.     The  buccinator  muscle  seems  to  be  the  Urst  to  recover 


1570  TEXT-BOOK  OF  MEDICIKE 

its  tonic  power,  and  then  come,  in  tke  following  order,  the  zygomaticus 
major,  the  zygomaticus  minor,  the  levator  communis  alse  nasi  et  labii 
superioris,  the  muscles  of  the  pinna,  the  depressor  labii  inferioris,  the  depressor 
anguli  oris,  the  levator  menti,  the  orbicularis  oris,  the  orbicularis  palpe- 
brarum, the  frontalis,  the  corrugator  supercilii,  the  compressor  naris,  and 
the  dilator  alee  nasi.  These  details  are  of  importance,  because  if  one  of 
these  muscles  recovers  its  tonicity  more  rapidly  than  usual  (during  the  first 
week),  especially  when  the  muscle  recovers  its  tonicity  out  of  its  turn, 
it  means  the  commencement  of  a  contracture  which  will  accentuate  the 
features  more  than  in  the  normal  condition,  and  which  will  become  gradually 
worse  "  (Duchenne). 

The  contracture  rarely  afEects  all  the  paralyzed  muscles.  Certaia  muscles 
—the  zygomatic  muscles  and  the  buccinator — are  more  often  attacked  than 
the  others.  In  proportion  as  the  contracture  becomes  marked,  the  features 
of  the  face  which  were  defective  and  weakened  during  the  paralysis  first 
become  regular  and  then  deformed  in  an  opposite  direction,  the  face 
assuming  the  most  strange  expressions. 

The  contracted  muscles  are  often  affected  by  convulsive  movements. 
In  the  long  run  they  may  retract  and  greatly  impair  the  various  move- 
ments. The  causes  of  these  contractures  are  numerous,  but  it  is  certain  that 
the  improper  use  of  electrical  currents  plays  an  important  part. 

Diagnosis — Treatment. — The  diagnosis  of  facial  hemiplegia  is  easy. 
One  cause  of  error,  however,  deserves  notice.  We  must  not  attribute  the 
deviation  caused  by  a  contracture  of  the  left  side  to  a  paralysis  of  the  right 
side.  This  error  is  easily  avoided  when  the  contracture  is  well  marked  ; 
but  this  is  not  always  the  case,  and  if  the  reader  will  refer  to  the  section  on 
Hysteria,  he  will  find  that  several  authors  have  wrongly  described  a 
contracture  as  facial  hemiplegia,  because  facial  paralysis  is  rare  in  hysteria. 

The  treatment  of  facial  paralysis  varies  according  to  the  cause.  We 
must  always  think  of  syphilis,  which  may  in  aU  its  stages  be  the  cause 
of  facial  paralysis.  Faradization  is  the  best  treatment  for  facial  paralysis. 
The  treatment  is  the  same  in  the  case  of  contracture,  but  faradization  must 
be  used  with  the  greatest  care,  because  it  may  lead  to  the  development  of 
contractures. 

Summary. — 1.  Facial  paralysis  of  peripheral  origia  presents  the  follow- 
ing characteristics  :  The  hemiplegia  is  generally  total — that  is  to  say,  the 
inferior  and  the  superior  facial  nerves  are  afEected.  It  is  often  preceded 
or  accompanied  by  pain  in  the  paralyzed  regions.  It  completely  abolishes 
mimicry  and  expression  on  the  paralyzed  side.  The  reflex  movements  are 
lost,  and  various  changes  are  noticed  in  the  electrical  excitability.  Accord- 
ing to  circumstances,  the  paralysis  is  slight  and  easily  curable,  or  severe, 
of  long  duration,  and  sometimes  followed  by  contractures.     In  the  case  of 


I'AUALVSKS  1'.71 

Bcvorc  paralvsis  tho  sweating  reaction  caiisi'd  f)v  [iil<>(;ir[)in  is  (l«'la\<il  <iii 
the  paralyzed  side. 

2.  Facial  henii])legia  of  intratemporal  origin  presents  the  same  para- 
lytic symptoms  as  the  preceding  variety,  but  it  also  presents  change  of 
taste,  deviation  of  the  uvula,  and  excessive  aciiteness  of  the  sense  of  hearing, 
due  to  the  paralysis  of  the  nerve  branches  arising  in  the  interior  of  the 
Fallopian  aqueduct. 

3.  Facial  paralysis  of  bulbar  origin  resembles  paralysis  of  peripheral 
origin  in  many  symptoms,  but  it  differs  in  that  the  facial  hemiplegia  is 
accompanied  by  crossed  hemiplegia  of  the  limbs. 

4.  Facial  paralysis  of  central  origin  differs  from  the  preceding  varieties 
in  many  ways.  It  is  this  variety  which  accompanies  common  hemiplegia. 
The  paralysis  spares  the  superior  facial  nerve  and  the  orbicularis  palpe- 
brarum, and  only  attacks  the  inferior  facial  nerve.  The  reflex  movements 
are  preserved  ;  the  faradic  contractions  are  normal ;  the  sweating  reaction 
with  pilocarpin  is  identical  on  both  sides  ;  the  facial  paralysis  is  on  the 
same  side  as  the  hemiplegia  of  the  limbs ;  secondary  contractures  are 
extremely  rare. 

5.  Facial  paralysis  of  cortical  origin  closely  resembles  facial  hemiplegia 
of  central  origin.  The  inferior  facial  nerve  alone  is  paralyzed.  The  electro- 
muscular  contractility  is  preserved,  and  the  facial  hemiplegia  is  associated 
with  paralysis  of  the  limbs  on  the  same  side.  Nevertheless,  this  association 
is  less  complete  than  in  the  central  form.  The  facial  paralysis  is  the  chief 
feature,  and  monoplegia  or  aphasia  is  joined  to  it,  according  to  the  site  and 
to  the  extent  of  the  cortical  focus. 

II.  SYPHILITIC  FACIAL  PARALYSIS. 

Syphilitic  paralysis  of  the  facial  nerve  may  be  early  or  late  :  early  when 
it  appears  during  the  secondary  stage  ;  late  when  it  supervenes  years  after 
the  infection  during  the  tertiary  stage.  Between  these  two  extreme.^, 
every  intermediate  variety  is  met  with. 

1.  Early  Paralysis. 

Clinical  Cases. — A  young  woman  under  my  care  had  been  suflFering  from  syphilis 
for  three  months  ;  she  had  a  maculo- papulous  roseola,  mucous  patches  in  the  throat, 
and  enlarged  glands  in  the  groin.  Since  the  appearance  of  these  secondary  symptoms 
the  patient  complaiued  of  pain  in  the  ear  and  in  the  right  side  of  the  face  ;  the  headache 
was  so  severe  that  she  could  not  sleep.  She  had  lost  her  appetite,  and  was  so  tired  that 
she  was  often  compelled  to  keep  her  bed— symptoms  frequent  in  a  woman  at  the 
commencement  of  syi^hihs,  as  Foumier  has  pointed  out.  One  morning  the  patient 
perceived  that  her  mouth  was  shghtly  diawn  to  the  left ;  she  could  not  close  her  left 
eye,  and  the  tears  flowed  on  to  her  cheek.  The  earache  grew  worse.  When  I  examined 
the  patient  (eight  days  after  the  commencement  of  the  paralysis),  I  found  right  facial 


1572  TEXT-BOOK  OF  MEDICINE 

hemiplegia :  the  mouth  was  diawii  over  to  the  left,  the  Lines  of  the  face  and  of  the 
forehead  were  effaced  on  the  right  side,  and  the  right  nostril  was  partially  closed ;  the 
right  eye  was  wide  open,  and  could  not  be  completely  closed ;  epiphora  was  present ; 
the  sense  of  taste  in  the  right  half  of  the  tongue  was  blunted ;  no  deviation  of  the 
uvula  and  no  auditory  troubles  were  present.  I  prescribed  mercury  and  iodide  of 
potassium.  The  first  result  of  the  treatment  was  to  diminish  the  headache,  and  to 
reheve  the  insomnia.  In  ten  clays  noticeable  amehoration  of  the  facial  paralysis  was 
evident :  the  mouth  was  less  twisted,  the  eye  closed  better,  and  the  epiphora  was 
insignificant.     In  three  weeks  recovery  was  complete. 

Bahuaud  :  A  man  had  a  chancre  and  glands  in  the  left  groin.  Eighteen  days  later 
a  roseola  appeared,  and  eight  days  later — that  is  to  say,  twenty-six  days  after  the 
chancre — the  patient  perceived  that  the  left  side  of  his  face  was  paralyzed.  He 
consulted  Bahuaud,  who  found  facial  hemiplegia.  The  left  side  of  the  face  was 
expressionless ;  the  cheek  was  fiaccid  and  pendulous,  and  was  often  nipped  between 
the  teeth  during  the  movements  of  speech  ;  the  food  collected  between  the  jaw  and  the 
cheek ;  and  the  mouth  was  drawn  upwards  and  outwards.  The  patient  could  neither 
whistle  nor  retain  the  air  in  his  mouth  during  the  efforts  of  expiration.  The  left  eye 
did  not  close,  and  the  movement  of  winking  was  impossible.  No  other  cause  except 
syphihs  could  be  discovered  to  explain  the  facial  paralysis.  Mercurial  treatment  was 
immediately  commenced.  In  a  week  the  patient  was  better.  The  deviation  of  the 
mouth  was  less  marked;  expectoration  was  more  easy.  In  three  weeks  recovery  was 
complete. 

The  following  cases  are  taken  from  Dargaud's  thesis  : 

Marty  :  A  man,  aged  twenty-five  years,  with  chancre  and  glands  in  the  groin, 
was  seized,  five  weeks  later,  with  roseola  and  paralysis  of  the  right  side  of  the  face.  The 
eye  could  not  be  closed ;  the  right  nostril  could  not  be  dilated  ;  the  mouth  was  drawn 
over  to  the  left ;  the  saliva  escaped  continually  from  the  right  angle  of  the  mouth  ;  the 
cheek  was  flaccid,  and  the  food  accumulated  behind  the  dental  arch.  Vidal  de  Cassis : 
A  man  had  a  syphihtic  chancre  in  February.  The  roseola  appeared  soon  afterwards, 
and  in  April — that  is  to  say,  two  months  after  the  syphihtic  infection — facial  hemiplegia 
of  the  left  side  declared  itself,  with  loss  of  taste  in  the  left  half  of  the  tongue.  After 
eight  days  of  mercurial  treatment  the  paralysis  had  disappeared. 

In  all  these  cases  of  early  syphilitic  paralysis  the  paralysis  was  unilateral. 
In  other  cases  the  paralysis  is  double,  and  attacks  both  facial  nerves.  To 
quote  an  example  ; 

A  man  was  admitted  to  the  Necker  Hospital  with  a  papular  roseola,  mucous  patches 
in  the  throat,  and  facial  paralysis  on  the  left  side.  The  infection  was  of  two  months' 
duration.  The  paralysis  was  classical.  The  patient  was  put  on  specific  treatment  (piUs 
of  proto-iodide  of  mercury  and  iodide  of  potassium).  A  week  later  facial  paralysis  of 
the  right  side  (facial  diplegia)  appeared.  The  face  then  assumed  the  strange  aspect  of 
an  expressionless  mask.  The  improvement  was  gradual,  and  the  cture  supervened  in 
two  months. 

Double  syphilitic  facial  paralysis  has  been  laiown  for  a  long  time.  In 
1836  BeU  reported  a  case  seen  by  Dupuytren  in  1828. 

Foumier :  In  a  man  who  had  two  syphihtic  chancres  facial  paralysis  of  the  left  side 
declared  itself  three  months  after  the  infection.  The  mouth  was  drawn  over  to  the 
right ;  the  right  cheek  was  flaccid,  and  was  shghtly  puffed  out  during  expuration. 
The  patient  could  neither  whistle  nor  blow  ;  he  could  only  half  close  the  right  eye. 
Two  days  later  facial  paralysis  appeared  on  the  right  side.     "  The  face,"  said  Fournier, 


PARALYSES  1573 

"  prcsontod  a  strange  oxprossion  of  iiiiinol)ility  and  HottiBlincsB."  The  difliuiiltv  in 
mastication  was  so  groat  that  tho  food  accumulated  botweon  the  tooth  and  the  lifis, 
and  then  foil  out  of  tho  mouth.  Tho  mercurial  and  iodide  treatment  was  proscribed  as 
soon  as  the  paralysis  appeared.  In  thirteen  days  the  effect  was  noticeable  :  the  patient 
could  close  liis  eyes  almost  complott^ly,  tho  movements  of  the  lips  wereea.sier,  and  food 
was  bott^ir  rotnined  in  tho  mouth.  .After  twonty-threo  days'  treatrnc^nt  tho  improvement 
was  very  apparent :  the  oj^os  closed  completely,  tho  patient  ate  with  much  greater  ease. 
In  two  months  "  there  was  not  a  trace  of  tho  double  facial  paralysis  with  which  the 
patient  had  been  afleeted." 

Bouvorot :  A  man  had  on  tho  dorsal  surface  of  his  prepuce  the  indurated  cicatrix  of 
a  chancre  iind  enlarged  glands  in  both  groins.  Over  the  whole  of  tho  body  there  was  a 
fading  roseola.  During  the  course  of  the  secondary  troubles,  probably  in  tho  second  or 
third  month  after  infection,  facial  paralysis  of  the  left  side  appeared.  When  tho  patient 
was  admitted  to  hospital,  the  paralysis  had  existed  for  about  a  fortnight :  inability 
to  close  the  eye  and  marked  epiphora  ;  great  deviation  of  the  right  angle  of  the  mouth  ; 
immobiUty  and  pulhng  do\vn  of  the  left  angle  ;  inabiUty  to  whistle.  Specific  treatment 
was  at  once  prescribed.  The  facial  hemiplegia  on  the  left  side  was  improving,  when 
paralysis  of  the  right  side  set  in.  The  improvement  was  gradual,  and  the  patient  left 
the  hospital  before  the  complete  cure  of  this  double  facial  paralysis. 

•  I  have  quoted  several  cases  in  order  to  convince  the  reader  that  early 
syphilitic  facial  paralysis  is  not  rare.  We  can  count  by  dozens  the  cases  of 
unilateral  or  of  bilateral  facial  paralysis  supervening  within  a  few  months 
of  the  syphilitic  infection.  Many  years  ago  Foumier  expressed  this  opinion, 
which  has  since  been  absolutely  justified.  "  Of  the  paralyses  in  secondary 
syphilis,"  said  he,  "  the  most  common  is  facial  hemiplegia.  Let  me  add 
that  it  is  also  the  earliest."  The  precocity  of  this  syphilitic  complication 
is,  in  fact,  remarkable.  In  looking  over  fifteen  cases  in  which  the  onset  of 
the  paralysis  is  clearly  stated,  I  find  the  following  distribution  : 

The  facial  paralysis  appeared  once  in  the  seventh  month  of  the  syphilitic 
infection,  once  in  the  sixth  month,  once  in  the  fourth  month,  four  times 
in  the  third  month,  seven  times  in  the  second  month,  and  once  in  the  first 
month. 

The  name  of  "  early  "  is,  therefore,  well  applied  to  this  kind  of  paralysis, 
as  its  most  common  time  of  appearance  is  two  or  three  months  after  the 
infection.  Even  the  most  severe  syphilitic  troubles  may  appear  a  few 
months  after  the  infection.  It  is  important  to  remember  this  fact,  as  I 
never  fail  to  point  out  whenever  the  opportunity  presents  itself.  In  my 
lectures*  on  syphilitic  nephritis  I  have  quoted  cases  in  which  acute  sj^hilitic 
nephritis  appeared  in  the  second,  third,  and  fourth  months  of  the  infection. 
In  the  section  on  Cerebral  Syphilis  I  have  reported  several  examples  of 
early  cerebral  arteritis,  supervening  only  a  few  months  after  the  chancre, 
and  ending  in  apoplexy  and  in  death  by  the  rupture  of  an  aneurysm,  or 
in  hemiplegia,  by  obliteration  of  the  vessel  (obliterating  endarteritis).     I 

*  "  Nephrite  SyphiUtique  et  Syphilis  du  Rien  "  (Clin.  Med.  de  VHotel-Dieu,  Paris, 
1898,  p.  242). 

II.  100 


1574  TEXT-BOOK  OF  ilEDICINE 

have  repeatedly  met  Trith.  early  syphilitic  myelitis  supervening  during  the 
first  year  of  the  infection,  and  ending  fatally  in  some  cases. 

I  repeat,  then,  that, -with  regard  to  events  in  syphilis,  "time  has  nothing 
to  do  Tvith  the  case,"  because  grave  troubles  may  appear  verv  soon  after 
the  infection.  We  must  finish,  once  and  for  always,  with  the  narrow 
classification,  "  secondary  troubles  and  tertiary  troubles."  It  has  been 
the  custom  to  consider  the  secondary  (or  early)  troubles  as  being  much 
less  formidable  than  the  tertiary  (or  late)  ones.  In  manv  cases  this  is 
true,  but  the  exceptions  are  so  numerous  that  they  have  been  classified 
under  the  rubric  of  "  early  tertiarism  "  (Fournier). 

Description. — Let  us  consider  the  history  of  early  syphilitic  facial 
paralysis.  The  onset  is  sudden,  and  from  the  outset  the  facial  nerve  is 
paralyzed  throughout  its  entire  extent.  The  paralysis  does  not  instal  itself 
in  a  slow  and  progressive  manner.  "We  do  not  see  it  commencing  in  the 
mouth  and  spreading  in  a  few  days  to  the  cheek  and  the  eyelid.  From 
its  appearance,  or  thereabouts,  the  paralysis  attacks  the  whole  of  one  side 
of  the  face.  The  patient  notices  that  his  mouth  is  twisted,  and  at  the 
same  time  he  finds  some  difficulty  in  closing  his  eye.  The  saliva  drools 
from  the  angle  of  the  mouth  and  the  tears  fall  on  to  the  cheek.  From  the 
outset  the  paralysis  is  general,  like  the  peripheral  form  due  to  cold.  The 
superficial  branches  of  the  facial  nerve  may  be  alone  attacked,  or  the  deep 
branches  (intratemporal)  may  be  also  afiected.  Loss  of  taste  in  the  anterior 
two-thirds  of  the  tongue  on  the  paralyzed  side  (chorda  tjnnpani),  deviation 
of  the  uvula  (palatine  nerves),  changes  in  the  power  of  hearing  (nerves 
supplying  the  motor  system  of  the  ossicles),  are  seen  in  the  intratemporal 
form  of  facial  paralysis. 

The  interpretation  of  these  early  paralyses  is  difficult.  Are  they  due 
to  an  osseous  or  a  meningeal  lesion  compressing  the  facial  nerve  at  its 
entrance  into,  or  during  its  course  through,  the  aqueductus  FaUopii  ?  While 
it  is  not  impossible,  it  is  not  probable.  Are  they  due  to  a  central  lesion  of 
the  nuclei  of  origin  of  the  facial  nerve  ?  This  is  hardly  likely,  because  the 
whole  nerve  is  affected  from  the  outset,  whilst  the  nuclei  of  the  superior 
and  inferior  facial  branches  are  distinct  in  the  bulb.  It  is  more  rational 
to  admit  a  toxic  peripheral  neuritis. 

This  theory,  applicable  to  unilateral  facial  paralysis,  is  less  admissible 
when  the  paralysis  is  double.  In  the  latter  case,  is  the  paralysis  due  to  a 
central  lesion  instead  of  peripheral  neuritis  ?  I  do  not  think  so.  In  the 
first  place,  the  paralysis  is  not  double  at  first.  In  two-thirds  of  the  cases 
which  I  have  quoted  the  second  paralysis  supervened  some  days  after  the 
first,  and  it  is  therefore  reasonable  to  suppose  in  such  a  case  that  syphilis 
determines  two  symmetrical  paralyses,  symmetry  being  fairly  common 
in  syphilis.     "WTien  the  Sylvian  artery  or  some  other  artery  at  the  base  of 


PARALYSES  1575 

the  skull  is  attacked  by  syphilitic  arteritis,  it  is  common  to  find  a  hviu- 
motrical  lesion  in  the  artery  of  the  opposite  side.  When  a  patient  has 
syphilitic  hemiplegia,  due  to  obliterating  endarteritis  of  one  Sylvian 
artery,  we  sometimes  see  a  second  hemiplegia  (I  have  met  with  such  a 
case)  caused  by  a  symmetrical  lesion.  In  a  case  in  which  Lcudet  was  able 
to  observe  closely  8\^hilitic  obliterating  arteritis  of  the  left  superficial 
temporal  artery,  he  found  later  a  symmetrical  arteritis  of  the  right  super- 
ficial temporal  artery.  We  have,  then,  numerous  examples  of  syphilitic 
symmetry.  I  am,  therefore,  of  opinion  that  facial  paralysis,  becoming 
double  within  a  few  days,  is  a  question  of  symmetry. 

Diagnosis. — Let  us  next  consider  the  question  from  another  point  of 
view.  Facial  paralysis  in  a  syphilitic  patient  does  not  make  its  appearance 
without  causing  some  trouble  to  the  patient  and  to  the  physician.  We  ask 
whether  the  paralysis  is  not  an  indication  of  more  or  less  grave  cerebral 
lesions  (early  syphilitic  hemiplegia  being  common).  An  individual  who 
has  had  a  syphilitic  chancre  and  secondary  symptoms  for  some  months 
wakes  up  with  his  mouth  twisted.  He  fancies  that  he  is  threatened  with 
apoplexy.  If  we  examine  him  carefully,  we  find  immediately  that  we  have 
to  deal,  not  with  paralysis  of  the  inferior  facial  nerve  associated  with  symp- 
toms of  hemiplegia,  but  with  paralysis  of  the  entire  facial  nerve.  WTiether 
the  paralysis  is  slight  or  severe,  all  the  superficial  branches  of  the  facial 
nerve  are  involved,  and  sometimes  also  the  deep  branches.  The  mouth 
and  the  face  are  drawn  over  to  the  healthy  side  (region  supplied  by  the 
inferior  facial  nerve) ;  the  eye  on  the  paralyzed  side  remains  wide  open, 
the  patient  being  unable  to  close  it ;  the  act  of  winking  is  affected  (region 
supplied  by  the  superior  facial  nerve),  and  a  few  tears  flow  on  to  the  cheek. 
Electrical  examination  often  reveals  a  more  or  less  marked  reaction  of 
degeneration.  Under  such  circumstances  we  can  give  a  favourable  prog- 
nosis as  to  the  localization  of  the  lesion.  The  patient  need  not  fear  hemi- 
plegia or  apoplexy.  The  facial  paralysis  is  not  the  result  of  a  cerebral  lesion, 
because  it  afl'ects  the  superior  and  inferior  facial  nerves.  It  is  peripheral, 
and  though  it  may  last  for  some  time,  it  is  not  of  evil  omen.  Moreover, 
the  most  minute  examination  of  the  patient  fails  to  reveal  any  trace  of 
brachial  or  of  crural  hemiplegia.  The  hand  shows  no  loss  of  power ;  the 
arm  is  not  heavy,  and  easily  executes  all  movements ;  the  gait  is  natural, 
and  the  patient  does  not  drag  his  leg  or  trip  when  going  upstairs. 

S}T)hilitic  facial  paralysis,  limited  to  the  inferior  facial  nerve,  is  very 
different.  In  such  a  case  only  the  lower  part  of  the  face  is  paralyzed.  The 
mouth  is  deviated,  the  angle  is  drawn  over  by  the  muscles  of  the  healthy 
side,  the  cheek  is  flaccid,  and  the  act  of  whistling  or  of  blowing  is  diflicult 
or  impossible  ;  but  the  muscles  supplied  by  the  superior  facial  nerve  have 
apparently  lost  none  of  their  functions.     The  eye  closes  as  well  as  the  one 

100—2 


1576  TEXT-BOOK  OF  MEDICINE 

on  the  opposite  side  ;  the  act  of  winking  is  normal ;  there  is  no  epiphora. 
In  such  a  case  th^  lesion  is  of  cerebral  origin.  The  electro-muscular  con- 
tractility of  the  paralyzed  muscle  is  preserved. 

Moreover,  we  find  that  the  paralysis  is  not  limited  to  the  lower 
part  of  the  face.  The  arm  and  the  leg  on  the  same  side  are  also  paralyzed — 
in  short,  there  is  hemiplegia.  The  symptoms  of  this  hemiplegia  may  be 
slight  or  severe,  but,  however  slight  they  are,  they  nevertheless  exist.  If 
we  question  the  patient,  he  will  say  that  he  has  less  power  in  the  hand,  that 
the  arm  appears  to  be  heavy,  and  that  his  walk  is  defective.  "  All  these 
things  came  on,"  says  he,  "  at  the  same  time  as  the  deviation  of  the  mouth, 
with  or  without  some  speech  troubles." 

This  last  variety  of  facial  paralysis  (affecting  only  the  inferior  facial 
nerve)  comes  under  the  early  syphilitic  hemiplegia,  which  may  supervene 
during  the  first  months  after  infection.  The  dominating  factor  is  not  the 
paralysis  of  the  face ;  it  is  the  more  or  less  marked  hemiplegia  which  strikes 
the  whole  of  one  side  of  the  body,  and  which  is  irrefutable  evidence  of  a 
cerebral  lesion,  the  prognosis  of  which  may  be  very  grave. 

Early  sjrphilitic  facial  paralysis  may,  therefore,  show  two  very  different 
forms.  In  the  first  form,  which  is  the  more  frequent,  the  paralysis  affects 
the  superior  and  the  inferior  facial  nerves  at  the  same  time  ;  the  nerve 
only  is  in  evidence  ;  the  brain  is  spared ;  the  limbs  are  not  paralyzed ;  the 
prognosis  is  benign,  and  the  disease  ought  to  be  called  "  facial  paralysis,  or 
paralysis  of  the  facial  nerve."  In  the  second  form  the  disease  ought  to 
be  called  "  hemiplegia."  The  facial  paralysis  attacks  only  the  inferior 
facial  nerve.  On  the  other  hand,  we  find  a  more  or  less  marked  paralysis 
of  the  arm  and  of  the  leg.  The  lesion  is  cerebral,  and  the  prognosis  is 
doubtful,  being  at  times  very  grave. 

2.  Late  Syphilitic  Paralysis. 

In  these  cases  the  paralysis  appears  many  years  after  the  infection. 
The  pathogenic  criterion  may  not  be  as  conclusive  as  in  the  early  form, 
because  paralysis  supervening  in  an  old  S5rphilitic  patient  may  not  be  syphi- 
litic.    Nevertheless,  the  following  cases  appear  to  me  to  be  conclusive  : 

A  man  admitted  into  the  Hotel-Dieu  said  that  he  had  been  ill  for  the  last  five 
weeks.  At  first  he  felt  very  sharp  pains  in  the  face,  followed  about  a  week  afterwards 
by  general  facial  paralysis  of  the  left  side.  His  mouth  was  drawn  over  to  the  right,  the 
left  cheek  was  flaccid  and  immovable,  the  left  eye  remained  open,  and  winking  was 
impossible.  On  admission  I  found  all  the  symptoms  of  facial  paralysis  :  asymmetry 
between  the  two  sides  of  the  face  ;  immobility  of  the  features  on  the  left  side,  contrasting 
with  the  animation  of  the  features  on  the  right  side.  The  cheek  was  flaccid  and  blown 
out  Mke  an  empty  sail  at  each  expiration,  and  the  mouth  was  strongly  pulled  over  to 
the  right.  When  he  took  a  deep  breath  the  left  nostril  did  not  expand.  The  left  eye 
was  open  more  widely  than  the  right  eye  ;  it  did  not  close  perfectly,  and  the  tears  flowed 


PARALYSES  J  577 

on  to  tli(>  chock.  MiiHlicafion  was  irii|N'(li'i|  \>y  (Im  fcxid,  wlii.h  follcclcd  liclwr-n  tho 
jiiw  and  t  ho  loft,  clu^ok. 

'I'lio  sonso  of  tasto  was  afTccjlod.  A  Rapid  HnhHtanci-,  phu cd  on  thc!  ant<Tior  two- 
thirds  of  tho  li'ft  half  of  tho  tongue,  caused  no  sonHation  of  ta.sl<\  Tho  mouth  wjw  dry, 
and  tlio  patient  noticed  a  diminution  in  tlie  salivary  80cretif>n.  'Jiio  wnsi!  of  hearing  on 
tho  left  side  was  bluntc^d.  Lacaillo  foimd  that  the  reaction  of  degcncfration  woh  very 
marked.  Tlio  patient  was  therefore  sufTering  from  jieriplu'ral  facial  paralysiH  of  the 
loft  side  {infratemporal  variety),  attacking  most  of  tho  8Uf)erfi(ial  and  deep  branches 
of  tho  facial  nervo.  Tliis  facial  paralysis  was  not  accompanied  by  any  woaloiess  in 
the  arm  or  in  the  leg.     There  was  therefore  no  question  of  any  cerebral  lesion. 

I  have  remarked  that  in  this  cixse  tho  paralysis  had  been  preceded  by  very  intense 
pains  in  tho  face,  which  still  continued  at  tho  time  of  his  admission  into  lio.spital.  I 
think  it  well  to  discuss  the  nature  of  these  pains  wliich  constitute  "  the  painful  paralysis 
of  the  seventh  pair."  The  pains  had  commenced  about  eight  days  prior  to  tho  paralysis  ; 
they  involved  tho  entire  left  half  of  the  face.  It  was  evident,  however,  that  their 
distribution  over  tho  face  coincided,  not  wth  the  distribution  of  the  trifacial  nerve 
(sensory  nerve),  but  with  that  of  the  facial  (motor)  nerve.  Tho  pains  had  commenced 
in  tho  ear,  and  had  reached  their  maximum  in  the  auricular  region.  On  the  cheek  and 
on  the  temi^le  tlie  patient  compared  them  to  a  strong  pressure ;  elsewhere,  especially 
in  front  of  and  behind  the  ear,  they  had  a  shooting  character.  Although  they  were 
continuous,  they  also  took  tho  form  of  repeated  paroxysms  during  the  twenty-four  hours. 
During  the  m'ght  they  were  severe  enough  to  keep  the  patient  awake.  These  pains  are 
far  from  I'are  in  facial  paralysis  (whether  the  paralysis  is  or  is  not  syphihtic).  They  were 
very  acute  in  the  ear  and  in  the  face  on  the  right  side  in  one  of  my  patients.  One 
of  i\Iauriac's  patients  "  experienced  very  severe  pains  beliind  the  left  ear  and  in  tho 
mastoid  region."  I  saw  formerty,  with  Vulpian,  a  lady  in  whom  the  pains  preceded  the 
facial  paralysis,  and  persisted  for  six  months.  I  once  had  in  my  ward  a  young  patient 
in  whom  the  painful  paralysis  of  the  facial  nerve  was  accompanied  by  zona.  According 
to  Weber,  the  pains  are  said  to  exist  in  more  than  half  the  cases  of  facial  paralysis. 
The  pains  sometimes  precede  the  paralysis,  sometimes  they  appear  with  it,  and  they 
may  survive  it.  They  are  usually  situated  in  or  behind  the  ear,  in  the  cheek,  in  the 
temple,  and  in  the  forehead. 

What  is  the  meaning  of  these  pains  ?  Are  they  due  to  neuralgia  of  the  trifacial 
nerve  running  parallel  with  the  paralysis  of  the  facial  nerve  ?  Are  they  due  to  a  reaction 
on  the  nervous  filaments,  amongst  others  the  auricular  branch  of  the  pneumogastric, 
which  anastomoses  with  the  facial  nerve  ?  The  explanation  of  these  pains  is  fairly 
simple,  since  we  know  that  the  facial  nerve  is  both  sensory  and  motor.  Wrisberg's 
nerve  appears  to  be  the  sensory  portion  of  the  seventh  pair.  This  nerve,  intermediate 
as  regards  its  situation  between  the  facial  and  the  auditory  nerves,  extends  from  the 
bulbar  exit  of  these  two  nerves  to  the  geniculate  ganglion  of  the  facial  nerve.  "  Its 
signification  remained  doubtful  for  a  long  time.  Anatomists  and  physiologists  looked 
upon  it  as  the  sensory  portion  of  the  facial  nerve,  but  ^vithout  positive  proof,  imtil 
Duval,  by  virtue  of  its  central  origin,  showed  that  it  was  the  detached  or  aberrant 
portion  of  the  glosso- pharyngeal  nerve.  Numerous  researches  have  definitely  proved 
that  it  is  the  equivalent  of  a  posterior  spinal  root ;  it  is  the  posterior  root  of  the  facial 
nerve,  and  its  ganghon  is  the  geniculate  ganglion  "  (Poirier). 

Painful  paralysis  of  the  facial  nerve  is  thus  explained.  This  painful  type  only 
exists  in  paralysis  of  peripheral  or  intratemporal  origin  ;  it  does  not  occur  when  the 
paralysis  is  hmited  to  the  inferior  facial  nerve,  and  forms  part  of  a  hemiplegia  of  cerebral 
origin. 

Let  us  now  return  to  the  patient  who  was  suffering  from  painful  paralysis  of  the 
facial  nerve.  We  had  to  ascertain  the  cause  of  his  paralysis.  There  was  no  evidence  in 
favour  of  cold.     On  the  contrary,  we  had  to  think  of  syphilis,  for  which  he  had  formerly 


1578  TEXT-BOOK  OF  MEDICINE 

l^een  treated  in  Algeria  during  his  term  of  military  service.  Relying  on  this  hypothesis, 
I  prescribed  injections  of  biniodide  of  mercury,  and  the  result  was  remarkable.  We 
must  not  forget  that  in  this  case  the  pains  were  so  severe  that  sleep  was  impossible. 
After  the  fifth  injection  the  pains  disappeared  and  the  insomnia  ceased.  At  the  same 
time  the  paralytic  symptoms  improved  rapidly,  the  deviation  of  the  mouth  grew  less, 
closure  of  the  eye  became  possible,  and  the  sense  of  taste  returned  in  the  tongue.  After 
the  fifteenth  injection  recovery  was  complete.  The  reaction  of  degeneration,  very 
pronounced  before  the  treatment,  had  disappeared  six  weeks  later. 

The  rapid  effect  of  the  mercurial  treatment  would  be  sufficient  to  show  in  this  case 
the  syphihtic  nature  of  the  paralysis,  but  I  have  other  arguments  to  adduce  in  favour 
of  this  opinion.  Three  months  later  the  man  came  back  completely  cured  of  the  facial 
paralysis,  but  this  time  he  had  paralysis  of  the  third  pair,  with  headache.  We  know 
how  frequent  syphilitic  paralysis  of  the  common  oculo -motor  nerve  is.  The  patient  was 
again  submitted  to  mercurial  injections,  and  the  paralysis  of  the  third  nerve  was  cured, 
just  as  the  facial  paralysis  had  been.  He  left  the  hospital,  and  came  back  two  months 
later  with  severe  headache.  There  was  not  the  sHghtest  trace  of  any  paralysis  being  left. 
The  mercurial  treatment  was  again  given,  and  the  headache  disappeared. 

What  do  we  know  about  late  sypMlitic  facial  paralysis  ?  We  must 
divide  it  also  iuto  two  varieties.  To  the  first  variety  belongs  facial  paralysis, 
properly  so  called,  affecting  the  entire  nejve,  the  limbs  being  absolutely 
free  from  any  paralysis.  To  the  second  variety  belongs  the  paralysis  of  the 
inferior  facial,  associated  with  a  more  or  less  complete  paralysis  of  the  limbs. 

The  late  form  of  this  facial  paralysis  rarely  affects  the  entire  facial  nerve, 
and  therefore  differs  from  the  early  form.  The  late  form  "  is  only,  to  speak 
the  truth,  the  previous  erpression  of  a  total  hemiplegia.  It  is,  in  technical 
terms,  a  segment  of  dissociated  hemiplegia  "  (Foumier).  It  is  a  hemi- 
plegia in  which  the  inferior  facial  nerve  participates,  but  the  superior  facial 
nerve  remains  free.  The  eye  closes  well,  the  act  of  winking  is  normal,  and 
the  tears  do  not  flow  on  to  the  cheek.  On  the  other  hand,  symptoms  of 
hemiplegia  are  seen  in  the  limbs  :  the  hand  is  awkward,  the  arm  is  heavy, 
the  leg  is  dragged — in  a  word,  there  is  hemiplegia,  and  the  lesion  is  cerebral. 
In  such  circumstances  the  prognosis  must  be  reserved.  It  always  has  a 
certain  gravity,  whereas  peripheral  facial  paralysis  is  practically  benign. 

III.  PAEALYSIS  OF  THE  MOTOR  NERVES  OF  THE  EYE. 

The  motor  muscles  of  the  eye  are  supplied  by  three  cranial  nerves — ^the 
common  oculo-motor  (third  pair),  the  pathetic  (fourth  pair),  the  external 
oculo-motor  (sixth  pair). 

I  shall  describe  isolated  paralysis  of  these  three  nerves,  next  their 
associated  paralysis,  and,  finally,  ophthalmoplegia. 

1.  Paralysis  of  the  Common  Oculo-Motor  Nerve. 

Anatomy  and  Physiology. — This  nerve  arises  in  the  motor  cells,  below  the  floor 
of  the  aqueduct  of  Sylvius.  From  these  cells  (nucleus  of  origin)  there  arise  certain 
distinct  root  filaments,  which  pass  through  the  cerebral  peduncles,  and  emerge 
outside  the  nerve  centres  in  the  interpeduncular  space,   where    they  unite  into  a 


PARALYSES  1579 

single  trunk,  whioli,  af<cr  s  short  course  aloriR  the  base  of  the  skull,  lies  against 
the  oxt-omal  wall  of  the  cavomous  sinus,  and  then  enters  the  orbit,  whore  it 
soparatos  into  two  branches:  an  up{x>r  branch,  which  supplies  a  twig  to  the  h'vator 
palpobra?,  and  another  to  the  rectus  superior ;  and  a  lower  branch,  which  suppiitis 
three  branches  to  the  internal  rectus,  the  inferior  rectus,  and  the  inferior  oblique  muscle. 
Furthermore,  the  branch  to  the  oblique  muscle  gives  oflF  the  motor  root  of  the  ophthalmic 
gangUon,  and  consequently  furnishes  the  nerve  supply  of  the  iris  and  the  ciliary  muscle. 
The  nervo  therefore  divides  in  the  orbit  into  as  many  branches  as  there  are  muscles  to 
supply. 

If  the  reader  will  refer  to  the  anatomical  points  mentioned  in  the  section  on  Poho- 
encephalitis,  he  will  see  that  the  nucleus  of  the  third  pair,  a  grey  column  situated  under 
the  Hoor  of  the  aqueduct  of  Sylvius,  is  in  reality  formed  of  a  series  of  five  small  nuclei 
for  the  principal  portion  of  the  nucleus,  and  two  in  number  for  the  other  portion  of  the 
nucleus,  situated  in  the  third  ventricle.  The  result  is  that  the  nucleus  of  origin  of  the 
third  nerve  is  divided  into  exactly  as  many  small  secondary  nuclei  as  the  muscles  to  bo 
supplied.  Each  one  of  these  secondary  nuclei  is,  in  fact,  the  nucleus  of  origin  of  the 
fibres  wliich  go  to  each  of  the  muscles  of  the  eye  (Hensen  and  Voelkers,  Kahler  and 
Pick).  The  root  filaments  which  issue  from  each  of  these  nuclei  are  clearly  defined  in 
the  cerebral  pedimcle,  but  soon  unite  to  form  the  common  trunk  of  the  third  nerve. 

It  will  now  be  understood  that  the  paralysis  of  a  certain  muscle  of  the  eye  may  be 
isolated,  the  lesion  attacking  the  terminal  network  of  the  nerve,  or  its  nucleus  of  origin. 
We  can  thus  explain  the  partial  paralyses  of  the  third  pair  of  nerves,  which  in  that 
respect  differ  from  the  paralyses  of  the  sixth  and  of  the  fourth  pair ;  the  latter  are  of 
necessity  always  total,  because  each  of  these  nerves  supplies  only  a  single  muscle,  and 
has  only  one  nucleus  of  origin. 

The  nuclei  of  origin  of  the  nerves  and  the  muscles  of  the  eye  which  these  nerves  supply 
are  situated  on  the  same  side,  the  only  exception  being  the  pathetic  nerve.  This  nerve 
undergoes  total  decussation  in  the  valve  of  Vieussens,  so  that  the  right  nucleus  supplies 
the  left  superior  oblique  muscle,  and  vice  versa.  Let  us  add  that  there  are  between 
certain  nuclei  very  important  connections  for  the  purpose  of  associating  the  muscles 
that  perform  the  same  movement  in  both  eyes. 

Summary. — The  common  oculo-motor  nerve,  by  virtue  of  its  distribution,  presides 
over  the  movements  of  raising  the  upper  eyelid,  over  all  the  movements  of  elevation 
and  of  convergence,  over  almost  all  the  movements  of  lowering  and  rotating  the 
eye  beyond  its  antero-posterior  axis.  We  see  that  abduction  belongs  rather  to  the 
other  nerves  of  the  eye.  The  oculo-motor  nerves  also  govern  the  movements  of  the 
sphincter  of  the  iris,  and  the  function  of  accommodation. 

This  brief  description  shows  the  importance  of  the  total  paralysis  of  the  common 
oculo-motor  nerve,  and  the  disturbance  wliich  it  causes  in  the  external  and  in  the  internal 
movements  of  the  eyeball. 

etiology. — In  proportion  as  the  domain  of  neuropathology  extends, 
the  aetiology  of  ocular  paralysis  becomes  more  exact,  and  we  are  led  to 
abandon  almost  entirely  the  old  denominations  of  essential  and  of  reflex 
paralyses — terms  greatly  abused.,  especially  with  reference  to  the  oculo- 
motor nerve.  It  is  better,  then,  to  mention  cold,  rheumatism,  gout,  etc., 
as  causes  often  invoked,  although  it  is  not  possible  to  give  a  satisfactory 
explanation  of  their  action.     Diabetes  deserves  special  mention. 

The  common  oculo-motor  nerve  is  sometimes  affected  in  the  intoxica- 
tions. The  paralyzing  action  of  lead  on  this  nerve  seems  to  be  fairly  well 
established,  and  Mallet  has  collected  a  considerable  nmuber  of  cases  of 


1580.  TEXT-BOOK  OF  MEDICINE 

paralysis  due  to  the  ingestion  of  black-puddings  and  of  "  liigh  "  sausages.  In 
these  cases  the  action  of  the  ptomaines  is  clearly  established.  Mydriasis 
is  one  of  the  first  symptoms  of  belladonna-poisoning.  We  may  compare 
the  toxic  paralysis  of  the  third  nerve  with  the  paralysis  of  the  accommoda- 
tion so  often  met  with  in  diphtheria. 

Syphilis  often  affects  the  nerve,  either  directly  in  the  form  of  neuritis 
(peripheral  neuritis),  or  indirectly  by  lesions,  such  as  exostoses,  periostitis, 
sclerotic  and  gummatous  meningitis,  arterial  lesions,  gummata,  and  cerebral 
sclerosis.  Meningeal  exudates,  tubercles,  and  orbital  suppuration  may 
compress  the  third  nerve  ;  it  may  be  bruised  or  torn  by  traumatism  or  by 
fracture  of  the  skull.  In  the  new-bom  infant  paralysis  of  the  levator 
palpebrse  is  fairly  frequent,  whether  it  is  a  case  of  accidental  and  transient 
ptosis,  due  to  the  action  of  the  forceps  on  the  branch  to  the  levator,  or 
another  variety,  which  really  deserves  the  name  of  "  congenital  ptosis," 
and  which  seems  to  be  dependent  on  an  arrest  in  the  development  of  the 
nucleus  of  origin  of  the  nerve.  The  most  common  causes  of  paralysis  of  the 
third  nerves  are  affections  of  the  nerve  centres — lesions  of  the  peduncles, 
such  as  gummata,  tubercles,  haemorrhage,  or  softening  ;  changes  in  the 
corpora  quadrigemina,  in  the  grey  matter  below  the  aqueduct  of  Sylvius, 
and  in  the  nuclei  of  the  ventricles.  Tabes,  especially  at  the  commencement, 
brings  on  various  dissociated  transient  and  mobUe  paralyses,  due  either  to 
peripheral  neuritis  or  to  lesions  of  the  nuclei  of  origin. 

The  paralysis  of  the  upper  eyelid  may  depend  on  a  cerebral  lesion  of 
cortical  origin.  In  several  cases  the  blepharoptosis  has  been  associated 
with  a  lesion  in  the  posterior  region  of  the  parietal  lobe,  as  though  the 
levator  palpebrae  had  a  motor  centre  in  the  angular  gyrus.  In  such  a  case 
the  ptosis  is  isolated,  or  is  associated  with  hemiplegia.  The  blepharoptosis 
is  situated  on  the  same  side  as  the  hemiplegia.  It  is  on  the  side  opposite 
to  the  cerebral  lesion. 

In  some  cases  the  paralysis  of  the  oculo-motor  nerve  alternates  with  the 
hemiplegia  of  the  limbs.  This  alternate  paralysis  generally  points  to  a 
lesion  in  the  cerebral  peduncle.  As  a  matter  of  fact,  the  cerebral  peduncle 
contains  the  motor  and  sensory  conductors  which  unite  the  brain  to  the 
periphery.  The  motor  bundles  are  said  to  be  situated  in  the  internal  portion 
of  the  peduncle  and  the  sensory  bundles  in  its  external  portion  (Maynert). 
The  conmion  oculo-motor  nerve  emerges  from  the  internal  surface  of  the 
peduncle,  the  fibres  having  traversed  the  peduncle  without  decussating. 
The  result  of  this  disposition  is  that  a  lesion  of  the  peduncle  may  attack 
at  the  same  time  the  oculo-motor  nerve  and  the  motor  tracts  for  the  limb 
muscles  prior  to  their  decussation.  The  paralysis  will  then  be  crossed^ 
direct  as  far  as  the  motor  nerve  of  the  eye  is  concerned,  and  crossed  in  refer- 
ence to  the  hemiplegia  of  the  limbs. 


PARALYSES  ir.81 

Symptoms. — Tlic  paralysis  may  be  comploto  or  incomplete  (dissoci- 
ated). Let  us  take  a  case  of  complete  paralysis.  The  first  thing  to  striice 
lis  is  ptosis  of  the  upper  eyelid.  The  levator  palpebrto  b  'ing  paralyzed,  the 
eye  remains  more  or  less  closed  by  the  contraction  of  the  orbicularis  supplied 
by  the  facial  nerve.  The  patient,  in  spite  of  every  effort,  cannot  open  the 
eye  ;  in  order  to  see,  lie  throw.s  his  head  backwards,  and  lowers  the  eyeball 
as  much  as  possible  by  means  of  the  superior  oblique  muscle.  This  attitude 
is  characteristic. 

The  globe  of  the  eye  is  motionless,  except  for  certain  movements  down- 
wards and  outwards.  There  is  divergent  strabismus  from  the  contraction 
of  the  external  rectus  (sixth  nerve),  and  the  globe  is  turned  downwards 
by  the  contraction  of  tlie  superior  oblique  muscle  (fourth  pair).  This  devia- 
tion causes  diplopia.  The  subject  sees  two  crossed  images,  with  consequent 
vertigo  and  erroneous  projection  of  objects  in  space.  When  the  ptosis 
is  complete,  as  the  patient  sees  with  the  healthy  eye  alone,  there  is  neither 
diplopia  nor  vertigo. 

The  pupil  is  dilated  and  fixed.  This  mydriasis  is  explained  in  the 
following  manner  :  The  muscular  fibres  of  the  iris,  which  co-operate  in  the 
dilatation  of  the  pupil,  are  supplied  by  the  great  sympathetic  nerve,  and 
the  muscular  fibres  which  co-operate  in  the  contraction  of  the  pupil  come 
from  the  third  nerve,  and  reach  the  iris  through  the  medium  of  the  oph- 
thalmic ganglion.  The  paralysis  of  the  constrictor  fibres  permits  free 
action  to  the  dilator  fibres  of  the  great  sympathetic. 

The  power  of  accommodation  may  be  paralyzed,  because  the  third 
nerve  supplies  the  ciliary  muscle,  which  plays  an  important  role  in  the  act 
of  accommodation  (Briicke). 

Incom'plete  Paralysis. — The  paralysis  of  the  third  nerve  may  be  partial, 
affecting  a  single  branch.  In  this  case  we  may  notice  only  one  isolated 
symptom  — for  instance,  ptosis  in  paralysis  of  the  levator,  mydriasis  in 
paralysis  of  the  sphincter  iridis. 

Paralysis  of  the  internal  rectus  is  the  most  frequent  of  the  partial 
paralyses  of  the  third  nerve.  Its  principal  characteristics  are  defective 
movement  of  the  eye  inwards,  divergent  strabismus,  deviation  of  the  head 
away  from  the  paralyzed  eye,  crossed  diplopia,  with  separation  of  the  images, 
increasing  in  proportion  as  the  object  is  moved  in  the  direction  of  the 
paralyzed  muscle. 

Paralysis  of  the  superior  rectus  is  characterized  by  inferior  and  external 
strabismus,  by  crossed  diplopia,  with  the  false  image  higher  than  the  true 
one,  and  inclined  towards  the  latter,  which  is  only  seen  when  the  patient 
looks  upwards. 

In  paralysis  of  the  inferior  oblique  the  strabismus  is  inferior  and  internal, 
the  diplopia  is  homonymous,  and  only  exists  in  the  upward  look.     The 


1582  TEXT-BOOK  OF  MEDICINE 

Images  are  inclined  in  sucli  a  manner  that  they  are  separated  above,  and 
approacli  one  another  below. 

When  the  inferior  rectus  is  paralyzed,  there  is  superior  and  slightly 
divergent  strabismus,  then  upward  diplopia,  crossed  on  looking  down- 
wards. The  difierence  of  level  in  the  two  images  increases  in  proportion 
as  the  object  is  lowered  and  abducted. 

In  paralysis  of  accommodation  mydriasis  is  nearly  always  present. 
Near  vision  is  indistinct,  and  the  object  is  smaller  than  normal  (micropsia). 

Diagnosis. — In  complete  paralysis  of  the  third  nerve  the  diagnosis  is 
obvious,  and  there  is  no  need  to  look  for  diplopia  and  for  the  respective 
position  of  the  images.  This  examination  is,  on  the  other  hand,  indispens- 
able when  the  paralysis  is  incomplete,  and  especially  when  there  is  simple 
paresis,  in  order  to  ascertain  which  branch  is  attacked,  or  in  order  not  to 
confound  paralysis  of  the  third  nerve  with  that  of  a  neighbouring  nerve.  I 
cannot  discuss  here  the  difierential  character  of  the  varieties  of  diplopia, 
already  described  under  the  symptoms  of  the  various  paralyses.  It  will 
suffice  to  compare  them  in  order  to  avoid  mistakes.  I  must,  however, 
explain  how  we  examine  for  diplopia.  The  patient  is  seated  in  front  of 
the  observer,  both  eyes  open,  and  one  of  them  covered  with  a  piece  of  red 
glass.  The  physician,  who  stands  with  a  lighted  candle  in  his  hand,  places 
himself  some  distance  from  the  patient,  moves  the  candle  to  all  the  points 
of  the  field  of  vision,  and  ascertains  in  the  various  situations  the  respective 
position  of  the  two  images,  an  easy  task,  because,  on  account  of  the  piece 
of  coloured  glass,  the  patient,  who  sees  a  red  and  a  white  image,  can  state 
precisely  their  respective  positions.  The  diagnosis  is  incomplete  if  we 
only  rely  on  the  memory,  the  iuterrogation,  and  the  general  condition  of 
the  patient.  In  paralysis  of  the  thicd  nerve  the  attention  of  the  physician 
must  be  directed  to  the  condition  of  the  central  nervous  system.  For 
example,  in  a  patient  previously  considered  to  be  suffering  from  rheuma- 
tism (because  he  has  complaiued  of  various  paias),  or  from  neuropathy, 
partial  paralysis  of  one  of  the  muscles,  we  may  find  slight  ptosis,  paresis 
of  the  pupH,  or  some  disturbance  of  accommodation,  appearing  suddenly, 
and  disappearing  in  the  same  manner.  We  must  think  of  tabes,  in  which 
these  transient  paralyses  are  often  the  first  symptom. 

I  would  point  out  that  syphilis  is  one  of  the  most  frequent  causes  of 
paralysis  of  the  third  nerve.  If  the  origin  of  the  disease  remains  obscure, 
antisyphilitic  treatment  should  always  be  employed. 

I  have  already  shown  under  the  aetiology  the  great  importance  of  certain 
paralyses  of  the  oculo-motor  nerve  as  regards  cerebral  localizations  (cortical 
paralysis,  crossed  paralysis). 

Course — Duration. — The  commencement  of  the  paralysis  may  be 
sudden  or  gradual.     The  duration  and  the  course  depend  on  the  cause.     In 


PAKALY8ES  lo83 

patients  suffering  from  ataxia,  if  the  paralysLs  of  tlio  onset  is  transient, 
appearing  and  disappearing  several  times,  the  paralysis  of  the  terminal 
period  often  becomes  definite.  The  paralysis  of  cerebral  origin  is  more 
obstinate  than  the  peripheral  paralysis.  Paralysis  of  a  syphilitic  origin  is 
easily  cured,  especially  if  treatment  is  inaugurated  from  the  commence- 
ment— inunction  of  mercury  and  iodide  of  potassium.  A  duration  of  two 
to  three  months  is  not,  however,  exceptional. 

2.  Paralysis  of  the  Fourth  Nerve. 

This  nerve  supplies  the  superior  oblique  muscle,  which  moves  the  eye 
downwards,  and  at  the  same  time  rotates  the  vertical  meridian  inwards. 
It  assists  to  a  slight  extent  the  external  rectus  in  the  movements  of 
divergence,  and  to  a  greater  extent  the  inferior  rectus  in  movement 
downwards. 

Description. — The  objective  symptoms  are  less  pronounced  than  in 
the  other  varieties  of  paralysis.  The  movements  of  the  eye  are  hardly 
affected.  Strabismus  upwards  and  inwards  is  but  little  marked.  The 
head  is,  however,  inclined  downwards  and  towards  the  paralyzed  muscle. 

Diplopia  is  noticed  as  soon  as  the  patient  looks  do-wnwards.  It  is  very 
troublesome,  because  it  interferes  with  walking  and  often  causes  dangerous 
falls.     The  images  are  homonymous. 

The  false  image  is  the  lower  one.  The  difference  of  height  increases 
in  adduction  in  proportion  as  the  object  is  lowered.  It  diminishes  in 
abduction.  The  false  image  is  inclined  in  such  a  manner  that  its  upper  end 
is  near  to  the  true  image.  The  false  image  appears  nearer  than  the  true 
image. 

3.  Paralysis  of  the  Sixth  Nerve. 

Anatomy. — The  sixth  nerve  arises  in  the  floor  of  the  fourth  ventricle,  on  either  side 
of  the  median  raphe,  from  nuclei  which  are  very  close  together  ;  this  origin  explains  the 
fact  that  the  paralysis  is  so  often  double.  The  nerve  has  a  long  course  in  the  cranial 
cavity,  approaching  the  base  of  the  skull,  and  coming  in  relation  vrith  the  apex  of  the 
petrous  bone.  These  anatomical  facts  show  why  the  sixth  nerve,  which  is  very  slender, 
is  often  ruptured  in  fractures  of  the  base  of  the  skuU  (Chevallereau). 

The  sixth  nerve  supplies  the  external  rectus,  which  moves  the  eye  outwards  without 
having  any  influence  on  the  height  or  on  the  vertical  meridian  of  the  pupil ;  it  is 
therefore  a  pure  abductor. 

Description. — This  paralysis,  which  is  the  most  frequent  of  the  diabetic 
paralyses,  presents  very  exact  characters — diminished  mobility  of  the  eye 
outwards  ;  convergent  strabismus,  due  to  the  contraction  of  the  internal 
rectus ;  iacliaation  of  the  head  towards  the  side  of  the  paralyzed  muscle ; 
homonymous  diplopia,  in  which  the  separation  of  the  two  images  increases 
in  proporton  as  the  object  is  moved  towards  the  side  of  the  affected 
muscle. 


1584  TEXT-BOOK  OF  MEDICINE 

Graux  and  Fereol  have  pointed  out  a  rare  form  of  tHs  paralysis,  wliicli 
supervenes  when  the  lesion  occupies  the  nucleus  of  origin  of  the  sixth  nerve, 
and  which  is  accompanied  by  conjugate  deviation  of  the  other  eye. 

4.  Paralysis  of  Associated  Movements. 

These  paralyses  consist  in  the  abolition  of  a  movement  common  to  both 
eyes — the  movement  of  raising  or  of  lowering,  movement  of  convergence 
or  divergence,  lateral  movement  to  the  right  or  to  the  left.  Here  we  have 
not  to  deal  with  paralysis  of  a  certain  nerve  or  of  a  certain  muscle.  As 
Parinaud  has  correctly  said  :  "  We  have  to  deal  essentially  with  the  paralysis 
of  a  function  relating  to  the  nerve  supply  of  several  muscles  taking  part 
in  this  function,  whilst  respecting  the  innervation  of  these  same  muscles 
for  other  acts." 

Description. — The  paralyses  of  the  horizontal  and  lateral  movements 
are  the  most  frequent  and  the  most  interesting.  Their  explanation  gives 
rise  to  many  controversies.  In  order  to  explain  how  two  muscles  opposed 
in  function  (internal  rectus  on  one  side  and  external  rectus  on  the  other 
one),  and  supplied  by  different  nerves,  become  associated  in  order  to  perform 
the  same  movement,  we  must  remember  that  the  internal  rectus  may  con- 
tract in  order  to  execute  two  totally  different  movements  :  (1)  It  may  pro- 
duce a  converging  movement,  both  eyes  being  directed  towards  the  median 
line.  In  this  case  the  right  internal  rectus  has  as  its  associated  muscle 
the  left  internal  rectus.  (2)  It  may  produce  lateral  movements,  both  eyes 
being  directed  to  the  same  side  of  the  body.  In  looking  to  the  left,  the  right 
internal  rectus  has  as  its  associated  muscle  the  left  external  rectus,  and 
vice  versa.  In  order  to  produce  these  varieties  of  movements  the  internal 
rectus  receives  a  double  nerve  supply.  It  receives  a  nerve  filament  from 
its  special  nucleus  (nucleus  of  the  third  pair)  on  the  corresponding  side. 
This  filament  governs  convergence,  but  for  the  lateral  movement  the  nucleus 
of  the  internal  rectus  receives  a  nerve  filament  from  the  nucleus  for  the 
external  rectus  of  the  opposite  side.  The  existence  of  this  anastomotic 
filament  explains  the  various  types  of  associated  paralysis  for  lateral  move- 
ments. 

As  a  matter  of  fact,  the  nucleus  of  the  sixth  nerve  on  the  left  side,  for 
instance,  supplies  the  left  external  rectus,  and  by  its  anastomotic  branch 
it  also  supplies  the  right  internal  rectus.  It  results  therefrom  that  a  central 
lesion,  destroying  the  nucleus  of  the  sixth  nerve  on  the  left  side,  produces 
paralysis  of  the  conjugate  movements  to  the  left — that  is  to  say,  the 
left  external  rectus  and  the  right  internal  rectus,  which  move  the  eyes  to 
the  left,  are  paralyzed. 

If  the  lesion  is  peripheral,  and  if,  instead  of  affecting  the  nucleus,  it 
affects  the  trunk  of  the  sixth  nerve  or  the  anastomotic  branch  to  the  internal 


PARALYSES  1585 

rectus  of  the  opposite  side,  two  very  diflcrcut  clinical  typos  result  thcrefroia. 
In  the  first  type  the  external  rectus  of  one  side  is  paralyzed,  and  the  internal 
rectus  of  the  other  side  is  in  a  condition  of  spasm.  The  eye  to  which  the 
paralyzed  external  rectus  belongs  can  no  longer  turn  outwards.  The  other 
eye,  however,  is  strongly  drawn  in  that  direction  by  the  spasm,  and  conse- 
quently turns  inwards  (Parinaud).  In  the  second  type  there  is  paralysis 
of  the  internal  rectus  on  the  one  side,  with  spasm  of  the  external  rectus  of 
the  opposite  side.  In  this  case  the  eye  to  which  the  internal  rectus  belongs 
can  no  longer  move  inwards,  whilst  the  other  eye  is  turned  outwards. 
Diplopia  is  often  absent  in  these  paralyses  of  the  associated  horizontal 
movements,  and,  when  it  exists,  it  is  of  only  secondary  importance.  Par- 
alyses of  this  kind  are  especially  recognizable  by  objective  examination  of 
the  ocular  movements. 

Let  us  next  consider  the  associated  paralyses  of  the  vertical  movements. 
They  involve  in  both  eyes  at  the  same  time  the  movement  of  elevation  or 
the  movement  of  lowering,  or  both  these  movements  together.  In  the 
three  cases  paralysis  of  the  movement  of  convergence  coexists.  The 
horizontal  movements  are  preserved  in  a  lateral  direction. 

Paralysis  of  convergence  is  characterized  by  the  abolition  of  the  three 
muscular  acts  which  determine  the  fixing  of  a  near  object — convergence, 
accommodation,  and  contraction  of  the  pupil  (Parinaud).  The  symptoms 
are  as  follows  :  Lack  of  convergence  in  the  eyes  ;  crossed  diplopia  persisting 
throughout  the  whole  extent  of  the  field  of  vision,  without  noticeable 
separation  of  the  images ;  double  paralysis  of  accommodation,  without 
mydriasis  ;  absence  of  the  pupil  reflex  of  accommodation.  We  find  side 
by  side  with  this  typical  form  of  paralysis  of  convergence  another  form, 
in  which  the  paralysis  coexists  with  associated  paralysis  of  the  vertical 
movements.  As  regards  the  so-called  paralysis  of  divergence — a  trouble 
characterized  by  inability  to  bring  the  visual  axes  parallel,  with  only 
slightly  pronounced  homonymous  diplopia — ^it  seems  that  it  is  rather  a 
contracture  of  convergence  than  a  paralysis  of  the  opposite  movement. 

Pathogenesis. — The  cause  of  paralysis  of  the  associated  movements  is 
stiQ  obscure.  Paralysis  of  the  horizontal  movements,  accompanied  by 
deviation  of  the  head  (conjugate  de^^ation),  is  met  with  in  some  cerebral 
lesions  (hsemorrhage,  softening,  etc.).  The  pure  forms  of  this  afiection  have 
been  noticed  in  certain  cerebro-spinal  afEections — insular  sclerosis,  cerebral 
syphilis.  They  may  foUow  a  stroke,  and  may  be  accompanied  by  various 
kinds  of  paralysis.  Essential  paralysis  of  convergence  has  been  met  with 
in  neurasthenia,  in  hysteria  (Borel),  in  certain  cases  of  intoxication  by 
morphia,  or  by  alcohol  (D.  Graefe),  in  locomotor  ataxy  (Hiibscher),  and  in 
exophthalmic  goitre  (Mobius). 

Where  are  the  lesions  situated  in  paralysis  of  the  associated  move- 


1586  TEXT-BOOK  OF  MEDICINE 

ments  ?  Are  tlie  nuclei  of  tlie  muscles  wliicli  co-operate  in  tlie  same  move- 
ment joined  together  by  anastomotic  filaments,  or  are  there,  below  tliese 
nuclei,  centres  for  co-ordiaatiag  tlie  movements  ?  The  question  is  far  from 
being  solved.  Paralysis  of  the  horizontal  movements  is  readily  explained 
by  the  existence  of  the  anastomotic  filament,  which  is  said  to  pass  from  the 
nucleus  of  the  sixth  nerve  to  the  opposite  internal  rectus  ;  but  it  must  be 
added  that  the  very  existence  of  this  filament  has  been  doubted,  and  that 
this  explanation,  besides,  is  opposed  to  what  we  know  concerning  the 
other  forms  of  associated  paralysis,  which  appear  to  be  due  to  lesions 
of  the  co-ordiaating  centres  — corpora  quadrigemina,  vermis  inferior 
(Henoch). 

The  treatment  is  that  of  the  cerebral  affection  which  has  caused  the 
paralysis.  In  a  case  of  syphilis  at  the  Necker  Hospital  rapid  recovery 
took  place. 

IV.  OPHTHALMOPLEGIA. 

Description. — External  ophthalmoplegia  is  a  clinical  type  due  to  the 
paralysis  of  aU  the  extrinsic  muscles  of  the  eye,  or  at  least  to  the  paralysis 
of  all  the  muscles  supplied  in  the  same  eye  by  two  different  nerves,  one  of 
them  always  being  the  third  nerve.  The  aspect  of  the  patient  is  most 
characteristic.  The  eyelids  droop,  the  forehead  is  wrinkled,  the  eyebrows 
are  arched  (to  remedy  the  blepharoptosis  caused  by  the  contraction  of  the 
frontalis  muscle),  the  eyes  are  immovable,  and  when  the  eyelids  are  lifted 
up  by  the  fingers  the  eyeball  looks  as  though  it  were  made  of  wax  (Benedikt). 
Finally,  the  patient  is  obliged  to  supplement  the  defective  movements  of 
the  eyes  by  moving  the  head  and  the  neck. 

Internal  ophthalmoplegia  is  the  paralysis  of  the  entire  intrinsic  muscu- 
lature of  the  eye  (sphincter  of  the  iris  and  the  ciliary  muscle).  These  two 
forms  together  constitute  total  ophthalmoplegia.  Each  form  may  be 
unilateral  or  bilateral.  Ophthalmoplegia  may  be  divided,  according  to 
the  site  of  the  lesion,  into  cortical,  supranuclear,  nuclear,  or  radicular,  the 
cortex,  the  co-ordinating  centres  of  the  muscles  of  the  eyes,  and  the  nuclei, 
the  nerve  roots  being  respectively  affected.  The  nerve  trunks  may  be 
affected  at  the  base  of  the  skull  or  in  the  orbit,  thus  producing  basilar  or 
orbital  ophthalmoplegia.  Ophthalmoplegia  may  also  be  caused  by  peri- 
pheral neuritis. 

I  have  previously  described  nuclear  ophthalmoplegia. 

Supranuclear  ophthalmoplegia  (Sauvineau)  is  always  bilateral,  and  is 
due  to  lesions  affecting  the  co-ordinating  centres  above  the  nuclei  (corpora 
quadrigemina,  subependymal  grey  matter).  The  lesions  of  these  centres 
provoke  paralyses  of  the  associated  and  conjugate  movements  of  the  eye. 
When  these  paralyses  affect  at  once  the  different  associated  movements  they 


PAUALYSKS  1587 

constitute  ophthalmoplegia.  Supranuclear  ophthalmoplegia  usually  takes 
an  acute  form,  and  is  accompanied  by  the  most  grave  cerebral  phenomena. 

Cortical  ophthalmoplegia  exclusively  affects  the  voluntary  movements 
which  are  abolished,  whilst  the  automatic  reflex  movements  are  preserved. 
This  dissociation  appears  to  be  peculiar  to  hysteria.  It  has  been  met 
with  in  exophthalmic  goitre  (Ballet),  but  it  is  likely  that  it  is  here  due  to 
hysteria,  which  in  the  cases  quoted  accompanied  Basedow's  disease. 

Radicular  ophthalmoplegia  affecting  the  roots  of  the  motor  nerves  of 
the  eye  at  their  exit  from  the  nuclei  does  not  exist,  and  cannot  exist.  The 
fourth  nerve,  in  fact,  does  not  traverse  the  peduncles,  and,  on  the  other 
hand,  the  radicular  filaments  of  the  third  nerve  and  those  of  the  sixth 
nerve  are  at  a  considerable  distance  from  one  another.  It  is  simply  a 
question  of  paralysis  of  the  sixth  nerve  or  of  paralysis  of  the  third  nerve, 
with  hemiplegia  of  the  opposite  side. 

Ophthalmoplegia  of  basilar  origin  is  generally  unilateral.  The  paralysis 
is  always  mixed  and  total,  because  a  lesion  of  the  base  of  the  skull  can 
hardly  injure  in  the  trunk  of  the  third  nerve  all  the  filaments  which  go  to 
the  motor  muscles  of  the  eye  without  affecting  the  filaments  which  go  to 
the  internal  muscles.  It  may  be  laid  down  as  an  axiom  that  every  case  of 
ophthalmoplegia  which  is  external  alone,  is  not  of  basilar  origin. 

It  is  often  dijB&cult  to  distinguish  orbital  ophthalmoplegia  from  nuclear 
ophthalmoplegia.  We  must  look  for  the  cerebral  symptoms,  such  as  head- 
ache, vomiting,  etc.,  which  are  caused  by  a  lesion  of  the  base  of  the  skull, 
and  we  must  rely  on  the  lesions  of  the  optic  nerve  (amblyopia,  optic  neuritis 
of  the  paralyzed  eye),  of  the  olfactory  nerve  (unilateral  olfactory  paralysis), 
or  of  the  trifacial  nerve.  Hemianopia  is  not  characteristic  of  a  lesion  at  the 
base  of  the  skuU. 

The  usual  causes  of  basilar  ophthalmoplegia  are  basal  meningitis  (tuber- 
cular and  syphilitic),  meningeal  haemorrhage,  lesions  of  the  bloodvessels  and 
neoplasms. 

Orbital  ophthalmoplegia,  due,  perhaps,  to  a  primary  lesion  of  the  retro- 
bulbar ceUular  tissue,  or  to  a  lesion  of  the  extrinsic  muscles,  is  generally 
caused  by  a  change  in  the  nerves  themselves  or  in  their  terminal  branches. 
These  cases  of  ophthalmoplegia  are  generally  unilateral,  mixed,  and  accom- 
panied by  more  or  less  pronomiced  exophthalmos  and  pain. 

Peripheral  ophthalmoplegia,  though  very  rare  in  the  infectious  diseases 
and  in  the  intoxications,  is  sometimes  due  to  injury  (Morel).  It  has  been 
noticed  particularly  in  tabes,  in  the  form  of  an  early  and  transient  paralysis. 
The  principal  characteristics  are  curability  (Dejerine),  and  the  existence  of 
spasms  in  the  associated  muscles — retraction  of  the  levator  palpebree  of  the 
diseased  eye,  spasms  of  the  associated  muscles  of  the  healthy  eye  (Pariuaud). 


1588  TEXT-BOOK  OF  MEDICINE 

V.  PARALYSIS  OF  THE  MUSCULO-SPIRAL  NEEVE. 

Description.- — Of  the  brandies  of  the  brachial  plexus  the  musculo- 
spiral  nerve  is  the  one  most  often  paralyzed.  The  paralysis  generally 
announces  itself  by  formication  and  numbness,  and  the  loss  of  movement 
gradually  becomes  complete. 

In  paralysis  of  the  musculo-spiral  nerve  the  attitude  of  the  hand  is 
characteristic.  If  the  patient  raises  the  arm,  the  hand  drops  on  to  the  fore- 
arm, and  it  is  impossible  to  lift  it,  because  the  extensor  muscles  of  the  wrist, 
the  two  radial  extensors,  and  the  extensor  ulnaris  are  paralyzed.  A  more 
careful  study  shows  the  following  symptoms  : 

The  dorsal  surface  of  the  hand  is  slightly  rounded,  and  the  palmar 
surface  is  hoUowed,  because  the  muscles  of  the  thenar  and  hypothenar 
eminences  are  no  longer  opposed  by  the  extensor  muscles. 

When  the  hand  and  the  forearm  are  placed  on  a  horizontal  surface,  the 
patient  cannot  execute  any  lateral  movement  of  the  wrist,  because  the 
extensor  muscles  are  also  paralyzed — the  extensor  ulnaris  muscle  being 
an  adductor  muscle,  and  the  extensor  radialis  longior  being  an  abductor 
muscle  (Duchenne). 

The  fingers  are  bent  on  the  metacarpus,  and  the  patient  cannot  extend 
them,  on  account  of  the  paralysis  of  the  common  extensor. 

The  extension  of  the  last  two  phalanges  is  possible  because  this  movement 
is  performed  by  the  interosseous  muscles  (Duchenne) ;  this  extension  of  the 
last  two  phalanges  is  only  possible  if  care  be  taken  to  make  up  for  the 
deficiency  in  the  action  of  the  common  extensor  by  previously  lifting  the 
metacarpal  phalanges. 

The  movements  of  flexion  of  the  fingers  are  also  affected,  and,  in  spite 
of  every  effort,  the  patient  cannot  bring  the  extremities  of  the  fingers  in 
contact  with  the  thenar  and  hypothenar  regions.  This  weakness  of  the 
flexor  muscles  is  only  apparent.  It  is  due  to  the  shortening  of  these  muscles 
by  the  paralysis  of  the  extensors  (Duchenne),  and  the  movements  of  flexion 
regain  their  power  if  care  is  taken  to  raise  the  patient's  wrist. 

The  long  and  short  supinator  muscles  are  paralyzed,  which  is  never  the 
case  in  lead  palsy.  The  paralysis  of  the  long  supinator  is  readily  discovered. 
The  patient  is  asked  to  flex  and  to  pronate  the  forearm,  whilst  the  movement 
is  being  opposed  by  drawing  the  forearm  into  the  position  of  supination. 
It  is  then  seen  that  the  long  supinator  does  not  stand  out  in  relief.  It  does 
not  contract. 

Condition  of  Sensation.  —  In  musculo-spiral  paralysis  there  is  no 
anaesthesia  of  the  posterior  and  external  half  of  the  forearm  and  of  the 
hand,  parts  which  receive  their  sensory  innervation  from  the  musculo- 
spiral  nerve.     This  fact  is  peculiar,  and  we  may  ask  how  the  same  cause 


PARALYSES  ir.SO 

actiii}:;  on  a  inixi'd  nerve  spares  the  sensory  filaments  of  this  nerve  when 
it  affects  the  motor  fihimcnts.  Several  explanations  have  been  i^ivcn. 
The  sensation  is  said  to  be  preserved,  not  because  the  sensory  filaments 
of  the  nerve  are  spared,  but  because  the  deficiency  is  supplied  by  other 
nerve  brandies.  Tlio  pliysiological  researches  of  Arloinj;,  Tripier,  and 
Vulpian,  and  the  clinical  observations  of  Weir  Mitchell,  Kichet,  etc.,  prove 
that  the  cutaneous  sensibility  may  be  preserved  in  a  region  deprived  of  its 
ordinary  cutaneous  nerve.  This  phenomenon  is  based  on  the  following 
anatomical  conditions  :  If  the  motor  root  of  a  mixed  nerve  is  cut,  it  will  be 
seen  that  the  peripheral  end  of  the  cut  nerve  is  still  sensitive  on  account  of 
the  recurrent  sensory  fibres  which  come  from  the  posterior  roots  and  go 
to  the  anterior  roots.  When  a  cutaneous  nerve  of  the  paw  is  cut  in  a  dog 
(Arloing  an'l  Tripier),  it  is  seen  that  the  peripheral  end  of  the  cut  nerve 
contains  some  fibres  which  do  not  degenerate.  They  are,  consequently,  in 
relation  uith  the  spinal  cord,  and  probably  come  from  the  anastomoses  of 
the  collateral  nerves  of  the  digits  (Sappey)  or  from  the  plexuses  formed  by 
their  terminal  ramifications.  These  peripheral  recurrent  fibres  do  not  go 
as  far  as  the  centres  with  the  nerve  which  they  accompany.  They  lose 
themselves  on  the  road  in  order  to  enter  the  skin.  It  is,  therefore,  by  this 
means  of  supplying  the  deficiency  that  the  sensation  is  re-established  after 
the  section  of  the  cutaneous  nerve  of  the  hand,  and  this  explanation  has 
been  given  to  explain  the  conservation  of  the  sensation  in  paralysis  of  the 
musculo -spiral  nerve. 

Nevertheless,  certain  writers  (Onimus),  though  recognizing  the  possi- 
bility of  supplementing  the  deficiency  by  recurrent  means,  have  looked 
elsewhere  for  the  cause  of  this  phenomenon.  When  the  musculo-spiral 
nerve  is  attacked  at  its  seat  of  election,  either  by  compression  or  by  cold, 
it  cannot  for  a  moment  be  admitted  that  the  motor  fibres  only  are  affected, 
the  sensory  fibres  being  spared  ;  but  what  can  be  admitted  is  that  the  resist- 
ance of  the  sensory  fibre  is  greater  than  that  of  the  motor  fibre.  It  may 
be  still  further  admitted  that  the  functions  of  sensation  are  more  difficult 
to  abolish  than  those  of  motion.  We  meet  with  an  analogous  case  in  the 
spinal  cord.  We  know  (Vulpian)  that  sensation  does  not  follow  in  the 
spinal  cord  a  path  marked  out  in  advance ;  it  passes,  according  to  circum- 
stances, through  the  grey  matter  or  through  the  posterior  columns.  When 
one  of  these  parts  is  compromised,  the  other  may  supply  the  deficiencv, 
and  these  parts  must  be  destroyed  over  a  large  extent  in  order  that  the 
anaesthesia  of  the  corresponding  regions  may  be  complete.  In  other  words, 
the  conductors  of  sensory  impressions  easily  make  up  for  mutual  deficiencies, 
and  the  preservation  of  a  small  number  of  them  explains  the  persistence  of 
the  sensation  when  an  analogous  lesion  of  the  motor  conductors  would 
produce  paralysis. 

n.  101 


1590  TEXT-BOOK  OF  MEDICINE 

Faradic  Contractility. — The  electro-muscular  contractility  is  preserved 
in  paralysis  of  the  musculo-spiral  nerve,  whilst  it  is  lost  in  paralysis  of  the 
facial  nerve  (I  am  speaking  of  what  takes  place  in  severe  cases  of  facial 
paralysis).  These  differences  in  the  condition  of  the  electro -muscular 
excitability  have  been  variously  interpreted.  Duchenne  says  :  "  If  it  be 
true  that  cold  causes  swelling  of  the  nerve,  the  Fallopian  aqueduct,  which 
is  traversed  by  the  facial  nerve,  must  oppose  this  increase  in  size,  and, 
consequently,  compress  the  nerve,  so  as  to  diminish  the  irritability  of  the 
muscles  to  which  it  is  distributed.  As  this  cause  of  compression  does  not 
exist  in  the  case  of  the  musculo-spiral  nerve,  it  is  clear  that  the  paralysis  of 
this  nerve  may  exist  without  the  electro-muscular  contractility  being 
weakened."  The  explanation  given  by  Duchenne  is  not  sufficient.  It 
rests  on  two  hypotheses,  which  mutually  destroy  one  another.  The  first 
is  that  the  facial  nerve  is  always  compressed  in  the  Fallopian  aqueduct, 
which  is  not  proved,  and  the  second  that  musculo-spiral  paralysis  is  always 
due  to  cold,  whereas  it  is  often  due  to  compression ;  and  if,  according  to 
Duchenne,  the  compression  of  the  facial  nerve  in  the  Fallopian  aqueduct 
suffices  to  abolish  the  electro-muscular  contractility,  compression  of  the 
musculo-spiral  nerve  ought  to  bring  about  a  similar  result ;  but  this  does 
not  take  place.  We  must,  therefore,  look  for  other  explanations.  Accord- 
ing to  Onimus,  the  apparent  difierence  in  the  electro-muscular  reactions 
in  cases  of  musculo-spiral  and  of  facial  paralysis  is  only  a  question  of  degree. 

-ffitiology — Pathogenesis. — The  pathogenesis  of  musculo-spiral  paralysis 
is  obscure,  and  its  mode  of  production  is  in  dispute.  Without  speaking  of 
rare  cases,  such  as  compression  of  the  nerve  by  the  use  of  crutches,  by 
wounds,  tumours,  fractures,  dislocations,  and  occupation  paralysis  (water- 
carriers),  it  may  be  said  that  the  usual  aetiology  of  musculo-spiral  paralysis 
can  be  summed  up  in  two  words — cold  and  compression. 

According  to  Duchenne,  the  paralysis  is  always  due  to  the  action  of 
cold,  and  is  improperly  named  rheumatic  paralysis.  We  find  in  the  works 
of  Duchenne  great  stress  laid  on  cold  as  the  cause.  If  the  patient  has 
lain  down  on  the  grass  or  on  the  damp  ground,  if  he  has  gone  to  sleep  in  a 
chair  with  his  arms  crossed,  or  if  he  has  left  them  outside  the  bedclothes, 
Duchenne  speaks  of  the  action  of  cold. 

In  opposition  to  the  exclusive  opinion  of  Duchenne,  another  equally 
exclusive  opinion  attributes  the  paralysis  to  the  compression  of  the  nerve. 
Panas  denies  the  action  of  cold,  and  declares  that  "  in  the  immense  majority 
of  cases,  not  to  say  in  all,  the  paralysis  is  due  to  compression  of  the  nerve 
trunk.  "  This  compression  is  favoured  by  the  superficial  situation  of  the 
nerve,  which  beqomes  subcutaneous  as  it  winds  round  the  outer  border  of 
the  humerus,  to  descend  into  the  muscular  interspace  between  the  supinator 
longus  and  the  brachialis  anticus.     The  compression  of  the  nerve  at  this 


PARALYRES  1591 

point  may  be  accomplished  by  various  mecliaiiisms.  In  some  cases  tho 
patient  {joes  to  sleep  with  his  arm  under  his  head  ;  at  otlier  times  he  goos  to 
sleep  with  liis  arm  leaning  on  a  hard  surface  (bed,  table,  back  of  a  chair, 
step),  which  compresses  the  nerve. 

Paralysis  of  the  musculo-spiral  nerve  by  compression  is  accepted  by 
everybody.  Panas  deserves  credit  for  having  brought  it  into  relief.  Jiut 
why  reject  absolutely  paralysis  a  frigore?  Why  should  not  cold,  which 
causes  paralysis  of  the  facial  nerve  and  of  the  external  larvngeal  nerve 
(paralysis  of  the  crico-thyroid  muscle)  also  cause  paralysis  of  the  musculo- 
spiral  nerve  ? 

One  of  the  principal  reasons  leading  Panas  to  reject  musculo-spiral 
paralysis  a  frigore  is  its  localization.  Thus,  the  triceps  never  participates 
in  the  paralysis,  whUst  the  supinator  longus  is  always  paralvzed ;  and  this 
localization,  easily  explained  in  the  case  of  compression,  cannot  be  explained 
by  cold. 

This  argument  does  not  appear  to  me  to  be  sufl&cient,  because  as  far  as 
localization  is  concerned,  we  find  at  every  turn  examples  which,  though 
inexplicable,  are  nevertheless  positive.  Why,  for  instance,  is  lead  palsy, 
which  so  closely  resembles  musculo-spiral  paralysis,  localized  in  the  extensor 
muscles,  whilst  it  spares  the  supinator  longus  ?  Why  does  progressive 
muscular  atrophy  always  commence  in  the  abductor"^ brevis  muscle  of  the 
thenar  eminence  ?  Why  does  glosso-labio-laryngeal  paralysis  at  first  and 
above  all  attack  the  superior  lingual  muscle  ?  These  facts  are  undeniable, 
and,  as  far  as  the  localization  of  musculo-spiral  paralysis  is  concerned,  if 
cold  spares  the  nerve  in  its  superior  parts  and  abolishes  its  functions  in  the 
region  of  the  supinator  longus,  it  is  no  doubt  because  it  attacks  it  at  the 
point  where  the  superficial  position  renders  the  nerve  more  accessible  to 
external  agents.  Besides,  there  are  undeniable  cases  of  musculo-spiral 
paralysis  a  frigore  (Chapoy,  Vicente,  Duplay).  It  is  true  that  it  has  been 
asserted  (Richet)  that  even  in  the  case  of  cold  the  paralysis  is  due  to  com- 
pression, because  the  nerve,  swollen  in  the  interior  of  its  osteo-fibrous 
canal,  undergoes  a  kind  of  strangulation.  This  hypothesis,  advanced  by 
Erb,  with  regard  to  paralysis  of  the  facial  nerve  a  frigore,  appears  to  me 
to  be  only  applicable  in  some  cases,  because  other  motor  or  mixed  nerves 
are  paralyzed  as  the  result  of  cold,  although  it  is  not  possible  to  invoke  the 
strangulation  or  the  compression  of  the  nerve  in  a  rigid  canal. 

The  diagnosis  is  simple.  I  have  already  said  that  paralysis  of  the 
musculo-spiral  nerve  dilSers  from  lead  palsy  of  the  extensors  in  that  the 
latter  is  not  accompanied  by  paralysis  of  the  supinator  longus. 

The  course  and  duration  of  musculo-spiral  paralysis  vary  according  to 
its  causes  and  to  its  varieties.  The  paralysis  recovers  after  a  longer  or 
shorter  time.     Faradization  is  absolutely  indicated. 

101—2 


1592  TEXT-BOOK  OF  MEDICINE 

VI.  RADICULAR  PARALYSIS— RADICULAR  PARALYSIS  OF  THE 

BRACHIAL  PLEXUS. 

The  spinal  nerves  sometimes  present  changes  between  their  exit  from 
the  spinal  cord  and  their  entrance  into  the  various  plexuses,  shown  clinically 
by  paralyses.  These  paralyses  have  received  the  name  of  radicular 
paralyses. 

There  exist  as  many  varieties  of  radicular  paralysis  as  there  are  plexuses. 
Those  dependent  on  lesions  of  the  first  cervical  nerves  and  of  the  sacral 
nerves  have  not  yet  been  described.  The  radicular  paralyses  of  the  lumbar 
plexus  are  very  obscure.  They  are  generally  met  with  during  pregnancy, 
and  especially  after  delivery,  and  are  attributed  to  the  compression  exer- 
cised by  the  head  of  the  foetus  on  the  nerve  roots.  They  generally  afiect 
the  lumbo-sacral  nerve  (fourth  and  fifth  lumbar  nerves)  as  it  winds  behind 
the  prominence  of  the  brim  of  the  pelvis.  They  give  rise  to  a  limited 
paralysis  in  the  area  supplied  by  the  external  popliteal  nerve,  and  sometimes 
(Vinay)  in  the  area  of  the  superior  gluteal  nerve — gluteus  medius  and 
minimus  and  tensor  fasciae  latse. 

The  radicular  paralyses  of  the  brachial  plexus,  on  the  contrary,  have 
been  during  the  past  few  years  the  object  of  much  important  research. 

Anatomo-physiological  Survey. — The  brachial  plexus  is  formed  by  the  last  four 
cervical  and  the  first  dorsal  nerves.  It  supplies  the  muscles  of  the  upper  limb,  some  of 
the  shoulder  muscles,  as  weU  as  the  subclavius,  serratus  magnus,  levator  anguh,  rhom- 
boids, pectorals,  and  latissimus  dorsi.  It  supphes  sensation  to  the  skin  of  the  upper  hmb, 
with  the  exception  of  the  internal  and  posterior  surface  of  the  arm,  as  well  as  a  portion 
of  the  point  of  the  shoulder.  The  nerves  which  supply  this  cutaneous  area  come  from 
the  second  and  third  intercostal  nerves.  Finally,  each  of  the  nerve  branches  forming 
the  brachial  plexus  gives  off,  immediately  after  the  union  of  its  two  roots  beyond  the 
spinal  gangUa,  communicating  branches,  which  form  the  trunk  of  the  great  sympathetic 
nerve. 

The  entanglement  formed  by  the  brachial  plexus  is  at  first  sight  inextricable,  but 
the  careful  researches  of  Fere  have  shown  the  part  taken  by  each  pair  of  spinal  nerves 
in  the  constitution  of  the  various  nerves  emanating  from  the  plexus.  Thus,  the  fifth 
and  sixth  cervical  nerves  give  rise  to  the  musculo -cutaneous  (biceps,  brachiahs  anticus, 
and  coraco -brachiahs),  to  the  circumflex  (deltoid),  to  the  nerves  of  the  supraspinatus 
and  infraspinatus,  the  teres  major,  the  latissimus  dorsi,  the  pectorahs  major,  and  the 
serratus  magnus,  as  well  as  to  the  fibres  of  the  musculo -spiral  nerve,  which  supphes  the 
supinators.  The  experiments  of  Ferrier  and  Yeo,  as  well  as  those  of  Forgues,  have 
proved  that  electrical  stimulation  of  these  two  pairs  of  nerves  in  the  monkey  causes 
the  contraction  of  these  muscles.  Finally,  Erb,  who  first  drew  attention  to  the  radicular 
localizations,  has  shown  that  in  man  the  electrical  stimulation  of  a  point  in  the  supra- 
clavicular hollow  produces  simultaneous  contraction  of  the  deltoid,  of  the  biceps,  of 
the  brachiahs  anticus,  and  of  the  supinator  longus.  This  point  is  about  an  inch  above 
the  clavicle,  immediately  external  to  the  posterior  border  of  the  stemo -mastoid,  over 
the  anterior  tubercle  of  the  transverse  process  of  the  sixth  cervical  vertebra. 

/Etiology. — The  radicular  paralyses  are  generally  the  result  of  injury- 
violent  faUs  on  the  shoulder,  sudden  traction  of  the  arm  (MiraUie),  reduc- 


PARALYSES  1  r.93 

t.ioti  of  dislocations,  gun-shot  wounds,  compression  by  tho  forceps  (Duclienno), 
vicious  {'alius  (fracture  of  tho  clavicle),  abscess  (Pott's  dis(!aso),  and  glandiil.ir 
tumours.  They  may  be  the  result  of  cold,  or  tiiey  may  be  of  reflex  origin 
(Rendu),  being  then  dependent  on  a  gastro-hepatic  affection.  Finally,  in 
sonu>  cases  the  cause  is  unknown. 

Symptoms. — The  ]>aralysis  may  be  total  or  partial. 

1.  When  total,  it  affects  all  the  roots  of  the  plexus :  the  arm  falls  lifeless, 
the  point  of  the  shoulder  is  lowered  and  flattened,  and  the  patient  cannot 
bend  the  forearm  or  move  the  fingers.  The  anaesthesia  is  complete  in  the 
hand  and  in  the  forearm,  and  ascends  more  or  less  high  to  the  arm  and  the 
shoulder.  The  reflexes  are  abolished.  The  muscles  present  the  reaction 
of  degeneration,  and  stimulation  at  Erb's  point  produces  no  contraction. 
Muscular  atrophy  occurs  early.  The  trophic  troubles  commonly  met  with 
in  peripheral  nerve  lesions  are  very  complete — atrophied  and  glossy  skin, 
malformation  of  the  nails,  cyanosis,  suppression  of  the  sweat,  and  fall  in 
the  temperature,  at  times  amounting  to  2°  or  3°  F.  (Giraudeau),  sub- 
cutaneous adiposis,  fibrous  ankylosis,  etc. 

Oculo-pupillary  phenomena  may  also  be  noticed,  with  myosis  (paralysis 
of  the  radiating  fibres  of  the  iris,  supplied  by  the  sympathetic),  with  con- 
striction of  the  space  between  the  eyelids  (paralysis  of  the  orbito-palpebral 
muscle),  and  at  times  smallness  and  retraction  of  the  eyeball  (Hutchinson, 
Le  Bret).  The  retracted  pupil  still  reacts  to  the  light,  but  less  so  than  the 
pupil  of  the  healthy  side.  These  disorders  of  innervation  are  connected 
with  the  destruction  of  the  communicating  branch  from  the  first  dorsal 
nerve,  as  the  experimental  researches  of  Klumpke  have  shown. 

We  must  distinguish  two  kinds  of  total  paralysis  (Raymond).  The 
lesion,  according  to  its  seat,  may  attack  the  plexus  at  the  very  exit  of  the 
roots  (tearing,  Pott's  disease,  etc.),  or  in  its  cervico- axillary  course  (fracture 
of  the  clavicle,  interstitial  haemorrhage  of  the  plexus,  exostosis,  etc.).  In 
the  first  case  (radicular  paralysis)  there  are  oculo-pupillary  troubles.  The 
anterior  and  posterior  roots  may  be  unevenly  affected,  whence  a  purely 
motor  or  purely  sensory  paralysis  (Raymond).  Finally,  the  anaesthesia 
reaches  the  deltoid  region.  In  the  second  case  no  oculo-pupillary  troubles 
are  observed,  and  the  anaesthesia  of  the  arm  does  not  ascend  higher  than  an 
oblique  line  drawn  from  the  epitrochlear  process  to  the  humeral  insertion 
of  the  deltoid  (paralysis  of  the  brachial  plexus,  properly  speaking). 

2.  Partial  Paralysis. — In  partial  paralysis  we  find  two  principal  types  : 
(a)  The  superior  type  comprises  the  paralysis  of  the  deltoid,  of  the 

biceps,  of  the  brachial  anticus,  and  of  the  supinator  longus.  It  corresponds 
with  the  distribution  of  the  fifth  and  sixth  cervical  nerves.  This  form 
attracted  the  attention  of  Duchenne.  The  muscles  of  the  point  of  the 
shoulder  may  be  involved.     Thus,  in  Giraudeau's  case  the  supraspinatua 


1594  TEXT-BOOK  OF  MEDICINE 

and  infraspinatus  were  paralyzed.  These  muscles  are  supplied  by  tlie  sub- 
scapular nerve,  whicli  arises  in  the  angle  of  union  between  tke  fifth,  and 
sixth  nerves  before  their  entry  into  the  plexus,  so  that  we  have  another 
proof  in  favour  of  the  radicular  theory  enunciated  by  Erb.  Sensory  and 
trophic  disturbances  are  wanting,  as  weU.  as  the  oculo- pupillary  troubles. 
Secretan  has  collected  twenty-eight  cases.  Guillain  and  Crouzon  have 
published  a  case  of  radicular  paralysis  (superior  tjrpe),  with  osseous  atrophy 
and  diminution  of  the  arterial  tension. 

(6)  The  inferior  type  is  much  rarer.  I  had  a  particularly  interesting 
case  of  this  kind  at  the  Hotel-Dieu. 

A  child  of  four  and  a  half  years  was  knocked  down  by  a  heavily-laden  cart.  Several 
injuries  resulted  therefrom,  in  particular  a  large  contused  wound  of  the  right  side  of 
the  head  and  the  neck,  followed  by  cicatricial  torticollis,  which  a  physician  reduced  by 
main  force.  The  right  arm  became  paralyzed,  and  the  child  grew  up  with  its  arm 
paralyzed  and  atrophied.  The  years  went  by,  and  at  the  age  of  thirty-three  the 
patient  was  admitted  under  my  care  for  phthisis.  The  findings  were :  The  right  arm 
showed  muscular  atrophy ;  the  radio-carpal  articulation  was  flail-hke  ;  the  forearm, 
semiflexed  on  to  the  arm,  was  in  the  position  of  forced  supination  ;  the  fingers  were 
flexed,  and  deprived  of  all  movement ;  the  elbow- joint  was  fixed  by  fibrous  adhesions 
in  semiflexion,  thus  forming  a  kind  of  hook,  on  which  the  patient  could  suspend  heavy 
objects.  The  deltoid,  the  supraspinatus,  and  infraspinatus  appeared  to  be  as  large  as 
their  feUows  of  the  opposite  side.  The  biceps  was  stiU  apparent,  but  powerless  to 
flex  the  forearm.  The  epicondylar  muscles  formed  an  appreciable  mass,  especially  in 
their  superior  portion,  but  the  epitrochlear  muscles  had  disappeared,  as  well  as  the 
extensors.  Finally,  both  pectoral  muscles  were  atrophied.  In  the  hand  the  thenar 
eminence  had  almost  disappeared.  There  were  no  sensory  troubles.  We  found, 
furthermore,  one  of  the  characteristic  signs  of  a  lesion  of  the  inferior  brachial  roots — 
viz.,  the  oculo -pupillary  phenomena  (myosis,  diminution  of  the  pupil  reflex,  constriction 
of  the  palpebral  aperture).  The  diagnosis  of  inferior  radicular  paralysis  was  therefore 
obvious. 

Some  time  later  the  patient  died  from  phthisis.  At  the  post-mortem  examination 
we  found  avulsion  of  the  eighth  cervical  and  of  the  first  dorsal  nerves.  The  dissec- 
tion of  the  arm  revealed  the  integrity  of  the  supraspinatus  and  infraspinatus,  of 
the  subscapularis,  teres  minor,  subclavius,  deltoid,  biceps,  supinator  longus,  and 
supinator  brevis,  and  the  radial  extensors.  All  the  other  muscles  of  the  arm  were 
completely  atrophied  and  degenerated.  The  pectoral  muscles  (including  the  clavicular 
head),  the  teres  major,  the  latissimus  dorsi,  the  coraco-brachiahs,  the  triceps,  the 
epitrochlear  muscles,  the  flexors  and  extensors  of  the  fingers,  and  the  muscles  of  the  hand 
had  disappeared.  Their  tendons,  though  stiU  recognizable,  were  lost  in  a  mass  of  greyish 
fibrous  tissue,  in  which  it  was  impossible  to  find  any  semblance  of  muscle.  The  locahza- 
tion  of  the  muscular  atrophies,  as  wiU  be  seen,  does  not  correspond  to  the  muscles  supphed 
by  any  of  the  nerves  of  the  arm.  In  fact,  amongst  the  atrophied  muscles,  some  received 
their  nerve  supply  from  the  ulnar  nerve  (hypothenar,  flexors,  etc.),  others  from  the 
median  (thenar,  epitrochlear),  others  from  the  musculo -spiral  (triceps,  extensors),  and 
others  from-  their  special  nerves  (pectorals,  teres  major).  The  musculo-spiral  nerve 
supphed  at  the  same  time  the  muscles  which  had  remained  healthy  (the  supinator 
longus,  and  the  radial  extensors)  and  those  which  were  atrophied  (triceps,  extensors). 
There  was  therefore  no  proper  relation  between  the  atrophied  muscles  and  the  distribu- 
tion of  a  nerve  trimk.  On  the  contrary,  there  was  an  intimate  relation  between  the 
atrophied  muscles  and  the  distribution  of  one  or  more  roots  of  the  brachial  plexus. 


PARALYSES  1595 

The  fttrophind  territory  oorrospondi-d  exactly  to  tlie  /one  of  dislrihution,  which  thn 
rpsciirchos  of  Fere  and  of  Korrior  have  attributed  to  the  two  iiifirior  rtKits  of  tin-  l.nw  Iil.vl 
piuxiis. 

Ck)urse. — According  to  Rendu,  the  radicular  paralyses  commence  with 
more  or  less  marked  pain,  which  in  certain  cases  passes  unnoticed. 
Tlic  motor  troubles  are  then  said  to  appear,  and  to  bo  accompanied  by 
atrophy  at  the  end  of  a  few  days.  The  paralysis  is  often  total  at  the  com- 
mencement. It  then  becomes  localized,  and  assumes  either  the  superior 
t}^e  or  the  inferior  type.  In  their  evolution  they  present  similar  characters 
to  those  of  peripheral  paralysis.  In  slight  cases  they  last  from  three  to  six 
weeks.     In  grave  cases  they  are  often  persistent. 

Diagnosis. — They  may  be  confounded  with  paralyses,  consequent  on 
injuries  of  the  shoulder  (dislocation  or  fracture),  but  in  the  latter  case  the 
muscles  of  the  scapiilo-humeral  zone  are  alone  affected,  and  the  shoulder- 
joint  becomes  ankylosed.  Hystero-traumatic  paralysis  (Charcot)  generally 
supervenes  six,  eight,  or  ten  days  after  the  accident.  It  is  accompanied  by 
complete  ansesthesia  of  the  upper  limb  or  by  hemianaesthesia.  It  is  sus- 
ceptible to  transference.  It  is  not  always  flaccid,  and  is  never  complicated 
by  oculo-pupillary  troubles.  Myelitis  is  often  bilateral.  The  sensory 
troubles  which  accompany  it  do  not  always  present  the  same  topography. 
The  reflexes  are  often  exaggerated,  and  the  electrical  reactions  are  different. 
The  paralyses  just  described  are  tributary  to  revulsives,  to  electricity,  and 
to  massage,  in  the  same  manner  as  peripheral  neuritis.  Duchenne  has 
noted  a  case  of  radicular  paralysis  which  was  suspected  of  being  due  to  a 
s}"philitic  exostosis.  The  patient  recovered  rapidly  under  the  influence  of 
specific  treatment. 


VII.  PARALYSIS  OF  THE  TRIGEMINAL  NERVE. 

This  nerve  is  formed  of  two  portions :  one,  the  sensory  portion,  comes 
from  the  large  root,  to  which  the  Gasserian  ganglion  is  attached,  and  gives 
off  three  sensory  nerves — the  ophthalmic,  the  superior  maxillary,  and  a 
portion  of  the  inferior  maxillary  nerve ;  the  other,  or  motor  one,  mutes 
with  the  branch  of  the  inferior  maxillary,  and  supplies  the  masseter,  tem- 
poral, pterygoid,  and  suprahyoid  muscles,  which  preside  over  the  act  of 
mastication. 

Complete  paralysis  of  the  fifth  nerve  includes,  therefore,  the  ansesthesia 
of  a  sensory  nerve  and  the  paralysis  of  a  motor  nerve. 

Description.  —  1.  Paralysis  of  the  0'phih(dmic  Branch.  —  The  oph- 
thalmic branch  is  distributed  to  the  eye,  after  having  divided  into  three 
branches — the  lachrymal,  the  frontal,  and  the  nasal.  The  paralysis  of  this 
nerve  causes  ansesthesia  of  the  skin  and  of  the  mucosae  in  the  area  supplied 


1596  TEXT-BOOK  OF  :^IEDICINE 

by  it — the  foreliead.  the  upper  eyelid,  the  nose,  the  conjunctiva,  and  the 
pituitary  membrane.  This  facial  anaesthesia  stops  at  the  median  line. 
The  remarkable  thing  is  that  the  whole  of  the  eye  may  be  insensitive, 
with  the  exception  of  the  cornea.  Bernard  explains  this  phenomenon  as 
follows  :  The  nasal  nerve  supplies  a  root  to  the  ophthalmic  ganglion,  but 
besides  the  indirect  filaments  which  the  nasal  branch  sends  to  the  eye  by 
way  of  the  ophthalmic  ganglion,  it  supplies  direct  ciliary  filaments  to  this 
organ.  The  sensation  which  the  eye  receives  by  means  of  the  indirect 
filaments  of  the  ophthalmic  ganghon  differs  from  the  sensation  which  it 
receives  from  the  direct  cihary  filaments  of  the  nasal  nerve.  The  iris  and 
the  conjunctiva  receive  both  kinds  of  filaments— the  direct  ciliary  nerves 
and  the  indirect  filaments — whilst  the  transparent  cornea  receives  only  the 
iudirect  filaments. 

It  may,  then,  be  supposed  that  a  lesion  may  cause  loss  of  sensation  in 
the  entire  eye,  with  the  exception  of  the  cornea,  and  reciprocally  that  the 
cornea  may  lose  sensation,  while  all  the  other  parts  of  the  eye  retain  it. 

The  starting-point  of  reflex  action  being  abolished,  winking  is  no  longer 
performed  automatically,  and  the  movements  of  the  iris  are  sluggish. 

2.  Paralysis  of  tlte  Superior  Maxillary  Nerve. — This  nerve  is  distributed 
to  a  portion  of  the  nose  and  of  the  cheek  iu  the  suborbital  region,  to  the 
gums,  the  lip,  and  the  upper  teeth.  It  also  supplies  the  mucous  membrane 
of  the  nose.  These  parts  become  insensitive  in  the  paralysis  of  the  nerve. 
The  excitation  of  the  mucosa  no  longer  causes  sneezing,  and  the  sense  of 
smell  is  imperfect.  If  the  sense  of  smeU  is  less  acute,  it  is  not  that  the 
maxillary  nerve,  like  the  olfactory  nerve,  has  a  special  sensibOity,  but  it 
appears  that  the  integrity  of  the  sensibility  of  the  mucosa  is  necessary  to 
the  proper  functional  action  of  the  sense  of  smeU. 

3.  Paralysis  of  the  Inferior  Maxillary  Nerve.— This  nerve  is  formed 
of  two  portions,  the  one  sensory  and  the  other  motor.  In  paralysis  of  the 
sensory  portion  the  anaesthesia  occupies  the  temporal  region,  part  of  the 
cheek,  the  mucosa  of  the  mouth  and  of  the  velum  palati,  the  teeth  and  the 
lower  gums,  the  anterior  two-thirds  of  the  tongue,  the  lower  lip,  and  the 
chin.  The  result  of  the  anaesthesia  of  the  buccal  mucosa  is  that  the  saKva 
flows  from  the  mouth,  and  that  food  accumulates  behind  the  teeth.  If  the 
patient  lifts  a  glass  to  his  mouth,  the  glass  appears  to  be  broken  in  the  middle, 
becatise  the  tactile  sensation  is  limited  to  the  lips  and  the  teeth  of  the 
healthy  side.  This  symptom  is  characteristic.  The  velum  palati  is  insen- 
sitive. It  may  be  touched  without  reflex  movements  being  provoked.  The 
act  of  swallowing  is  impeded.  The  lingual  nerve  supphes  the  general 
sensibilitv  to  the  tongue,  and  is  associated  with  the  chorda  tympani  in 
supplving  the  sense  of  taste  in  the  anterior  two-thirds  of  the  tongue,  the 
glosso-pharyngeal  nerve  being  reserved  for  the  posterior  portion.    Paralysis 


PARALYSES  ir.'.i7 

of  the  inferior  maxillary  nerve,  therefore,  seriously  afTects  the  sense  of  taste 
in  the  corresponclin^  half  of  the  tongue. 

4.  Motor  Branch. — In  paralysis  of  the  motor  branch  of  the  trifacial 
nerve  the  muscles  of  mastication  are  paralyzed,  and  the  lower  jaw  is  pulled 
over  towards  tlio  hoaltliy  side. 

The  trophic  troubles  which  at  times  accompany  paraly.sis  of  the  trifacial 
nerve  have  been  described  under  neuralgia  of  this  nerve. 

etiology. — Paralysis  of  peripheral  origin  is  either  total  or  partial.  Cold 
produces  both  varieties.  As  to  the  various  lesions  which  have  been  noticed 
(cancer,  exostosis,  chronic  meningitis,  contusions,  and  wounds),  they  pro- 
duce partial  paralysis  if  they  affect  one  of  the  branches  of  the  nerve,  and 
total  paralysis  if  they  attack  the  nerve  before  it  reaches  the  Gasserian 
ganglion. 

Paralysis  of  Central  Origin. — Paralysis  of  the  trifacial  nerve  may 
depend  on  a  change  in  its  nuclei  of  origin,  such  as  is  seen  in  locomotor  ataxy. 
A  lesion  of  the  pons  may  affect  the  sensory  bundle  of  the  trifacial  nerve  at 
the  same  time  as  the  general  sensory  tract.  The  result  is  facial  hemi- 
anaesthesia,  with  hemiansesthesia  of  one  entire  side  of  the  body.  The  two 
cerebral  senses,  sight  and  smell,  are  the  only  ones  preserved  (Couty). 

Complete  hemianaesthesia,  with  loss  of  the  senses  of  sight  and  of  smell, 
may  exist  when  the  cerebral  lesion  is  seated  in  the  most  posterior  part  of 
the  internal  capsule.  Apart  from  hysteria,  in  which  this  hemianaesthesia 
may  exist  alone,  it  is  rare  for  ordinary  hemiplegia  or  paralysis  of  the  cranial 
nerves  not  to  exist  at  the  same  time,  according  to  the  seat  of  the  lesion. 
Aphasia  has  been  noticed. 


CHAPTER  IX 
TROPHIC  AND  VASOMOTOR  TROUBLES 

I.  TROPHIC  TROUBLES  IN  GENERAL— DYSTROPHIES. 

Description. — Lesions  of  the  nerve  centres  and  of  tlie  nerves  sometimes 
cause  disorders  of  nutrition,  known  as  trophic  troubles.  These  disorders 
affect  the  skin,  the  mucosse,  the  cellular  tissue,  the  muscles,  the  bones,  the 
joints,  and  the  viscera.  They  give  rise  to  eruptions,  losses  of  substance, 
ulcerations,  atrophy,  gangrene,  necrosis,  and  arrested  development ; 
sometimes,  on  the  contrary,  they  reveal  themselves  by  excess  ot  develop- 
ment. 

Most  of  the  trophic  troubles  have  been  described  under  the  Diseases  of 
the  Nerve  Centres  and  of  the  Nerves  ;  the  others  will  be  discussed  in  the 
following  sections.  I  shall  here  mention  in  general  terms  certain  clinical 
types  of  dystrophic  origin. 

1.  Skin. — Trophic  changes  in  the  skin  are  frequent.  The  eruptions  of 
herpes  sometimes  affect  the  form  of  zona.  Eczematous,  pemphigoid,  and 
erythematous  eruptions  supervene  in  diseases  of  the  nerves  (neuritis,  peri- 
pheral neuritis,  neuralgia,  and  wounds),  and  in  diseases  of  the  spinal  cord 
(tabes  dorsalis  or  tumours).  Pustules  and  eschars  of  rapid  course  (decubitus 
acutus)  are  met  with  in  lesions  of  the  brain  and  of  the  spinal  cord.  Lesions 
of  the  brain  (haemorrhage,  softening)  are  accompanied  by  the  gluteal  bed- 
sore ;  acute  infective  or  traumatic  myelitis  is  complicated  by  the  sacral 
bedsore.  Eschars  of  slow  development  are  met  with  in  the  perforating 
disease  of  the  hands  and  feet  and  in  symmetrical  gangrene  of  the  extremities. 
The  hairs  (decoloration  and  falling  out  of  the  hair)  participate  in  these 
trophic  troubles  (neuralgia  of  the  trifacial  nerve,  facial  trophoneurosis, 
hysteria).  The  so-called  glossy  skin,  which  ends  in  the  atrophy  of  -the 
sebaceous  glands,  in  a  cracked  condition  of  the  skin,  and  in  sclerosis,  is 
seen  in  lesions  of  the  nerves  and  in  sclerodermia.  Calcification  of  the  skin 
has  been  noted  by  Renon  and  Dufour  in  a  man  who  had  hard  nodules  in 
the  skin,  with  pigmentation  and  muscular  atrophy.  The  nodules  were 
composed  of  tribasic  phosphate  of  lime  and  of  fibrous  tissue. 

3598 


TROPHTO  AND  VASOMOTOR  TROUBLES  ir.09 

Vitiligo  is  a  trophio  disorder  of  the  skin,  charaoterized  hy  thfi  develop- 
ment of  wliitisli  patches,  surrounded  by  a  ])igrnented  area.  It  oecurs  in 
the  course  of  the  most  varied  nervous  affections,  such  as  hysteria,  insanitv, 
tabes,  and  syphilis  of  nervous  system,  where  it  may  coi^xist  with  Argyll- 
Robertson's  sign. 

2.  Cellular  Tissue. — The  cellular  tissue  sometimes  disappears,  as  in 
facial  trophoneurosis.  At  other  times  adiposis  occurs,  as  in  deutero- 
pathic  muscular  atrophy.  In  myxoedema  it  is  swollen,  oedematous,  and 
indurated. 

This  adiposis  may  show  different  forms.  It  affects  the  supraclavicular 
regions  in  the  shape  of  an  elastic,  painless  swelling,  called  the  supra- 
clavicular pseudo-lipoma  (Potain).  It  may  invade  the  legs  and  the  thighs 
(neuropathic  pseudo-elephantiasis  of  Mathieu).  Each  segment  of  the  limb 
may  be  affected  alone  (segmentary  cedema  of  Debove).  Symmetrical 
adeno-lipomatosis  of  the  cervical  region  is  a  very  curious  form  (Lannois  and 
Bensaude).  The  description  is  given  later.  Meige  has  described  another 
form  of  dystrophy  of  the  cellular  tissue  under  the  name  of  hereditary 
chronic  trophoedema. 

3.  Mucosae. — Herpes  of  the  nasal  mucosae,  of  the  tongue,  of  the  lips, 
and  of  the  conjunctiva,  and  ulceration  of  these  mucous  membranes  accom- 
pany lesions  of  the  trifacial  nerve  and  zona. 

4.  Muscles. — The  muscular  atrophies  following  on  diseases  of  the  spinal 
cord  may  be  di\'id6d  into  two  classes.  In  the  one  the  anatomical  and 
clinical  evolution  of  the  atrophy  is  acute  (acute  myelitis,  hsematomyelia, 
infantile  paralysis).  Progressive  muscular  atrophy  is  the  t}npe  of  the  second 
class.  The  change  in  the  muscles  is  variable.  Sometimes  it  takes  the  form 
of  pure  muscular  atrophy ;  in  other  cases  the  atrophy  is  accompanied  by 
fatty  or  fibrous  degeneration.  These  muscular  atrophies  must  be  attributed 
to  a  change  in  the  anterior  cornua  of  the  spinal  cord. 

Under  the  influence  of  the  lesions  of  the  motor  nerves  (especially  trau- 
matic lesions)  the  muscles  undergo  more  or  less  rapid  change,  and  their 
electrical  contractility  disappears  completely  or  in  part. 

The  atrophies  seen  in  alcoholism  and  in  lead-poisoning  are  types  of 
neuritic  atrophy.  Peripheral  neuritis  plays  a  great  part  in  these  trophic 
disorders. 

Muscular  atrophy  is  one  of  the  trophic  troubles  found  in  hysteria.  In 
some  cases  the  muscle,  instead  of  bemg  atrophied,  appears  to  be  hyper- 
trophied,  the  hj'pertrophy  being  due  to  overgrowth  of  the  connective  tissue 
(pseudo-hypertrophic  muscular  paralysis).  Finally,  myopathy  occurs  in 
some  patients.  The  trophic  trouble  is  not  in  the  spinal  cord  or  in  the 
nerves.  It  appears  to  reside  in  the  muscle  itseK  (Landouzy-Dejerine 
type). 


1600  TEXT-BOOK  OF  MEDICINE 

5.  Nerves. — The  fibrous  tissue  of  the  nerves  is  markedly  liypertropliied 
in  tlie  curious  affection  called  general  neurofibromatosis  (Recklingbausen's 
disease).  It  is  characterized  by  a  triad  of  symptoms  (Landowski) — tumours 
of  the  skin  and  of  the  nerves,  pigmentation  of  the  skin,  with  slowness  of  the 
movements,  cramps  in  the  legs,  and  mental  depression.  It  ends  in  cachexia 
and  death. 

6.  Cartilages.  —  Achondroplasia  (Parrot)  betrays  itself  by  an  increase 
in  the  size  of  the  head,  and  by  dwarfism.  The  limbs  are  exceedingly  short. 
"  In  Anatole,  forty-one  years  of  age,  the  leg  was  3  inches  shorter  than  that 
of  an  eight-year  old  child.  In  Gaudius,  eighteen  years  of  age,  the  leg  was 
6  inches  shorter  than  the  leg  of  a  child  of  eight  years  of  age  "  (Marie).  The 
hand  looks  like  a  "  square."  The  fingers  of  the  same  hand  are  almost 
equal  in  size,  and  are  separated  from  one  another  by  their  extremities. 
The  hand  sometimes  has  the  shape  of  a  trident  (Marie). 

7.  Bones. — The  bones  show  rarefying  osteitis.  They  become  fragile 
in  tabes  dorsalis,  and  are  atrophied  in  facial  trophoneurosis.  They  undergo 
an  arrest  of  development  in  infantile  paralysis,  and  they  become  hyper- 
trophied  in  acromegaly  (Marie)  and  in  hypertrophic  pulmonary  osteo- 
arthropathy.    They  are  deformed  in  Paget's  disease  (osteitis  deformans). 

8.  Articulations. — The  joint  changes  differ  in  lesions  of  the  skull  and 
of  the  spinal  cord.  In  lesions  of  the  skuU  the  changes  develop  after  a  few 
weeks,  during  the  period  of  secondary  contractures.  The  pain  and  the 
swelling  of  the  joint  simulate  articular  rheumatism.  In  the  diseases  of  the 
spine  the  arthropathy  is  acute,  if  the  myelitis  is  acute ;  in  tabes  dorsalis 
the  arthropathy  is  not  accompanied  by  pain  and  fever,  and  is  characterized 
by  enormous  swelling  of  the  articulation,  with  rapid  wearing  away  of  the 
bony  surfaces.  Articular  dystrophy  accounts  for  the  strange  afiection 
described  by  Marie  under  the  name  of  spondylose  rhizomelique,  characterized 
by  an  almost  complete  ankylosis  of  the  vertebral  column  and  of  the  shoulder 
and  hip  joints.  The  vertebral  colunm  is  welded  together.  The  patient, 
in  order  to  maintain  the  erect  position,  stands  in  the  form  of  the  letter  Z, 
the  upper  portion  of  the  body  being  carried  forward,  while  the  knees  are  more 
or  less  bent.  In  1906  we  had  in  the  Hotel-Dieu  a  case  of  osteo-hyper- 
trophic  vascular  nsevus.  The  clinical  aspect  is  the  same  in  all  the  pub- 
lished cases — a  more  or  less  extensive  zoniform  nsevus  on  one  limb  and 
hypertrophy  of  the  bone.  The  juxtaposition  of  these  lesions  gives  the 
diagnosis. 

Pathogenesis.  —  Several  theories  are  given  in  explanation  of  these 
trophic  troubles.  At  first  paralysis  of  the  vasomotor  nerves  was  suggested, 
but  the  numerous  experiments  of  Bernard  and  of  Brown-Sequard  show 
us  that  the  only  result  of  the  paralysis  of  the  motor  nerves  is  to  cause 
congestion  of  the  part  which  they  supply.     "  Atrophy  of  the  muscles  of  the 


Tliol'illC  XNT>  VASOMOTOR  TROUBLES  MJOl 

head  has  never  been  met  with  in  animals  after  cutting  the  cervical  cord  of 
the  great  sympathetic  nerve  "  (Vul[)ian). 

Another  tlicorv  has  been  proposed — the  theory  of  trophic  nerves 
(Samuel).  The  trophic  nerves  are  said  "  to  make  the  exchanges  whicjj  con- 
stitute anabolisiu  and  katabolism  more  active  in  the  depth  of  the  tissues." 
The  existence  of  trophic  nerves  as  distinct  nerves  is  not  adnii.ssible,  but  we 
are,  nevertheless,  face  to  face  with  the  undeniable  fact  that  the  nerves 
derive  tlieir  trophic  properties  somewhere  in  the  nervous  system,  just  as 
they  derive  their  motor  and  sensory  properties. 

It  is,  therefore,  not  the  nerve  which  is  trophic,  but  the  nerve  centres 
which  communicate  this  property  to  the  nerve;  and  by  nerve  centres  I  not 
only  refer  to  the  collections  of  cells  in  the  spinal  cord  or  in  the  brain,  but 
also  to  the  peripheral  ganglia  found  in  the  neighbourhood  of  the  organs  and 
in  their  parenchyma. 

Are  the  trophic  troubles  due  to  a  suspension  or  to  an  exaggeration  of  this 
trophic  power  of  the  nerve  centres  ?  This  question  has  been  well  put  by 
Onimus.     I  will  give  a  brief  summary  of  it : 

In  a  general  wa}^  the  nutrition  of  the  cells  consists  in  an  incessant  interchange  of 
materials  :  this  is  anabohsm  and  katabohsm.  Some  of  the  lower  animals  possess  only 
one  propertj',  nutrition ;  in  them  the  nutrition  is  blended  with  the  function.  On  the 
other  hand,  in  highly-developed  organisms  the  function  is  aiiparentlj-  more  isolated  ;  it 
results  from  the  activity  of  the  elements,  and  from  the  manifestation  of  their  properties 
(movement,  sensation,  secretion),  and,  chemically,  it  consists  in  a  combination  of  the 
molecules  present,  a  combination  which  is  almost  always  an  oxidation.  The  function 
uses  what  nutrition  has  slowly  stored  up.  Nutrition  is  a  slow  oxidation  and  a  con-' 
tinuous  act ;  the  function  is  a  rapid  oxidation  and  a  more  or  less  intermittent  act. 

What  is  the  role  of  the  nervous  system  in  the  economy,  and  how  does  it  act  on  the 
nutrition  and  on  the  function  ?  In  the  end  it  always  acts  Hke  a  force  of  discharge 
through  the  intermediary  of  the  nerve.  The  nerve  is  a  conductor  which  always  plays 
the  same  part.  It  reveals  and  renders  active  the  properties  of  the  elements  ivith  which 
it  communicates  :  it  makes  them  act ;  or,  in  other  words,  it  provokes  the  oxidation  of 
the  immediate  principles  which  compose  them,  and  the  more  it  causes  them  to  act, 
the  more  it  uses  them  up,  so  that  the  nervous  system  is  rather  antitrophic  than  trophic 
(Onimus).  It  is  said  to  be  trophic  when  nutrition  and  function  counterbalance  ;  anti- 
trophic,  when  the  income  does  not  balance  the  expenditure.  In  this  case  there  is  auto- 
phagia  of  the  element.  Under  the  influence  of  the  nervous  lesions  above  described 
(irritative  lesions),  the  elements  act  (or  destroy  one  another,  which  comes  to  the  same 
thing)  more  quickly  than  they  are  nourished ;  this  rapid  wear  and  tear  provokes  dys- 
trophic or  atrophic  troubles. 

While  this  theory  is  attractive,  it  is  only  a  theory. 

II.  FACIAL  TROPHONEUROSIS. 

Description. — Facial  trophoneurosis,  or  progressive  unilateral  atrophy 
of  the  face,  may  invade  in  succession  the  structures  of  the  face,  from  the 
skin  down  to  the  bone.     The  atrophy  is  unilateral. 

The  disease  commences  in  the  skin  in  the  shape  of  patches  that  are  white 


1602  TEXT-BOOK  OF  MEDICINE 

at  first,  and  then  become  coloured.  They  may  be  isolated  or  confluent, 
and  they  may  or  may  not  coincide  with,  the  anatomical  course  of  a  nerve 
branch.  These  patches  are  found  at  various  points  on  the  chin,  on  the 
cheek,  or  above  the  eyebrows.  Their  edges  are  ill-defined.  Over  the  patch 
the  skin,  grows  thia,  and  becomes  depressed.  It  is  hard  to  the  touch,  like 
scar  tissue.  The  beard,  the  hair,  and  the  eyebrows  lose  their  pigment,  and 
fall  out.  As  the  subcutaneous  tissue  becomes  atrophied,  the  side  of  the 
face  affected  by  the  trophoneurosis  grows  thin,  wrinkled,  and  hollow.  The 
sebaceous  secretion  disappears,  the  skin  is  dry,  and  the  secretion  of  the 
sweat-glands  is  diminished. 

The  smooth  muscles  of  the  skin  are  partly  atrophied.  They  preserve 
their  power  of  contraction  and  often  present  fibrillary  twitchings.  Atrophy 
of  the  muscles  of  mastication  has  been  noticed  (nerve  supply  of  the  facial 
nerve).  The  cartUages  of  the  nose,  the  superior  maxiUa,  the  inferior 
maxilla,  and  the  malar  bones  may  be  attacked  by  atrophy.  The  teeth  fall 
out.  The  tongue,  the  velum  palati,  and  the  uvula  sometioies  participate 
in  the  atrophy. 

The  arteries  are  not  atrophied.  The  lachrymal  and  salivary  secretions 
are  not  affected.    The  temperature  remains  the  same  on  both  sides  of  the  face. 

In  many  cases  the  disease  commences  insidiously,  without  prodromata. 
At  other  times  it  is  associated  with  facial  neuralgia,  or  with  convulsive  move- 
ments of  the  face.  Its  coarse  is  extremely  slow,  and  it  lasts  from  fifteen  to 
twenty  years,  without  endangering  the  patient's  life.  Long  remissions 
have  been  met  with,  and  in  some  cases  the  progressive  course  of  the  atrophy 
has  been  arrested. 

Raymond  and  Sicard  have  described  a  special  type  of  trophoneurosis 
— total  and  family  hemiatrophic  trophoneurosis.  In  their  cases  the 
atrophy  affected  not  only  the  face,  but  also  the  whole  of  one  side  of  the 
body.  It  was  progressive,  attacking  the  deep  and  superficial  structures. 
The  family  feature  was  found  in  two  generations. 

Pathogenesis. — The  aetiology  of  facial  trophoneurosis  is  very  obscure. 
The  pathogenesis  is  no  better  elucidated.  It  is  evidently  the  result  of 
trophic  troubles.  Why  do  these  troubles  supervene  ?  Which  are  the 
centres  and  which  are  the  nerves  primarily  affected  ?  It  has  been  suggested 
(Gintrac,  Lande)  that  the  connective  tissue  is  the  initial  seat  of  the  trophic 
lesion.  The  cellulo-adipose  tissue  is  said  to  disappear,  with  the  exception 
of  the  elastic  fibres.  Retraction  of  the  skin  and  atrophy  of  its  elements  are 
said  to  result  therefrom.  Several  objections  have  been  made  to  this  theory. 
How  are  we  to  reconcile  it  with  the  atrophy  of  the  deep  parts  of  the  face, 
with  the  changes  in  the  bones,  with  the  accurate  and  unilateral  localization 
of  the  disease,  when  the  lesions  which  commence  in  the  interstitial  tissue  are 
essentially  diffuse  ?     The  theory  which  places  the  initial  seat  of  the  mischief 


TRdl'IlK'  ANJ)   VASOMOTOR  Tliol  I'.I.KS  1G03 

in  the  nervous  system  is,  in  my  opinion,  more  correct,  and  there  is  no 
question  here  of  circuhitory  disturbance  due  to  vascMiHttor  troubles.  It 
is  rather  a  question  of  trophic  troubles  arisin}^  in  tlui  sphere  of  the  tri- 
geminal nerve  and  of  the  facial  nerve,  and  also  in  the  sphere  of  the  cervical 
plexus,  because  facial  trophoneurosis  sometimes  extends  as  far  as  the 
neck. 

III.  SCLERODERMIA. 

Description. — Sclerodermia,  or  disseminated  trophoneurosis  (Hallo- 
peau),  is  in  character  and  nature  closely  allied  to  unilateral  atrophy  of  the 
face. 

First  Period. — Sclerodermia  usually  commences  with  nervous  troubles. 
Some  patients  experience  numbness,  formication,  and  shooting-pains, 
analogous  to  rheumatic  pains,  in  the  limbs.  The  pains  come  on  in  fits. 
They  may  last  for  several  months,  and  may  be  sometimes  accompanied  by 
cutaneous  eruptions  (herpes,  zona,  pemphigus,  or  ecthyma).  In  this  period 
we  also  find  vasomotor  troubles — excessive  pallor  or  congestion  of  the 
skin,  cramps,  contractures,  and  hyperidrosis. 

Second  Period. — TNTien  the  sclerema  first  appears,  the  condition  is 
that  of  oedematous  sclerema.  Later  the  skin  and  the  cellular  tissue  attacked 
by  sclerema  become  as  hard  as  wood  and  look  like  stone. 

The  patches  of  sclerodermia  appear  in  various  regions  of  the  body.  They 
are  white  or  dark  coloured,  according  as  there  is  or  is  not  an  accumulation 
of  pigment.  These  patches  may  be  confluent  or  discrete.  They  are  usually 
symmetrical,  and  present  a  metameric  disposition  (Raymond).  The  skin 
of  the  patch  is  thin,  indurated,  and  analogous  to  scar  tissue.  "  The  charac- 
teristic feature  of  the  disease  is  a  special  induration,  affecting  a  more  or 
less  considerable  area  of  the  skin,  and  accompanied  by  a  certain  degree  of 
immobility  of  the  affected  parts  "  (Thirial). 

When  the  sclerema  is  situated  in  the  fingers,  they  become  rigid  and 
diminished  in  size.  The  atrophy  sometimes  attacks  the  palm  of  the  hand, 
and  the  retraction  of  the  skin  flexes  the  fingers  and  the  metacarpus,  and 
holds  them  fixed  in  this  position.     Ankylosis  sometimes  supervenes. 

Sclerema  of  the  neck  impedes  the  movements  of  the  head,  which  seems 
to  be  fixed  on  the  shoulders.  In  the  face  the  affection  attacks  both  sides. 
The  face  resembles  a  wax  mask,  and  the  natural  orifices  undergo  marked 
narrowing.  The  eyehds  are  retracted.  The  alae  nasi  are  thin  and 
flattened.  The  lips  become  small,  and  the  patient,  being  unable  to  open 
and  close  his  mouth  properly,  cannot  retain  the  food  and  the  saliva.  The 
troubles  of  mastication  and  of  deglutition  are  the  more  marked  because 
the  tongue  and  the  fracnum  are  sometimes  attacked  by  sclerodermia. 

In  the  limbs  the  embarrassment  of  the  movements  depends  on  the  seat 


1604  TEXT-BOOK  OF  MEDICINE 

and  the  extent  of  the  sclerodermia.  The  movements  of  flexion  of  the  fore- 
arm and  of  elevation  of  the  arm  are  very  limited.  The  affection  is  far  less 
common  in  the  lower  limbs. 

Sclerodermia  does  not  always  remain  limited  to  the  cutaneous  tissue. 
The  disease  also  attacks  the  deep  tissues,  and  in  this  case  the  word  "  sclero- 
dermia "  is  no  longer  sufficient,  and  the  denomination  disseminated  tropho- 
neurosis is  to  be  preferred  (Hallopeau). 

In  a  case  of  Ball  the  disease  made  its  appearance  in  the  fingers,  with  symptoms 
similar  to  those  of  local  asphyxia.  The  sclerodermia  appeared  later.  The  lower 
limbs  were  attacked,  and  the  bones  were  also  affected — atrophy  of  several  phalanges 
and  ankylosis  of  certain  articulations.  Vulpian  has  reported  a  case  of  sclerodermia, 
with  atrophy  and  disappearance  of  several  phalanges.  These  trophic  troubles  were 
not  accompanied  by  suppuration  or  by  the  formation  of  sequestra.  A  patient  seen 
by  HaUopeau  was  not  only  attacked  by  sclerodermia,  but  she  had  also  atrophy  of  the 
bones  and  arthropathy.  "  The  lingual  mucosa,  the  muscles  of  the  lips  and  of  the 
tongue,  and  probably  also  those  of  the  forearm,  were  atrophied.  Wherever  the  skin  was 
deeply  affected  the  subcutaneous  fat  had  to  a  large  extent  disappeared." 

We  see,  therefore,  that  sclerodermia  closely  resembles  facial  hemi- 
atrophy. In  some  cases  the  facial  hemiatrophy  was  not  only  limited 
to  the  face,  but  was  accompanied  by  sclerodermia  in  other  parts  of  the 
body.  Certain  changes  in  the  thyroid  body  (exophthalmic  goitre,  simple 
goitre,  and  atrophy  of  the  gland)  may  be  followed  at  an  earlier  or  later  date 
by  the  appearance  of  sclerodermia  (Jeanselme).  Let  me  also  add  that 
sclerodermia  has  some  relation  with  Rajmaud's  disease.  It  has  several 
times  commenced  with  the  same  symptoms,  so  that  some  writers  hold  that 
it  does  not  constitute  a  definite  morbid  entity.  According  to  Favier, 
"  sclerodermia  and  symmetrical  gangrene  of  the  extremities  are  closely 
related."  According  to  Apollinario,  "  there  is  a  close  affinity  between 
sclerodermia  and  local  asphyxia."  According  to  Grasset,  local  asphyxia, 
gangrene,  sclerodermia,  and  leprosy  are  all  manifestations  of  a  general 
pathological  condition. 

According  to  Brissaud,  every  case  of  sclerodermia  which  is  chronic  from 
the  outset  results  from  a  previous  affection  of  the  system  of  the  great 
sympathetic  nerve.  Lymphocytosis  has  been  observed  in  the  cerebro- 
spinal fluid. 

IV.  LOCAL  ASPHYXIA— SYMMETRICAL  GANGRENE  OF  THE 

EXTREMITIES. 

Under  the  name  of  "  local  asphyxia,"  or  symmetrical  gangrene  of  the 
extremities,.  Raynaud  has  described  a  form  of  dry  symmetrical  gangrene, 
affecting  the  fingers  and  the  toes,  and  more  rarely,  the  nose  and  the  ears. 

Description.^ — The  evolution  of  the  disease  may  be  divided  into  three 
periods  (Raynaud) ; 


TROPHIC  AND  VASiJMOToli  TliOlJIiLKS  um 

The  first  period,  which  is  generally  insidious,  lasts  from  a  few  days  to  a 
month.  It  is  characterized  by  local  asphyxia.  The  ends  of  the  fingers 
become  pale,  bloodless,  and  insensitive.  The  patient  lias  formication,  and 
the  lingers  feel  dead.  At  other  times  the  ends  of  tht^  fingrjrs,  instead  of 
being  bloodless,  become  livid  ;  there  is  a  venous  stasis,  or  local  asphyxia. 
The  invaded  parts  are  symmetrical.  The  thermomciter  shows  a  marked 
fall  of  temperature.  These  troubles  are  at  first  intermittent ;  later,  they 
become  continuous.  It  is  not  uncommon  to  see  hard  oedema  at  the  end  of 
the  affected  fiii^tTs. 

In  the  second  period,  or  stationary  stage,  the  formication  gives  place 
to  sharp  pain.  The  diseased  parts  assume  a  livid  tint,  and  sloughing  is 
imminent.  The  gangrene  is  sometimes  preceded  by  the  formation  of  pustules, 
which  break  and  leave  the  derma  exposed.  As  a  rule,  the  gangrene  is  super- 
ficial and  limited.  It  does  not  extend  below  the  superficial  layer  of 
the  derma,  and  the  nails  are  not  always  shed.  In  other  cases  the  entire 
phalanx  is  invaded,  and  the  dead  parts  become  as  black  as  coal.  The 
second  period  lasts  about  ten  days. 

In  the  third  period  we  find  elimination  of  the  eschars  and  cicatriza- 
tion. This  process  lasts  for  several  months.  When  the  gangrene  has  been 
very  superficial,  the  pulp  of  the  fingers  shows  whitish  parchment-like 
cicatrices.  The  end  of  the  finger  has  a  tapering  shape.  In  more  severe 
cases  a  line  of  demarcation  appears  at  the  base  of  the  gangrenous  part. 
The  suppuration  at  this  line  favours  the  tliro\ving  ofJ  of  the  slough. 

In  some  exceptional  cases  the  gangrene  is  not  confined  to  the  extremities 
of  the  fingers  and  of  the  toes.  It  also  invades  the  ears  and  the  tip  of  the 
nose  (Fischer),  and  it  may,  indeed,  be  limited  in  these  latter  parts,  whilst 
sparing  the  fingers  (Grasset). 

i^tiology  —  Diagnosis.  —  Symmetrical  gangrene  of  the  extremities 
usually  occurs  between  the  ages  of  eighteen  and  thirty  years.  Although  it 
is  rare  after  forty,  it  has,  nevertheless,  been  met  with  in  an  old  man  of 
seventy  years  of  age  (Renon).  It  is  more  frequent  in  women.  It  has  often 
been  apparently  associated  with  malaria  (Mourson),  with  sclerodermia, 
with  leprosy,  with  pericarditis  (Widal),  with  diabetes  (Apert),  with  ergotism 
(Ehlers),  and  with  tuberculosis  (Renon).  At  the  present  time  it  is  rather  a 
syndrome  than  a  proper  disease.  Certain  forms,  however,  appear  to  pre- 
serve their  autonomy.  It  is  probable  that  it  is  caused  by  a  tetanic  condition 
of  the  great  s\Tnpathetic  nerve,  thus  causing  contracture  of  the  arterioles 
(Ra\Tiaud). 

Goldschmidt  thinks  that  symmetrical  gangrene  of  the  extremities  and 
sclerodermia  must  be  placed  under  the  same  heading.  He  says  that 
obliterating  endarteritis  appears  to  be  the  primary  lesion,  which  depends, 
perhaps,  on  some  nervous  trouble. 

II.  102 


1606  TEXT-BOOK  OF  MEDICINE 

The  diagnosis  must  be  made  in  eacii  stage  of  the  disease.  It  must  not 
be  confounded  with  the  sensation  of  dead  fingers  met  with  in  consequence 
of  cold  and  in  hysteria  (Armaingaud).  I  have  described  the  symptom  of 
dead  fingers  in  Bright's  disease.  Gangrene  of  the  tips  of  the  fingers  has  been 
met  with  in  these  cases. 

The  so-caUed  senile  gangrene  is  due  to  vascular  lesions.  It  is  not  sym- 
metricalj  and  is  not  limited  to  a  single  focus. 

Apropos  of  treatment,  I  would  recommend  the  employment  of  super- 
heated air. 


PART   V 

GENERAL  AND  INFECTIOUS  DISEASES 

CHAPTER  I 
ERUPTIVE  FEVERS 

I.  VARIOLA. 

Trousseau  wTote  as  follows  on  variola  :  "  Variola,  whether  it  is  or  is  not 
modified,  assumes  two  chief  forms  :  it  may  be  discrete  or  confluent,  and 
whatever  form  it  takes,  it  is  normal  or  abnormal  in  its  course.  These  two 
forms  must  be  carefully  distinguished,  since  discrete  variola  is  usually  free 
from  danger,  while  the  confluent  form  is  nearly  always  fatal.  Their  course 
and  termination  are  so  difierent  and  their  characteristics  are  so  weU  defi.ned 
that  it  is  most  important  to  foUow  Sydenham's  example,  and  study  them 
separately." 

Discrete  and  Confluent  Variola. 

Description.  —  Discrete  variola  is  characterized  by  an  eruption  of 
pustules,  separated  from  one  another  by  large  areas  of  healthy  skin.  The 
febrile  remission  is  well  marked,  the  apyretic  periods  are  clearly  defined, 
and  the  prognosis  is  usually  good. 

Confluent  variola  is  characterized  by  an  eruption,  so  closely  set  that 
all  trace  of  healthy  skin  disappears.  The  febrile  remissions  are  incomplete 
or  of  short  duration,  and  the  prognosis  is  usually  bad. 

We  find  varieties  which  have  been  called  coherent-confluent.  They 
occupy  an  intermediate  place  between  the  two  chief  forms,  and  commence 
like  discrete  variola ;  but  the  pustules  suppurate,  and  finally  become  confluent 
by  fusion.  These  cases  are  not  confluent  from  the  outset,  and  are  far  from 
presenting  the  grave  prognosis  of  true  confluent  variola  ;  we  must  therefore 
be  careful  not  to  confound  the  two  forms. 

Incubation. — The  duration  varies  from  seven  to  fourteen  days,  irre- 
spective of  the  kind  of  variola.  It  is  customary  to  describe  four  phases 
of  the  disease — invasion,  eruption,  suppuration,  and  desiccation. 

1607  102—2 


1608  TEXT-BOOK  OF  MEDICINE 

1.  Invasion. — In  discrete  variola  the  phase  of  invasion  is  marked  by 
one  or  more  chills,  which  in  children  are  often  replaced  by  convulsions. 
By  the  end  of  the  first  day  the  thermometer  shows  a  reading  of  103°  or 
104°  F.,  and  the  temperature  remains  at  its  maximum,  with  some  oscilla- 
tions, during  the  whole  of  this  period.  Perspiration  is  seen  with  the  onset 
of  suppuration,  and  at  the  same  time  headache,  nausea,  and  vomiting 
appear.  Pains  in  the  loins  are  constant,  and  constipation  is  the  rule.  In 
some  cases,  however,  these  symptoms  are  not  clearly  defined. 

In  confluent  variola  the  symptoms  of  invasion  are  practically  the 
same,  although  constipation  is  often  replaced  by  diarrhoea,  and  perspira- 
tion is  absent ;  but  at  this  period  the  difierence  between  the  symptoms  is 
not  sufficiently  marked  to  enable  us  to  say  whether  the  eruption  will  be 
discrete  or  confluent.  Indeed,  we  see  patients  in  whom  the  symptoms  of 
invasion  are  very  severe,  but  only  result  in  an  eruption  of  a  few  papules. 
The  backache,  which  is  one  of  the  symptoms  of  this  phase,  appears  to  be 
due  to  congestion  of  the  spinal  cord,  which  may  be  so  severe  as  to  cause 
pain  in  the  limbs  and  paraplegia,  with  or  without  retention  of  urine. 

The  primary  rash  which  precedes  the  true  eruption,  and  which  English 
authors  have  called  the  "  variolous  rash,"  belongs  to  the  period  of  invasion. 
The  rash  assumes  two  chief  forms.  These  are  hyperaemic  and  hsemorrhagic, 
and  develop  either  alone  or  simultaneously  in  the  same  patient.  The 
hypersemic  rash  may  resemble  the  eruption  of  measles,  erysipelas,  erythema, 
or  urticaria  ;  but  the  hsemorrhagic  rash  is  scarlatiniform.  The  former  is 
very  extensive.,  fades  on  pressure,  and  lasts  only  one  or  two  days.  The 
latter  appears  a  little  later,  and  is  composed  of  plaques  with  a  red  base, 
upon  which  several  small  ecchymoses  are  found,  which  do  not  disappear 
on  pressure,  although  the  red  base  becomes  pale  for  a  moment.  The  rash 
is  caUed  "  astacoid  "  {aaraKofi,  boiled  lobster)  when  the  redness  is  intense. 
This  rash  is  usually  confined  to  the  axillse  and  the  groins,  but  it  may  become 
general,  lasting  several  days,  and  disappearing  slowly.  We  must  not 
confound  the  scarlatiniform  rash,  which  is  slightly  hsemorrhagic,  and  with- 
out dangerous  signification,  with  the  purpuric  eruption  met  with  in  hsemor- 
rhagic variola. 

The  frequency  of  the  rash  varies  in  different  epidemics,  and  has  been 
noted  forty-four  times  in  395  cases  by  Barthelemy.  It  is  found  in  all  forms 
of  variola,  and  has  neither  the  benign  nor  grave  prognosis  which  has  been 
attributed  to  it. 

The  presence  of  the  rash  may  be  of  assistance  in  the  diagnosis  of  variola 
in  a  difficult  case,  but  we  must  be  careful  not  to  make  the  mistake  of 
taking  the  morbilliform  rash  for  measles  and  the  scarlatiniform  rash  for 
scarlatina. 

What  is  the  duration  of  the  invasion  ?     The  classical  opinion  held  by 


EIUTTTVK  FEVERS  1G09 

Sydenham  and  Trousseau  has  lately  been  criticized.  According  to  these 
great  observers,  the  period  of  invasion  is  longer  in  discrete  than  in  con- 
fluent variola,  and  lasts  three  full  days — that  is  to  say,  the  eruption  appears 
at  the  end  of  the  third  day  or  in  the  course  of  the  fourth,  Init  very  rarely 
on  the  second  day.  In  confluent  variola  the  period  of  invasion  is  shorter, 
and  the  eruption  a])}>ears  at  the  end  of  the  second  or  in  the  course  of  the 
third  day.  To  this  rule,  however,  there  are  exceptions,  \vithout  speaking 
of  abnormal  cases. 

2.  Eruption. — In  discrete  variola  at  the  time  of  the  eruption  the  patient 
feels  better,  the  symptoms  of  the  period  of  invasion  disappear,  and  the 
fever  gradually  falls  in  twenty-four  or  in  thirty-six  hours.  The  eruption 
first  appears  on  the  face,  the  neck,  and  the  scalp  (Borsieri),  and  is  always 
most  marked  on  the  face,  whatever  the  variety  of  the  variola.  It  invades 
the  rest  of  the  body  almost  simultaneously,  and  is  complete  in  thirty-six 
hours.  The  eruption  at  its  onset  is  present  on  the  face,  in  the  form  of 
scattered  macules  or  of  papules,  which  are  red  and  slightly  pointed.  During 
the  next  few  days  these  little  papules  change  into  vesicles  of  unequal  size, 
in  which  a  milky  fluid  begins  to  form.  This  period  marks  the  onset  of 
suppuration.  The  papules  on  the  face  are  not  umbilicated,  but  those  on 
the  trunk  and  limbs  often  show  a  central  depression,  called  "  umbilication." 
However  slight  the  eruption  on  the  face  may  be,  it  produces  swelling,  which 
chiefly  invades  the  eyelids. 

The  eruption  appears  on  the  mucosae  at  the  same  time  as  on  the  skin 
(mucous  membrane  of  the  mouth,  pharynx,  larynx,  and  conjunctiva),  and 
produces,  according  to  its  situation,  dysphagia,  cough,  hoarseness,  or 
ocular  symptoms. 

In  confluent  variola  the  eruption  shows  quite  a  different  course.  T^Hiile 
in  the  discrete  and  coherent  forms  we  always  find  intervals  of  healthy  skin 
between  the  initial  papules,  in  this  form,  on  the  contrary,  the  face  is  invaded 
by  a  diffuse,  erysipelatous  redness,  and  the  eruption  occurs  nunc  erysipe- 
latis  ritu,  nunc  morhUlorum  (Sydenham).  The  papules  become  confluent, 
so  that  the  skin  often  looks  "  sad,"  like  shagreen.  On  the  second  and  third 
day  of  the  eruption  the  papules  become  vesicular,  but  the  vesicles  are  smaller 
than  those  seen  in  discrete  variola.  They  open  into  one  another,  lift  up 
the  epidermis,  and  commence  to  fill  with  milky  serous  fluid.  The  face 
is  swollen,  and  the  onset  of  suppuration  is  now  seen.  Similar  phenomena, 
although  they  are  less  marked,  occur  on  other  parts  of  the  body.  The 
eruption  on  the  mucosae  is  more  general  than  in  the  discrete  forms.  The 
pustules  invade  the  mouth  and  phar^mx  (dysphagia),  the  conjunctivae 
and  corneas  (photophobia),  and  the  lar}Tix  (cough  and  dyspncea).  They  may 
even  spread  to  the  intestine,  vagina,  and  urethra.  Orcliitis  has  been  seen 
in  variola. 


1610  TEXT-BOOK  OF  MEDICINE 

While  complete  defervescence  with  tlie  period  of  eruption  is  the  rule  in 
discrete  variola,  the  fever  persists  in  the  confluent  form,  or,  at  any  rate, 
the  defervescence  is  slow  and  incomplete,  and  some  patients  become 
delirious. 

3.  Suppuration. — In  discrete  variola  at  the  time  of  suppuration  the 
pustules  are  surrounded  by  an  inflammatory  areola,  and  the  umbilication 
disappears.  On  the  face  the  pustules,  which  are  more  or  less  spaced,  are 
at  first  soft  to  the  touch — leves  ad  tadum  (Sydenham)  —  but  later  they 
become  rough — as'periores — because  a  sero-purulent  oozing  takes  place  on 
their  surface,  and  then  they  dry  up.  On  the  body  suppuration  takes  place 
from  twenty-four  to  thirty-six  hours  later,  and  the  pustules  do  not  dry  up 
as  they  do  on  the  face,  but  burst,  and  allow  the  escape  of  the  contained 
pus.  On  the  hands  and  feet  suppuration  occurs  late,  and  is  accompanied 
by  pain  and  swelling,  while  the  pustules  often  resemble  "bright  drops  of 
pure  wax."  During  this  period  the  face  is  swollen,  there  is  profuse  lachryma- 
tion,  salivation  is  sometimes  abundant,  and  the  fever  reappears.  But  this 
fever,  which  marks  the  onset  of  suppuration,  and  occurs  about  the  eighth 
day  of  the  disease,  is  generally  of  slight  duration  and  moderate  intensity. 
Delirium,  when  present,  is  slight,  and  is  chiefly  seen  at  night. 

In  confluent  variola  events  take  a  different  course.  The  swelling  of  the 
face  is  universal,  and  the  angle  of  the  jaws  and  the  ears  are  almost  as  much 
swollen  as  in  erysipelas;  The  epidermis  is  raised  by  the  milky  secretion 
in  the  confluent  pustules.  Opaline,  greyish  blisters  appear,  and  give  the 
skin  of  the  face  the  appearance  of  a  parchment  mask  (Morton).  Later, 
these  blisters  become  yellowish  and  wrinkled,  and  exhale  a  most  foetid 
odour.  Similar  symptoms,  though  less  severe,  are  seen  on  the  other  parts 
of  the  body. 

When  suppuration  occurs,  the  fever  returns,  and  the  temperature  some- 
times exceeds  that  of  the  period  of  invasion.  The  fever  is  continuous, 
with  a  morning  remission,  and  lasts  during  the  whole  period  of  suppuration. 
Delirium  is  fairly  frequent,  and  sometimes  lasts  until  the  end  of  the  second 
week.  Salivation  is  excessive,  and  viscous  saliva,  which  soils  the  sheets 
and  pillows,  constantly  drools  away  from  the  mouth.  The  salivation 
diminishes  about  the  eleventh  day  of  the  disease,  and  the  swelling  of  the 
face  also  decreases  at  this  period ;  but  the  feet  and  hands  now  commence 
to  swell,  and  this  swelling  of  the  extremities  was  considered  by  Sydenham 
and  Trousseau  as  such  a  necessary  fact  that  its  absence  meant  a  most 
gloomy  prognosis. 

The  patient  suffers  excessively  during  the  whole  of  this  period.  The 
swelling  of  the  head  and  face  render  him  unrecognizable.  He  can  neither 
open  his  eyes  nor  move  his  lips  or  tongue.  Thick  mucus  oollects  in  the 
mouth  and  fauces,  and  the  dysphagia  is  so  great  that  he  may  find  it  difficult 


ERITPTIVE  FI':VF^:RS  1011 

to  quonoli  liis  tlilrafc.  TIk^  l)ro!it]iin{];  Ik  (•.oni|)r(nni.so(l,  apcech  is  diffioult, 
and  tlio  bed-linen  becomes  fcijiid  iiiui  soiled  with  pus,  in  spite  of  every  care. 
The  patient  is  indeed  fortunate  if  these  terrible  8ufT(»ring8  do  not  result  in 
death. 

4.  Desiccation. — In  discrete  variola  the  dry  pustules  become  covered 
with  crusts,  which  are  more  or  less  thick  and  yellowish,  soft  at  first  and 
then  hard.  When  the  crusts  fall  off,  they  leave  reddish  scars,  which  later 
become  depressed  and  white,  and  sometimes  persist  indefinitely.  In  the 
confluent  forms  the  crusts  are  not  isolated,  but  assume  the  appearance  of 
large  dark-coloured  scales,  which  are  imbricated  and  foul-smelling.  The 
resulting  scars  in  confluent  variola  (pitted  and  scarred  face)  cause  great 
deformity. 

Convalescence,  especially  in  the  confluent  forms,  is  not  free  from 
danger.  An  eruption  of  boils,  lasting  several  months,  may  appear  about 
the  fourth  week,  when  the  fever  has  fallen  to  normal  and  the  crusts  have 
all  dropped  ofl.  This  tendency  to  suppuration  is  also  shown  by  abscesses 
in  the  joints,  the  cellular  tissue,  and  the  muscles,  and  the  patient  often  dies 
from  prolonged  suppuration. 

Coherent  Variola. — The  differences  between  discrete  and  true  confluent 
variola  are  evident  from  the  preceding  description.  This  description,  how- 
ever, only  applies  to  typical  cases,  and  does  not  include  all  the  clinical  forms. 
Accordingly,  under  the  term  "  coherent "  writers  have  described  cases 
of  variola,  which  begin  like  the  discrete  form,  but  in  which  the  pustules 
are  so  numerous,  especially  on  the  face,  that,  although  isolated  when  the 
eruption  commences,  and  before  their  complete  development,  they  become 
confluent  when  they  reach  their  mature  stage.  This  secondary  confluence 
is  quite  different  from  true  confluent  variola.  These  cases  are  of  necessity 
more  serious  than  the  discrete  ones,  and  the  description  of  the  latter 
is  not  exactly  applicable  to  them,  and  yet  they  rarely  show  the  gravity  of 
true  confluent  variola. 

Varioloid. — This  term  does  not  signify  benign  variola,  for  varioloid 
may  be  very  severe  ;  neither  does  it  mean  very  discrete  variola,  for  it  may 
be  coherent.  The  term  "  varioloid  "  is  applied  to  any  case  of  variola 
which  does  not  suppurate,  or  which  shows  only  slight  suppuration.  The 
distinguishing -point  is  that  varioloid  does  not  end  in  a  stage  of  suppuration. 
The  symptoms  of  invasion  and  eruption  are  like  those  of  variola.  They  are 
generally  attenuated.  The  progress  of  the  eruption  is  then  arrested,  the 
secondary  fever  does  not  appear,  and  the  vesicles  dry  up ;  and  if  a  few  of 
them  do  suppurate,  they  become  horny,  without  leaving  scars.  Although 
varioloid  is,  as  a  rule,  quite  benign,  it  may  also  be  haemorrhagic.  Is  vario- 
loid variola  attenuated  by  vaccination  or  by  a  previous  attack,  or  is  it  rather 
a  special  form  of  variola  ?     In  no  case  must  it  be  confounded  with  varicella. 


1612  TEXT-BOOK  OF  MEDICINE 

Haemorrhagic  Variola, — It  is  necessary  to  distinguish  two  forms — the 
one  early,  which  precedes  the  eruption,  and  the  other  late,  which  appears 
during  the  course  of  the  eruption.  The  first  is  far  more  severe  than  the 
second.  It  is  always  fatal.  The  early  form  begins  like  ordinary  variola, 
but  the  patient  sometimes  sufTers  from  restlessness,  dyspnoea,  and  general 
malaise,  which  are  of  bad  augury.  A  haemorrhagic  and  purpuric  rash 
then  appears,  with  bluish  or  blackish  ecchymoses  in  the  groin,  upon  the 
neck,  the  face,  the  conjunctivae,  and  the  eyelids.  We  might  say  that  the 
patient  has  been  plunged  into  a  butt  of  wine  (Trousseau).  The  patient 
suffers  from  epistaxis,  haemoptysis,  and  haematuria  ;  blood  oozes  from  the 
gums  ;  the  skin  is  covered  with  blisters,  full  of  blackish  serum ;  and  the 
restlessness  and  dyspnoea  are  extreme.  The  tongue  is  dry,  the  breath  foetid, 
the  voice  is  reduced  to  a  whisper,  and  the  pulse  is  thready.  In  some  cases 
the  patient  retains  consciousness,  but  he  more  often  sinks  into  an  ataxo- 
adynamic  condition,  with  or  without  convulsions,  and  dies  on  the  third, 
fourth,  or  fifth  day,  either  before  the  appearance  of  the  eruption,  or  at 
any  rate  before  the  vesicles  have  definitely  appeared. 

The  late  form  of  haemorrhagic  variola  appears  in  the  course  of  the 
eruption,  which  is,  moreover,  often  retarded.  It  is  more  frequent  in  con- 
fluent than  in  discrete  variola.  The  haemorrhagic  symptoms  are  those 
which  I  have  just  described,  but  they  are  further  accompanied  or  preceded 
by  haemorrhages  into  the  pustules.  This  form  is  less  severe  than  the  pre- 
ceding one,  and  sometimes  recovers.  Haemorrhagic  variola  is  more  frequent 
in  some  epidemics.  It  was  terrible  during  the  epidemic  of  1871  (during  the 
war  and  the  Siege  of  Paris).  I  saw  a  large  number  of  cases  in  my  capacity 
as  house-physician  to  Ax:enfeld.  The  late  haemorrhages  are  favoured  by 
alcoholism  and  the  puerperal  state. 

Congenital  Variola. — When  variola  is  transmitted  by  the  mother  to  the 
foetus,  it  may  cause  different  clinical  varieties.  The  infant  may  be  born 
during  the  stage  of  incubation,  showing  at  the  time  no  signs  of  variola, 
which  appears  some  days  later,  and  carries  off  the  child.  The  incubation 
may  have  been  intra-uterine  ;  the  infant  is  born  with  the  eruption  well  out, 
and  death  supervenes  in  a  few  hours.  The  child  may  be  born  with  scars, 
or,  indeed,  without  any  trace  of  previous  variola,  and  is  immune,  being 
refractory  both  to  variola  and  to  vaccination.  The  liquor  amnii  is 
sterile. 

Anomalous  Variola. — The  following  description  will  indicate  the  meaning 
of  the  term  "  anomalous  variola  ":  An  individual  falls  sick  of  discrete 
variola,  which  is  apparently  quite  benign ;  but  the  eruption  appears  in  suc- 
cessive crops,  and  is  not  complete  until  the  sixth  or  seventh  day.  The 
pustules  develop  in  an  irregular  manner,  or  are  depressed  ;  perspiration  is 
absent,  and  cannot  be  induced  by  any  means  ;  the  urine  is  scanty  or  absent ; 


ERUPTIVK  FEVERS  1G13 

the  tnncuo  1)0^011103  dry  ;  the  pulso  is  small  ami  irrogulr^.r,  and  nervong  symp- 
toms (siibsultus  tt'udinum,  delirium,  dyspjuua,  and  coma)  herald  the  onset 
of  danger,  and  death  occurs  from  the  eighth  to  the  tenth  day,  because 
discrete  variola,  when  it  is  anomalous,  is  much  more  quickly  fatal  than  the 
confluent  form.  These  anomalous  or  malignant  cases,  as  Van  Swieten 
and  Borsieri  called  them,  are  most  frequent  in  some  epidemics.  Sydenham 
had  seen  them,  and  Trousseau  has  described  them ;  while  we  may  class 
them  with  anomalous  cases  of  scarlet  fever,  which  are  also  called  malignant. 

Prognosis — Complications. — According  to  the  general  law,  epidemic 
variola  is  much  more  serious  than  sporadic.  The  prognosis  of  variola  is 
benign  as  regards  the  discrete  form,  unless  the  case  is  an  anomalous  one, 
and  it  is  also  benign  in  varioloid.  It  is  much  more  serious  in  the  coherent 
forms,  and  fatal  in  the  confluent  and  hsemorrhagic  cases.  Patients  suffering 
from  confluent  variola  usually  succumb  from  the  twelfth  to  the  fourteenth 
day.  The  absence  of  vaccination  may  be  considered  as  making  the  prog- 
nosis serious,  even  from  the  onset  of  the  disease.  Variola  is  almost  always 
fatal  in  the  new-born  and  in  young  infants.  In  women  the  menses  generally 
appear  early  under  the  influence  of  variola,  and  metrorrhagia  is  common 
during  the  eruption  (Gubler).  In  the  pregnant  woman  miscarriage  is 
frequent  if  the  pregnancy  is  advanced  and  if  the  variola  is  severe.  The 
child  usually  dies,  and  the  mother  succumbs  in  60  per  cent,  of  the 
cases  ;  but  the  prognosis  is  less  serious  if  the  pregnancy  is  not  far 
advanced.  Ordinary  variola  may  become  hsemorrhagic  as  the  result  of 
the  puerperal  condition  and  from  the  second  day  after  the  confinement 
(Raymond). 

The  causes  of  death  in  variola  have  been  given  as  : — sideration  of  the 
nervous  system ;  changes  in  the  blood  resembling  those  caused  by  carbonic 
oxide  poisoning  ;  suppression  of  the  functions  of  the  skin,  causing  cutaneous 
asphyxia ;  pyaemia  consecutive  to  the  purulent  collections  in  the  skin. 
The  local  complications,  such  as  oedema  of  the  glottis  caused  by  the  erup- 
tion in  the  larynx  and  pleuro-pulmonary  inflammation,  which  tends  to 
suppurate,  may  be  added  to  these  causes. 

Broncho -pneumonia  (secondary  infection)  is  frequent  in  some  epidemics. 
It  is  insidious,  and  frequently  assumes  the  pseudo -lobar  form.  Myo- 
carditis and  cardiac  paresis  are  by  no  means  rare. 

The  endocarditis  of  variola  is  slight,  and  usually  leaves  no  trace.  The 
changes  in  the  larynx  may  result  in  necrosis  and  stenosis.  The  ophthalmia 
may  terminate  in  destruction  of  the  eye  and  loss  of  sight ;  the  otitis  may 
result  in  deafness ;  and  the  transient  paraplegia  of  the  period  of  invasion 
may  be  lasting.  In  the  course  of  variola  we  sometimes  see  secondary 
eruptions  of  ecth3ana  and  pemphigus,  which  become  a  serious  complication 
in  some  cases.     Dropsy,  with  or  without  albuminuria,  peripheral  neuritis. 


1614  TEXT-BOOK  OF  MEDICINE 

and  gangrene  of  the  mouth  and  of  the  parotid  glands,  have  also  been  seen. 
The  nephiitis  of  variola,  which  is  usually  transient  and  curable,  may  pass 
into  chronic  disease. 

etiology. — Variola  is  epidemic  and  contagious  at  every  period,  and 
here,  as  in  other  fevers,  the  contagion  is  direct  or  indirect.  The  agents  of 
contagion  are  the  blood  (Fournier),  the  pus,  and  the  crusts,  which,  in  a 
finely  divided  state,  preserve  their  virulence  for  a  long  time  in  rags,  linen, 
clothes,  rooms,  or  vehicles,  and  which,  being  light  and  mobile,  may  be 
carried  to  a  distance  and  meet  with  an  organism  in  a  state  of  receptivity. 
The  contagious  element  enters  the  system  through  the  respiratory  tract. 
The  specific  organism  has  not  yet  been  found. 

Diagnosis. — The  symptoms  of  variola  are  sudden  intensity  of  the  fever, 
headache,  vomiting,  and  backache.  The  presence  of  a  general  scarlatini- 
form  rash  may  for  a  moment  cause  doubt  between  scarlatina  and  variola, 
but  scarlatina  is  accompanied  by  angina,  and  not  by  backache.  The  erup- 
tion in  certain  vesicular  cases  of  measles  at  first  somewhat  resembles  that 
of  variola,  but  the  ocular,  nasal,  laryngeal,  and  bronchial  catarrhs  which 
characterize  the  invasion  of  measles  are  not  present  in  variola.  Pustular 
or  varioliform  acne  is  almost  always  limited  to  the  face  or  to  the  upper  parts 
of  the  back  and  of  the  chest,  while  the  pustules  present  a  comedo  in  their 
centre,  and  the  general  symptoms  of  variola  are  absent.  The  general 
erysipelatous  tint  of  the  face  which  follows  the  invasion  in  confluent  variola 
is  not  likely  to  be  confounded  with  the  clearly  defined  redness  and  prominent 
edge  in  erysipelas. 

Pathological  Anatomy. — At  the  onset  of  the  eruption  the  lesion  is 
situated  in  the  middle  portion  of  the  Malpighian  layer,  and  is  covered  by 
the  superficial  epidermis,  which  shows  no  change,  and  adheres  deeply  to 
the  papillary  layer.  The  section  of  a  ripe  pustule  shows  the  following 
points  :  At  the  edge  of  the  pustule  there  is  an  accumulation  of  young  cells 
arising  from  the  Malpighian  layer,  and  the  centre  of  the  pustule  is  parti- 
tioned ofi  by  threads,  and  contains  but  few  cells.  This  disposition  explains 
the  umbilication  of  the  pustules.  Complete  repair  is  possible  when  the 
Malpighian  layer  is  intact.  When  this  layer  is  completely  destroyed,  the 
scars  are  indelible. 

The  changes  in  the  blood  are  marked  The  gases  are  diminished  by 
one-half  in  the  haemorrhagic  forms  (Brouardel).  The  diminution  of  the 
haemoglobin  commences  before  the  eruption,  and  continues  to  the  end  of 
the  disease  (Quinquaud).  The  red  corpuscles  are  deformed,  and  lose  their 
power  of  taking  up  oxygen. 

The  other  lesions — granulo-fatty  degeneration  of  the  muscles  and  of 
the  heart,  changes  in  the  cells  of  the  liver  and  of  the  kidneys,  swelling  and 
softening  of  the  spleeu^are  common  to  all  severe  fevers. 


ERTTTIVE  FEVERS  1G15 

Treatment.—  Tlie  patient  should  be  placed  in  as  large  and  airy  a  room 
as  j)()ssihli'.  If  the  disease  is  mild,  it  will  suflice  to  prescribe  cool  drinks, 
gentle  laxatives,  broth,  and  milk.  If  the  disease  is  severe,  tonics  must 
also  be  employed.  Opium  should  be  used  for  the  nervous  complications, 
and  if  the  fever  is  severe  and  the  jiaroxysms  are  marked,  sulj)hate  of  quinine 
or  salicylic  acid  should  be  given.  When  suppuration  occurs,  the  most 
careful  nursing  is  necessary,  and  two  beds  should  be  employed,  so  that  the 
sheets  may  be  frequently  renewed.  Cool  baths  and  sponging  with  tepid 
water  are  indicated.  Trousseau's  custom  was  to  place  the  patient  in  a 
bath  and  pour  three  or  four  buckets  of  water  at  a  temperature  of  70"  F. 
over  him,  and  then  to  put  him  to  bed  wet  and  wrapped  in  a  blanket. 

Ducastel  has  employed  a  mixture  of  ether  and  opium,  giving  the  patient 
daily  6  spoonfuls  of  a  draught  in  which  opium  is  mixed  with  ether ;  but 
as  this  draught  is  often  nauseating,  it  may  be  replaced  with  advantage  by 
2  grains  extract  of  opium  in  the  twenty-four  hours,  and  a  subcutaneous 
injection,  containing  30  minims  of  ether,  morning  and  evening.  This 
treatment  does  not  appear  to  have  much  influence  on  the  general  intoxica- 
tion, but  in  some  cases  it  modifies  the  eruption  favourably,  and  appears 
to  lessen  the  degree  of  suppuration. 

Finsen,  by  placing  patients  suffering  from  variola  in  a  room  into  which 
only  the  red  rays  penetrate,  has  seen  the  eruption  come  out  more  rapidly. 
The  suppuration  diminishes,  and  the  scars  disappear  almost  completely. 
(Ettinger  has  confirmed  in  France  the  favourable  action  of  photo -therapy 
in  the  eruption  of  variola. 

Prophylactic  measures  cannot  be  too  rigorously  observed.  Patients 
must  be  isolated,  and  the  isolation  must  be  carried  out  in  a  thorough  manner. 
The  hospital  staff  who  are  brought  into  contact  with  patients  suffering  from 
variola  should  be  revaccinated.  The  patients  should  be  given  frequent 
baths.  We  must  not  forget  that  the  crusts  are  most  contagious,  and  that 
the  patients  must  be  isolated  until  every  crust  has  fallen  off. 

II.  VACCINIA. 

History. — Before  the  discovery  of  vaccinia  it  was  customary  to  inoculate  the  patient 
with  variola,  the  fluid  being  taken  from  the  vesicles  of  as  discrete  a  case  as  possible, 
and  inoculated  in  the  same  manner  as  in  the  case  of  arm-to-arm  vaccination.  Four 
days  later  a  vesicle  appeared,  and  soon  changed  into  a  pustule,  called  the  "  mother 
pustule,"  and  surrounded  by  secondary  pustules.  About  the  seventh  day  the  fever  of 
invasion  made  its  appearance,  and  the  variola  ran  its  course.  As  a  rule,  the  patient 
inoculated  with  discrete  variola  became  immune,  and  had  no  longei  cause  to  dread 
the  terrible  consequences  of  this  epidemic  scourge.  Unfortimately,  inoculation  some- 
times caused  severe  or  fatal  variola,  and,  in  addition,  the  patient  inoculated  with  variola 
became  an  epidemic  centre,  so  that  vaccination  was  preferred.  Vaccination,  however, 
was  not  accepted  at  first,  and  in  England  an  Act  of  Parliament  was  required  before 
vsccination  was  substituted  for  varioUzation. 


1616  TEXT-BOOK  OF  MEDICINE 

Although  Jenner  did  not  discover  the  vaccine,  yet  he  introduced  its  use  and  made 
it  popular,  so  that  the  honour  of  having  bequeathed  this  great  benefit  to  humanity 
belongs  to  him.  Jenner,  who  was  inoculator  for  his  own  district  (Gloucestershire), 
had  remarked  that,  according  to  popular  tradition,  milkers  who  came  in  contact  with 
the  cows  contracted  a  pustular  disease  known  as  cow-pox,  but  were  immune  during 
epidemics  of  variola.  Accordingly,  Jenner  inoculated  a  child,  eight  years  old,  with  the 
fluid  from  the  pustules  which  a  milkmaid  had  contracted  while  tending  to  her  cows. 
In  this  way  vaccine  was  discovered ;  the  child  was  vaccinated,  and  two  months  later 
an  attempt  at  variohzation  of  the  same  child  failed.  Such  is  the  origin  of  vaccina- 
tion, and  Jenner  pubhshed  his  first  paper  in  1798. 

Vaccinia  {vacca,  cow)  derives  its  origin  from  an  eruptive  disease  in  the  bovine  species 
which  attacks  cows,  and  especially  young  calves,  when  two  or  three  months  old.  This 
eruptive  disease,  cow-pox,  is  characterized  by  an  eruption  of  large  umbihcated  and 
flat  pustules  on  the  udder  of  the  animal.  The  horse  also  suffers  from  an  eruptive 
disease  of  the  same  nature,  the  pustules  being  situated  around  the  nostrils,  in  the  cavities 
of  the  nose  and  mouth,  and  also  on  the  lower  part  of  the  legs,  with  abundant  secretion. 
This  disease,  which  is  accompanied  by  marked  general  symptoms,  has  been  called 
horse-pox  (Jenner  called  it  "  grease  "). 

The  virus  of  cow-pox,  inoculated  into  the  human  species,  takes  the  name  of  vaccinia, 
and  prevents  variola.  Inoculation  of  human  beings  with  the  virus  of  horse-pox  gives 
the  same  result.  Is  the  vaccine  virus  simply  the  virus  of  variola,  modified  by  its  passage 
through  the  cow,  or  is  it  a  disease  special  to  the  bovine  species  ?  I  shaU  answer  these 
questions  by  quoting  Chauveau's  conclusions  : 

1.  Vaccinia,  no  matter  how  exalted  its  virus,  never  changes  into  variola. 

2.  We  may  inoculate  the  cow  with  variola,  but  it  never  becomes  vaccinia  in  passing 
through  the  bovine  species.  The  disease  is  variola,  remains  variola,  and  gives  rise  to 
variola,  if  it  is  reproduced  in  the  human  race.  This  statement  also  apphes  to  variola 
inoculated  in  the  horse  and  transferred  to  man.  The  virus  of  variola  and  that  of  vaccinia 
are  therefore  of  different  natures.  On  the  other  hand,  horse-pox  and  cow-pox  are  of 
the  same  nature,  although  the  vaccine  grows  better  in  the  cow  than  in  the  horse. 

Chauveau's  statements  have  not  been  accepted  without  dispute.  Depaul  was 
convinced  of  the  identity  of  variola  and  vaccinia,  while  numerous  experiments  under- 
taken in  Germany  and  Switzerland  would  also  tend  to  identify  the  two  diseases,  but 
these  experiments  are  not  yet  sufficiently  conclusive.  From  the  clinical  point  of  view, 
the  dualists  have  a  better  case  than  the  imicists.  We  see  clearly,  say  the  dualists, 
that  vaccinia  and  variola  are  different  diseases,  for  variola  is  essentially  contagious  and 
epidemic,  while  vaccinia  is  never  epidemic  and  never  contagious  (Bousquet,  Hervieux) ; 
we  must  admit  that  variola  and  vaccinia  are  two  different  diseases,  because  they  may 
run  their  course  simultaneously  in  the  same  individual  or  animal.  Moreover,  says 
Chauveau,  in  the  milUons  of  vaccinations  performed  since  Jenner's  time  we  have  never 
seen  vaccinia  recover  its  so-called  virulence  and  reappear  as  variola  ;  aU  these  successive 
passages  have  never  been  able  to  exalt  its  virulence.  We  have  never  seen  those  returns 
to  the  parent  form  which  are  "  so  characteristic  of  the  attenuated  virus,  and  of  which 
examples  are  fairly  frequent  with  the  most  perfectly  prepared  artificial  vaccine,  such  as 
the  vaccine  from  the  anthrax  pustule  made  by  Pasteur."  In  short,  until  there  is  proof 
to  the  contrary,  Chauveau's  opinion  must  stand  good. 

Pathological  Anatomy. — The  structure  of  the  pustule  in  vaccinia  is 
comparable  to  that  of  variola,  and  we  find  the  same  vacuolar  change  in 
the  cells  of  the  epidermis  and  the  same  necrosis.  The  base  of  the  pustule 
is  indurated,  the  cavity  is  divided  by  septa,  and  the  juices  with  which  it  is 
impregnated  form  the  lymph.     The  lymph,  which  is  clear  and  transparent 


EKUITIVE  FEVERS  Hi  1 7 

ill  iiKiii  up  to  the  sovcuth  day,  and  in  the  cow  ujj  to  tin-  flftli  day,  contains 
leu('«»cvt('s,  rod  corjUKscIcs,  ^raniilulions,  and  niicro-orgiinisniH. 

The  juicrohe  of  vaccinia  is  .still  unknown.  Strau.s  followed  day  by  day 
the  evolution  of  the  vaccine  pustule  in  the  (;alf,  and  by  means  of  histo- 
h)f^ical  ])re])arations  showed  its  difTcrent  i)liases.  We  see  clearly  in  these 
sections  colonies  of  nucrobes,  which  at  first  occupy  the  lips  of  the  inocula- 
tion wound,  then  pass  into  the  Malpighian  layer,  and  reach  the  lymphatic 
tracts. 

Various  microbes,  including  the  Stafhylococcus  aureus,  the  liaderium 
termo,  and  a  saccharomyces,  as  well  as  other  forms,  have  been  found  in 
vaccine  lymph  (especially  in  the  calf),  but  they  are  the  microbes  of  secon- 
dary infection.  The  absence  of  the  Streptococcus  pyogenes  would,  according 
to  Pfeiffer,  explain  the  rarity  of  erysipelas  in  vaccination.  A  coccus 
(Voigt),  to  which  a  certain  amomit  of  importance  has  been  assigned,  has 
also  been  noted  by  Garre. 

Yaccination. — Formerly  human  or  Jennerian  lymph  was  usually 
employed ;  animal  vaccination  has  now  rightly  become  the  proper  method. 

In  employing  animal  lymph,  the  following  are  some  of  the  previous 
conditions  formulated  by  Saint- Yves  Menard  as  being  necessary  to  obtain 
good  lymph  :  A  young  heifer,  which  has  already  been  weaned,  is  taken, 
because  we  can  thus  avoid  diarrhoea  and  other  diseases  frequent  in  the 
animal  before  weaning.  The  heifer  is  inoculated  with  horse-pox,  natural 
cow-pox  (when  obtainable),  or  cow-pox  from  other  heifers.  The  animal  is 
placed  in  the  stable  and  tied  up  with  a  short  cord,  in  order  that  it  may  not 
be  able  to  lick  the  wound.  The  fever  is  absent  or  insignificant.  The  lymph 
which  is  collected  on  the  fifth  or  sixth  day  is  the  best. 

It  may  be  prepared  as  a  pulp  or  a  powder,  and  every  antiseptic  pre- 
caution should  be  observed.  This  lymph  will  keep  for  a  long  while,  but  it 
is  obviously  less  likely  to  be  successful  than  vaccine  taken  directly  from 
the  heifer. 

Kelsch  has  made  an  important  communication  to  the  Academie 
concerning  the  action  of  the  surrounding  temperature  on  the  preservation 
of  the  vaccinal  pulp.  In  the  ordinary  refrigerator  at  the  Academie,  the 
tubes  of  pulp  are  kept  at  a  temperature  of  4-  5  to  -f  7.  Other  tubes  were 
kept  in  a  special  refrigerator  at  a  constant  temperature  of  —  12  to  —  15. 
After  six  months  in  these  two  kinds  of  refrigerator,  the  contrast  between 
the  two  sets  of  lymph  was  most  striking.  Four  infants  vaccinated  with 
the  Academy  lymph  showed  no  reaction ;  in  the  case  of  the  other  lymph, 
seven  infants,  varying  in  age  from  seven  to  twenty  months,  all  showed  a 
positive  reaction.  At  the  end  of  a  year  the  Academy  lymph  was  absolutely 
inert,  while  the  other  lymph  was  still  endowed  with  its  maximum 
efficiency. 


1618  TEXT-BOOK  OY  MEDICINE 

The  pulp,  after  being  pounded  up  and  mixed  with  glycerine,  was 
placed  in  the  ordinary  refrigerator ;  it  kept  its  active  properties  for  about 
five  weeks,  so  that  it  was  possible  in  due  time  to  the  recipients,  but  it  was 
necessary  for  them  to  use  it  promptly  because  it  rapidly  lost  its  vaccinal 
properties,  when  placed  even  in  a  cool  place.  Probably  many  vaccination 
failures  are  due  to  neglect  of  this  recommendation. 

The  eruption  of  vaccinia  corresponds  to  the  first  stage,  and  about  four 
days  after  vaccination  a  papule  forms.  It  becomes  umbilicated  on  the  fifth 
or  sixth  day,  and  filled  with  clear,  transparent  fiuid,  called  "  lymph."  On 
the  seventh  day  the  pustule  is  formed.  It  is  flat,  umbilicated  in  the  centre, 
swollen  at  the  periphery  by  the  lymph,  and  surrounded  by  a  reddish  areola. 
About  the  eight  day  the  mature  or  suppuration  period  begins,  when  fever, 
lassitude,  headache,  and  gastric  disturbance  are  sometimes  seen.  The 
corresponding  lymphatic  glands  are  painful,  the  pustules  become  of  a  whitish 
tint,  the  umbilication  disappears,  the  lymph  becomes  turbid  and  sero-puru- 
lent,  and  the  skin  of  the  region  is  red  and  shiny.  Desiccation  begins  about 
the  tenth  day.  A  brownish  spot  appears  at  the  centre,  and  then  invades 
the  whole  pustule.  Desiccation  ends  on  the  fourteenth  day,  and  we  see  a 
dry,  thick,  adherent  brownish  crust,  which  does  not  fall  off  until  the 
eighteenth  day.     Whitish  scars  are  left  by  the  pustules. 

False  vaccinia,  which  is  abortive  and  confers  no  immunity,  is  charac- 
terized by  vesicles  that  appear  on  the  day  after  vaccination.  They  are 
accompanied  by  sharp  itching,  dry  up  rapidly,  without  presenting  umbili- 
cation, and  sometimes  have  the  appearance  of  a  boil. 

Jennerian  and  animal  vaccine  give  the  same  results,  and  confer  the 
same  immunity  against  variola.  How  long  does  this  immunity  last  ?  It 
begins  about  five  days  after  vaccination,  and  as  the  usual  incubation  period 
of  variola  is  from  nine  to  thirteen  days,  vaccination  five  days  in  advance 
will  prevent  the  development  of  variola.  In  some  persons  vaccination 
confers  immunity  lasting  for  life;  but  in  others  the  period  of  immunity 
is  limited  to  eight  or  ten  years,  so  that  reYaccination  is  absolutely 
necessary,  especially  during  epidemics.  We  cannot,  then,  have  recourse 
to  vaccination  too  freely.  In  the  German  and  French  armies,  in  which 
vaccination  has  been  compulsory  for  many  years,  variola  may  be  said  to 
exist  no  longer.  "  In  the  Ear  East  no  more  deadly  scourge  than  variola 
exists.  No  one  who  has  not  seen  it  break  out  in  a  country  where  vaccina- 
tion has  not  penetrated  can  form  any  idea  of  the  incalculable  number  of 
its  victims "  (Jeanselme).  Accordingly,  all  possible  means  must  be 
employed  to  make  vaccination  compulsory. 

General  Vaccinia. — In  some  cases  the  eruption  is  not  limited  to  the  seat 
of  inoculation,  but  is  more  or  less  disseminated  over  different  parts  of  the 
body.     It  may  result  from  animal  or  from  Jennerian  vaccine.     It  would 


ERUPTIVE  FEVKRS  IHIO 

appear  chiefly  to  supervene  after  vaccination  with  horse-pox.  Certain 
derniatoHos  (eczema,  impctifro)  place  the  skin  in  a  state  of  receptivity,  and 
favour  the  disseniiiuition  of  the  vaccine.  The  eru[)tiou  in  general  vaccinia 
runs  its  course  at  the  same  time  as  that  of  inoculation,  the  two  eruptions 
being  contemporaneous,  which  proves  clearly  that  vaccinia  is  not  the 
result  of  auto-inoculation,  but  that  it  is  distinct,  and  constitutes  a  true 
eruptive  fever,  which  sometimes  determines  fatal  infectious  troubles  in 
children. 

Vaccinal  Eruptions. — From  the  eighth  to  the  twelfth  day  after  vacci- 
nation, when  the  vaccinal  eruption  is  at  its  height,  we  sometimes  see  various 
eruptions  appear  without  warning,  fever,  or  general  symptoms.  In  some 
cases  we  find  a  vaccinal  rash  which  may  resemble  the  rash  of  measles,  scarlet 
urti-fever,  or  erysipelas,  or  may  be  erythematous,  exudative,  papular,  or 
carial ;  it  commences  around  the  .pustules,  spreading  thence  to  the  neck, 
the  arms,  and  the  whole  of  the  body.  Sometimes  the  eruption  has  the 
appearance  of  miliaria,  being  vesicular,  and  accompanied  by  pruritiis 
and  desquamation.  Lastly,  in  very  rare  cases  the  eruption  is  pemphigoid 
or  purpuric.  These  vaccinal  eruptions  are  comparable  to  those  produced 
by  drugs,  or  to  the  rashes  caused  by  the  toxines  of  numerous  microbes,  and 
by  injections  of  serum. 

Complications  of  Vaccinia. — Vaccination  is  sometimes  followed  by 
complications,  of  which  some  are  benign,  while  others  are  grave.  There 
is  one — vaccinal  syphilis — which  exclusively  results  from  Jennerian 
vaccination. 

Vaccinal  Syphilis. — This  terrible  complication  of  vaccination  (Fournier) 
has  been  proved  clinically  by  cases  seen  at  Coblentz  (nineteen  persons  who 
became  syphilitic),  at  Rivalta  (thirty-nine  children),  at  Algiers  (fifty-eight 
soldiers),  and  at  Paris  (five  persons).  It  has  been  proved  experimentally  by 
Cory,  who  voluntarily  inoculated  himself  with  s}T)hilis  by  means  of  vaccine 
from  a  syphilitic  child.  The  vaccino-syphilitic  inoculation  assumes  the 
following  forms  :  (1)  Chancre  develops  alone,  and  vaccinia  is  absent ;  (2)  the 
chancre  develops  either  on  a  pustule  or  in  one  of  the  pimctures  which  have 
not  taken. 

Chronologically,  the  chancre  appears  several  weeks  after  the  vaccinia, 
and  the  vaccinal  eruption  has  long  since  ended  when  the  chancre  commences, 
for  syphilis  has  an  incubation  period  of  three  to  four  weeks.  This  is  one 
of  the  chief  distinctive  signs  from  ulcerative  vaccinia.  At  first  the  chancre 
has  the  appearance  of  a  papule,  which  becomes  encrusted.  Under  the 
crust  a  circumscribed  sore  with  an  mdurated  base  is  found. 

Contagion  may  occur,  although  the  giver  is  not  suffering  from  active 
syphilis,  but  only  from  latent  s}^hilis  (hereditary  or  acquired),  which  has 
not  shown  any  traces  upon  the  skin  or  elsewhere.     It  will,  therefore,  be 


1620  TEXT-BOOK  OF  MEDICINE 

seen  that  the  source  of  the  lymph  is  a  very  important  matter.  It  has  been 
asserted  that  all  accidents  may  be  avoided  by  taking  only  the  lymph,  and 
by  avoiding  lymph  mixed  with  blood.  To  this  the  answer  may  be  given 
that  it  is  non-proven  that  the  lymph  may  not  contain  at  one  and  the  same 
time  the  active  principle  of  vaccinia  and  of  syphilis,  and,  further,  no  matter 
what  precautions  are  taken,  red  corpuscles  are  always  found  in  vaccine 
lymph  collected  from  a  vaccinifer.  The  only  safe  method  of  preventing 
this  accident  is  to  employ  animal  lymph. 

Ulcerated  Vaccinia. — We  sometimes  see  ulcerations  instead  of  pus- 
tules between  the  eighth  and  twelfth  days  after  vaccination.  These  ulcera- 
tions may  exceed  the  size  of  a  sixpence.  They  are  deep,  hollowing  out  and 
destroying  the  skin.  The  edges  are  straight-cut,  and  the  base  is  anfrac- 
tuous, pulpy,  diphtheroidal,  or  gangreniform.  They  are  surrounded  by  a 
large  red  areola,  and  the  tissues  upon  which  they  rest  show  difiuse  inflam- 
matory induration.  In  some  cases  the  ulcers  unite,  the  suppuration  is 
abundant,  and  the  oedema  is  very  extensive.  Impetiginous  and  ecthy- 
matous  eruptions,  lymphangitis,  and  lymphatic  oedema,  may  complicate 
the  vaccinal  ulcer,  which,  as  a  rule,  is  not  painful.  These  troubles  cause 
indolent  and  hard  inflammation  of  the  glands,  while  fever  is  rare,  and  the 
general  health  does  not  suffer. 

These  ulcers  do  not  only  develop,  as  was  at  first  supposed,  in  feeble 
or  lymphatic  patients  :  they  occur  sometimes  in  epidemic  form  in  those 
who  are  in  good  health,  as,  for  instance,  in  the  epidemic  at  Motte-aux- 
Bois,  in  which  forty-two  children  suffered  from  vaccinal  ulcers. 

The  claim  that  ulcerative  vaccinia  is  more  frequent  when  animal  lymph 
is  employed  is  ill  founded,  since  in  several  epidemics  of  ulcerative  vaccinia — 
among  others,  that  at  Motte-aux-Bois — the  lymph  had  been  taken  from  a 
child,  and,  moreover,  appeared  to  be  perfectly  good.  This  ecthymato- 
ulcerative  vaccinia  is  certainly  the  result  of  secondary  infection,  and  due 
to  pathogenic  agents  developing  in  lymph  which  has  been  kept  too  long, 
and  has  become  purulent.  From  the  point  of  view  of  diagnosis  the  ulcera- 
tive vaccine  will  not  be  confused  with  vaccinal  syphilis,  because  the  chancre 
does  not  suppurate  or  form  an  ulcer,  while  its  edges  are  not  straight-cut. 
Lastly,  ulcerative  vaccinia  appears  from  the  eighth  to  the  tenth  day  after 
vaccination,  while  the  chancre  does  not  appear  until  three  weeks  after. 
Accordingly,  the  period  of  incubation  is  totally  different  in  the  two  cases. 

Vaccinia  in  some  cases,  which  are,  fortimately,  exceptional,  may  be 
followed  by  other  complications,  including  erysipelas,  profuse  inflammation, 
and  fatal  septicaemia  ;  but  these  complications  are  due  to  secondary  infection, 
which  may  easily  be  avoided. 

The  fear  of  vaccinal  tuberculosis  is  illusory.  Neither  animal  nor 
Jennerian  vaccination  is  capable  of  causing  tuberculosis.     There  is  not  a 


ERUPTIVE  FEVERS  1621 

single  positive  case.  Koch's  bacilli  have  never  boiiii  met  with  in  lymph 
taken  from  tuhcrciiiar  j)atieiits,  while,  if  tlie  iymjih  is  taken  from  nn  animal, 
we  must  remember  that  tuberculosis  in  young  calves  (which  are  used  as 
the  source  of  the  lymph)  is  so  rare  that  only  one  case  of  tuberculosis  has 
been  found  in  22,000  calves  slaughtered  in  the  abattoir  at  Augs})urg. 

We  can,  with  proper  precautions,  avoid  all  complications.  In  the  first 
place,  vaccinal  sy])hilis  is  no  longer  possible,  if  animal  lymph  be  employed. 
In  the  second  place,  we  can  prevent  any  other  complications  by  employing 
f resli  lymph  taken  on  the  fifth  day  from  the  calf,  or  on  the  seventh  day  from 
a  child,  and  by  being  careful  to  perform  inoculation  with  aseptic  instru- 
ments on  an  area  of  skin  which  has  previously  been  rendered  aseptic. 

Sero-thera'py. — The  first  experimental  point  to  establish  is  that  "serum 
of  a  vaccinated  heifer,  collected  after  the  virulent  period — i.e.,  ten  to  fifty 
days  after  vaccination — possesses  immunizing  properties  against  inoculated 
vaccinia  ";  and  it  further  exercises  "  in  vitro  on  the  vaccine  an  action  which 
may  be  called  antivirulent,  since  the  vaccinal  virus,  after  being  bathed 
in  this  serum,  can  no  longer  be  successfully  inoculated,  and  produces 
hardly  any  local  reaction.  The  attempts  of  sero-therapy  to  cure  variola 
with  serum  from  the  vaccinated  heifer  have  not  yet  given  any  conclusive 
result. 

III.  VARICELLA. 

Varicella  is  an  eruptive  fever,  contagious,  epidemic,  inoculable,  very 
benign,  and  distinct  from  varioloid,  from  which  it  differs  by  its  mode  of 
invasion,  the  character  of  its  eruption,  as  well  as  by  its  course  and  nature. 
It  presents  three  periods — incubation,  invasion,  and  eruption. 

Description. — The  incubation  period  of  varicella  is  a  fortnight  when  it 
results  from  contagion,  but  varies  from  three  to  seventeen  days  when  it 
is  caused  by  inoculation  (D'Heilly).  In  1895  Apert  saw  in  a  maternity 
hospital  an  epidemic  of  varicella  which  lasted  five  months,  and  attacked 
ten  children  and  two  wet-nurses.  The  cases  succeeded  one  another  with  an 
almost  mathematical  regularity  every  fortnight,  thus  allowing  the  duration 
of  the  incubation  to  be  fixed.  The  symptoms  of  the  period  of  invasion 
are  very  slight.  They  comprise  fever,  malaise,  and  loss  of  appetite.  In 
less  than  twenty-four  hours  small  rose-coloured  spots  can  be  seen  on  the 
skin.  Next  day  these  spots  form  vesicles,  filled  with  clear  or  slightly  coloured 
fluid.  By  the  second  day  the  bleb  is  fuUy  formed.  It  is  sometimes  umbHi- 
cated.  It  reaches  the  size  of  a  lentil  or  of  a  small  pea.  On  the  next  day 
it  is  surrounded  by  a  painfid  inflammatory  area,  and  the  fluid  in  it  becomes 
[  urulent.  It  then  breaks  and  dries  up,  leaving  a  blackish  crust,  like  that  which 
follows  a  pustule  of  ecth}'Tna.  The  evolution  of  the  bleb  is  therefore  com- 
plete in  three  days,  while  eight  days  are  necessary  for  the  pustule  of  variola. 

II.  103 


1622  TEXT-BOOK  OF  MEDICINE 

The  eruption  in  varicella  often  leaves  some  slight  scars,  especially  in 
children  who  scratch  themselves  and  pull  off  the  crusts. 

The  eruption  of  varicella  comes  out  in  successive  crops,  which  are  accom- 
panied by  fever,  and  follow  each  other  for  four  or  five  days,  and  even  a 
week  to  a  fortnight.  The  eruption  shows  no  especial  predilection  for  any 
part  of  the  body,  but  commences  and  spreads  at  the  same  time  on  the  face, 
trunk,  and  limbs.  On  the  first  day  a  dozen  papules  may  be  seen ;  on 
the  foUowing  day  thirty  to  a  hundred  may  be  counted,  and  so  on  for  several 
days.  Varicella,  however,  always  remains  more  or  less  discrete,  and  the 
eruption,  however  general  it  may  be,  does  not  become  confluent. 

Varicella  is  sometimes  accompanied  by  a  scarlatiniform,  morbilliform, 
or  erythematous  rash,  which  lasts  about  twenty-four  hours.  It  may 
follow  or  may  precede  the  true  eruption. 

The  eruption  of  varicella  may  invade  the  mucous  membranes  of  various 
regions  (mouth,  tongue,  uvula,  tonsils),  as  well  as  the  conjunctivse  and 
corneae  (kerato-conjunctivitis),  and  it  may  also  be  found  in  the  larynx, 
where  it  may  cause  laryngitis,  with  spasm  of  the  glottis  and  death.  In 
the  laryngeal  eruption  small  circular  ulcers  are  often  found  on  the  vocal 
cords. 

Complications  are  rare  in  the  course  of  varicella.  Nevertheless, 
nephritis,  which  is  usually  benign  and  transient,  has  been  seen  (Henoch). 
Gangrene  is  one  of  the  most  unusual  complications  in  varicella.  The 
disease  has  run  a  normal  course,  the  pustules  have  dried  up,  and  recovery 
is  at  hand,  when,  without  appreciable  cause,  and  without  warning,  some 
of  the  vesicles  become  injected  with  blood,  necrose,  and  ulcerate.  The 
gangrenous  ulcers  increase  in  extent  and  depth,  and  the  disease  generally 
ends  fatally.  Arthritis,  which  is  very  rare,  may  supervene  during  the 
decline  of  the  disease.  It  chiefly  attacks  the  large  joints — ^namely,  the 
knee,  shoulder,  and  hip.  The  arthritis  is  always  multiple,  and  the  strepto- 
coccus is  the  pathogenic  agent  (Braquehaye  and  De  EouvUle). 

Diagnosis. — The  vesiculo-bullous  appearance  of  the  eruption  which 
occurs  in  successive  crops  is  diagnostic  of  varicella.  On  examination  of  the 
eruption  over  the  whole  surface  of  the  body,  it  is  rare  that  we  do  not  find 
in  the  midst  of  growing  vesicles  and  of  vesico-pustules,  which  are  more  or 
less  purulent  or  dried  up,  some  adult  vesicles  in  the  form  of  crystalline 
blebs,  which  are  transparent,  rounded,  and  pathognomonic  of  varicella. 
The  distinction,  however,  between  varicella  and  modified  variola  is  some- 
times difficult.  Certain  diagnostic  points  are,  however,  present.  Thus, 
the  period  of  invasion  in  modified  variola  lasts  three  days  at  least,  and  the 
usual  symptoms  are  fever,  headache,  backache,  and  vomiting ;  while  in 
varicella  the  period  of  invasion  lasts  one  day,  and  the  symptoms  are  trifling 
(malaise,  lassitude,  and  slight  fever).     The  eruption  of   modified  variola 


ERUPTIVE  FEVERS  1 623 

does  not  appear  before  the  end  of  the  third  or  the  coinmencement  of  the 
fourth  day,  while  that  of  varicella  appears  in  twenty-four  hours. 

The  eruption  of  modified  variola  commences  on  the  face,  while  that  of 
varicella  commences  with  a  primary  crop  on  different  parts  of  the  hody. 
The  eruption  in  modified  variola  gradually  passes  into  the  umbilicated 
pustule,  while  that  of  varicella  results  within  twenty-four  hours  in  a  vesicle. 

This  discussion  upon  the  diagnosis  of  varicella  and  varioloid  brings  us 
to  another  question  of  primary  importance — viz.,  are  varicella  and  varioloid 
two  distinct  diseases,  each  showing  its  own  individuality  and  specific  nature, 
or  is  varicella  an  attenuated  variety  of  varioloid  ? 

Trousseau  was  the  first  to  separate  varicella  from  varioloid.  Varicella 
considered  in  a  general  manner,  said  Trousseau,  presents  clearly  marked 
differences  from  varioloid,  so  that  it  is  scarcely  comprehensible  how  con- 
fusion has  been  possible.  Indeed,  the  history  of  epidemics  teaches  us  the 
fact  that  variola  may  be  present  alone,  but  that  varioloid  is  never  present 
in  epidemic  form  without  being  accompanied  by  cases  of  true  variola. 
Variola  never  attacks  a  child  who  has  been  vaccinated  two  or  three  years 
previously,  and  the  inoculation  of  variola  may  be  attempted  with  im- 
punity ;  but  the  same  child  readily  takes  varicella  if  he  comes  in  contact 
with  another  child  suffering  from  this  disease.  Further,  if  an  individual 
who  has  just  had  varicella  is  placed  in  contact  with  variola,  he  ought  not 
to  contract  the  latter  disease  if  the  varicella,  of  which  he  still  carries  traces, 
is  only  modified  variola.  We  know,  on  the  contrary,  that  the  individual 
may  contract  true  variola.  Lastly,  these  two  exanthemata,  varicella  and 
varioloid,  may  occur  simultaneously  or  successively  in  the  same  patient. 
Varicella  and  variola  are  therefore  two  absolutely  distinct  diseases. 

The  great  authority  of  Trousseau  had  so  clearly  decided  the  question 
that  no  one  in  France  attempted  to  uphold  the  ancient  doctrine  of  the 
identity  of  varicella  and  varioloid.  Abroad,  on  the  other  hand,  some 
observers  were  of  the  opposite  opinion,  and  proclaimed  the  identity  of  the 
two  diseases  (Kaposi,  Hebra).  Their  opinions  have  recently  found  some 
partisans  in  their  own  country,  who  run  a  great  risk  of  remaining  isolated, 
for  Trousseau's  teaching  is  more  alive  than  ever.  The  ideas  which  our  great 
master,  with  so  much  reason  and  good  sense,  caused  to  prevail  in  the  name 
of  clinical  medicine  have  been  confirmed  by  indisputable  observations,  of 
which  I  give  a  resume. 

Senator  and  Tordeus  have  successfully  vaccinated  children  who  have 
had  varicella,  and  D'Espine  has  seen  varicella  occur  on  the  twenty-second 
day  in  a  case  of  variola.  Those  who  believe  in  the  identity  of  the  twc 
diseases  should  carefully  ponder  over  the  following  case  : 

A  child,  thirteen  months  old,  in  whom  (Ettinger  found  characteristic  varicella, 
was  sent  by  mistake  to  the  annex  for  cases  of  variola.     In  a  short  while  the  child 

103—2 


1624  TEXT-BOOK  OF  MEDICINE 

recovered  from  the  varicella.  CEttinger,  having  found  no  marks  of  previous  vaccination, 
had  very  properly  recommended  immediate  vaccination,  which,  however,  was  done 
only  ten  days  later.  Two  days  later  the  child  showed  symptoms  of  variola,  which 
proved  fatal,  although  the  vaccinal  pustules  had  appeared  at  the  three  inoculated 
points  at  the  same  time  as  the  eruption  of  variola.  This  case  is  most  instructive.  If 
varicella  and  variola  were  the  same  disease,  this  child,  who  had  just  had  the  former, 
would  not  have  contracted  the  latter  some  days  later,  and  if  varicella  and  vaccinia, 
were  the  same  disease,  as  some  authorities  have  upheld,  the  vaccine  would  not  have 
taken  in  the  child  who  had  just  had  varicella.  "  This  case,"  says  CEttinger,  "  in  con- 
junction with  one  of  Dr.  Sharkey  and  many  others,  is  another  plea  in  favour  of  the 
specific  nature  of  varicella.  It  is  only  one  case,  but  it  is  irrefutable,  and  should  prevail 
against  all  the  contrary  hypotheses  which  might  be  formulated." 

In  some  cases  varicella  suppurates.  Aiter  one  or  two  days  the  fluid 
in  the  vesicle  loses  its  limpid  character,  and  becomes  opalescent,  yellowish, 
and  purulent.  It  contains  polynuclear  leucocytes  in  large  number,  whUe 
the  citron-coloured  fluid  of  varicella,  like  the  purulent  fluid  of  the  pustule 
in  variola,  contains  chiefly  mononuclear  cells.  The  staphylococcus,  with 
or  without  the  streptococcus,  is  the  organism  which  produces  the  suppura- 
tion. This  suppuration  lasts  a  few  days,  and  ends  in  rupture  or  slow  desicca- 
tion of  the  vesicle,  with  the  formation  of  crusts  and  scars,  like  those  of 
variola.  The  appearance  of  pus  is  sometimes  accompanied  by  fever. 
Epidemics  of  suppurative  varicella  have  been  seen.  The  diagnosis  between 
variola  and  suppurative  varicella  is  not  always  free  from  difiiculty,  and 
yet  in  a  case  of  suppurative  varicella  we  always  find  clear  or  limpid  vesicles, 
which  permit  us  to  make  a  diagnosis. 

Treatment. — The  treatment  of  varicella  consists  in  attention  to  hygiene, 
mild  purgatives,  milk  diet,  and  the  application  to  the  vesicles  of  an  oint- 
ment, in  order  to  avoid  infection  (oxide  of  zinc,  1  part ;  powdered  talc, 
5  parts).  A  bath  is  given  when  the  disease  is  at  an  end,  and  until  then  the 
patient  should  be  isolated,  for  varicella  is  markedly  contagious  in  children. 
Infection  and  dissemination  take  place  with  the  greatest  rapidity. 


IV.  SGAKLATINA. 

Description. — I  shall  choose  as  my  type  a  case  of  scarlatina  of  moderate 
severity,  and  I  shall  then  describe  the  malignant,  hssmorrhagic,  and 
defaced  forms,*  which  are  far  more  rare. 

The  evolution  of  scarlatina  is  usually  divided  into  four  periods— incuba- 
tion, invasion,  eruption,  and  desquamation. 

Incubation. — The  period  comprised  between  the  introduction  of  the 
infective  agent  into  the  economy  and  the  appearance  of  the  first  symptoms 
has  not  been  exactly  determined.  Certain  facts  would  indicate  that  it 
mav  be  very  short— not  longer  than  twenty-four  hours  (case  reported  by 

*  See  p.  1629. 


ERUPTIVE  FEVERS  1025 

Tronsspan)— but  tho  averap^e  duration  is  four  to  seven  days,  while  it  mav  be 
more  than  a  fortnight.  During  the  period  of  incubation,  which  is  generally 
latent,  the  patient's  general  health  is  excellent.  Sometimes,  however,  the 
infective  process  which  is  going  on  in  the  economy  shows  itself  by  general 
malaise. 

Invas^ion. — Scarlatina  usually  commences  with  more  or  less  severe 
plienomena,  including  rigors,  quick  pulse  (110  in  adults  and  140  in 
children),  rise  of  temperature  to  104°  F.,  sore  throat,  and  headache. 
Nausea,  vomiting  of  food  or  of  bile,  and  convulsions  in  young  children, 
or  delirium  in  adults,  are  sometimes  seen  in  the  severe  forms.  In 
some  persons  the  vomiting  at  the  onset  of  scarlatina  is  frequent  and 
uncontrollable,  and  in  some  epidemics  it  has  been  the  chief  feature  (Greifs- 
wald  epidemic,  1826).  Sore  throat  is  the  symptom  noticed,  almost  to  the 
exclusion  of  others,  during  the  period  of  invasion.  I  may  say  that  most 
cases  of  scarlatina  in  children  commence  with  acute  tonsillitis,  which  is 
set  down  to  cold,  and  it  is  only  some  hours  later  or  on  the  next  day  that 
we  see  the  appearance  of  the  exanthem  in  the  mouth  and  pharynx,  or  of 
the  rash  upon  the  skin.  We  can  then  correct  an  erroneous  diagnosis,  or 
confirm  a  doubtful  one.  The  angina  causes  pain  on  swallowing  ;  the  throat 
is  dry,  and  the  tonsils  are  swollen,  as  at  the  onset  of  tonsillitis,  and  of  a 
dark  red  colour,  which  extends  to  the  throat  and  soft  palate.  The  retro- 
maxillary  glands  are  painful  and  enlarged.  The  tongue  is  coated,  but  red 
at  the  tip  and  edges.  Anorexia  is  present,  and  the  thirst  is  acute,  but 
diarrhoea  is  rare.  The  respiratory  system  remains  free.  Absence  of 
cough  is  the  rule — an  important  and  striking  contrast  to  the  invasion  of 
measles. 

Eruption. — The  period  of  invasion  usually  lasts  twenty-four  to  thirtv- 
six  hours.  It  may  last  only  a  few  hours,  and  the  eruption  and  sore  throat 
may  appear  at  the  same  time.  The  eruption  does  not  show  itself  first  on 
the  face,  as  in  measles  and  variola,  but  usually  begins  on  the  neck  and 
chest,  and  becomes  more  or  less  general,  the  hands  being  invaded  last. 

At  first  the  eruption  is  composed  of  red  spots,  which  are  small  and  not 
prominent.  They  quickly  unite,  without  leaving  intervals  of  healthy  skin, 
and  form  extensive  patches  of  a  strawberry  or  scarlet  colour ;  whence  the 
name  of  red  fever  formerly  given  to  scarlatina.  A  large  area  of  the  body 
may  be  thus  coloured  by  the  eruption,  but  the  tint  is  not  absoluteh'  uniform. 
A  darker  stippling  shows  on  the  red  ground  of  the  exanthem.  The  redness 
of  the  skin  is  most  marked  on  the  neck,  the  abdomen,  and  the  inner  surface 
of  the  thighs  and  arms.  When  we  press  on  the  parts  invaded  by  the  erup- 
tion, or  trace  lines  with  the  point  of  a  pencil,  the  redness  gives  place  for 
a  moment  to  a  whitish  colour,  which  contrasts  with  the  red  groimd. 

This  classical  description  of  the  eruption  does  not  include  all  cases,  for 


1626  TEXT-BOOK  OF  MEDICINE 

there  are  discrete  eruptions  in  scarlatina,  formed  by  a  multitude  of  little 
red  points,  rounded,  isolated  from  one  another,  and  somewhat  like  the 
eruption  of  measles. 

The  eruption  on  the  face  difiers  somewhat  from  that  on  the  body,  being 
streaky,  or  formed  by  red  and  white  tracts,  like  the  finger-marks  seen  after 
the  ears  have  been  boxed  (Trousseau).  In  addition,  the  face  is  puffy  and 
swoUen,  and  this  swelling  is  also  noticeable  in  the  feet  and  hands.  The 
swelling  begins  and  increases  with  the  eruption,  so  that  by  the  second  or 
third  day  it  hampers  the  movements  of  the  fingers  ;  but  it  is  not  painful, 
and  must  be  distinguished  from  the  rheumatic  swelling,  which  I  shall  describe 
later.  More  or  less  acute  itching  accompanies  the  eruption,  and  is  usually 
associated  with  the  benign  forms  and  with  abundant  sweating. 

The  eruption,  though  sometimes  transient,  usually  lasts  from  three  to 
five  days,  and  if  it  is  at  aU  confluent,  it  is  accompanied  by  a  crop  of  miliaria 
on  the  neck  and  the  abdomen.  The  miliary  eruption  gives  to  the  skin  the 
appearance  called  "  goose-flesh."  The  vesicles  of  the  miliary  rash  are 
perceptible  to  the  touch,  and  are  at  first  filled  with  a  colourless  fluid,  which 
thirty-six  hours  afterwards  becomes  milky. 

Can  any  relation  be  established  between  the  intensity  of  the  eruption 
and  the  gravity  of  the  fever  ?  Trousseau  held  the  following  opinion  :  It 
is  said  that  when  the  eruption  is  "  weU  out,"  in  vulgar  parlance,  the  patient 
has  less  chance  of  being  attacked  by  serious  complications.  The  contrary 
opinion,  however,  holds  good,  for  in  scarlatina,  as  in  the  other  eruptive 
fevers,  the  more  intense  the  eruption,  the  more  severe  is  the  disease.  This 
proposition,  however,  is  not  absolute,  and  in  scarlatina,  just  as  in  variola, 
if  the  eruption  is  prevented  by  some  grave  antagonistic  inflammation,  by 
severe  haemorrhage,  or  by  profound  nervous  disturbances,  it  does  not  appear 
in  a  typical  form,  but  is  iU-defined  and  incomplete.  This  occurs,  then,  in 
anomalous  scarlatina,  which  is  not  always  free  from  danger. 

The  angina  must  now  occupy  our  attention.  It  forms  from  the  onset 
of  scarlatina  the  chief  symptom,  and  increases  in  severity  during  the 
eruptive  period.  The  movements  of  deglutition  are  so  painful  that  the 
patient  cannot  swallow  the  saliva.  He  expectorates  continuously ;  he 
can  drink  only  at  the  risk  of  sharp  pain,  and  fluids  regurgitate  through  the 
nose ;  the  voice  is  nasal.  The  swelling  of  the  uvula  and  tonsils  may  em- 
barrass the  breathing.  On  examination  of  the  throat,  we  find  that  the 
tonsils  are  large,  the  uvula  is  oedematous,  the  mucous  membrane  is  swollen, 
and  a  diffuse  redness  (scarlatinal  exanthem)  invades  aU  these  regions, 
and  at  times  covers  the  mucosa  of  the  cheeks  and  lips.  On  the  third  or 
fourth  day  the  angina  becomes  pultaceous  {fvls,  pvltis,  pap),  and  on  the 
tonsils,  which  are  large  and  red,  we  see  in  the  crypts  a  deposit  of  small 
whitish  or  greyish  concretions,  forming  a  pultaceous  coating  that  is  not 


ERTTPTTVE  FEVERS  1G27 

adherent  to  tho  sul)jacoiit  parts,  and  is  readily  reiuuved  with  a  tamjjon  of 
wool.  This  pultaceous  coating  is  formed  by  tlu^  products  of  epithelial 
desquamation  »nd  by  the  mucus  secreted  by  the  follicles  of  the  tonsil.  It 
is  perfectly  soluble,  as  can  be  j)roved  by  shaking  it  for  a  few  moments  in  a 
glass  of  water.  The  angina  ends  in  three  or  four  days,  and  the  concretions 
disappear  from  the  tonsils,  which  remain  red  and  sometimes  excoriated 
(Trousseau). 

The  tongue  is  absolutely  characteristic.  After  the  coated  condition 
at  first  seen,  the  epithelium  is  gradually  laid  bare,  and  between  the  third 
and  sixth  day  of  the  disease  the  organ  presents  a  scarlet  surface,  which  is 
swollen  and  thickly  set  with  large  papillae,  giving  it  a  strawberry-like  appear- 
ance. iVbout  the  seventh  or  eighth  day  the  tongue,  although  it  preserves  its 
red  colour,  becomes  smoother,  and  loses  its  strawberry  appearance ;  but 
it  is  only  about  the  twelfth  day  that  its  appearance  approaches  the  normal, 
the  red  tint  being  still  marked. 

The  lesions  of  the  mouth  and  pharynx  affect  the  tonsils  (tonsillitis)  and 
the  mucosa  of  the  cavity  (bucco-pharATigeal  erythema).  Berger  has  even 
insisted  on  the  importance  of  the  dissociation  of  these  two  local  lesions  (of 
which  tonsillitis  is  the  first)  from  the  point  of  view  of  pathogenesis. 

Adenopathy  in  scarlatina  is  constant.  With  the  onset  of  angina  the 
glands  at  the  angle  of  the  jaw  become  painful,  enlarged,  and  indurated. 

Fever  persists  during  the  whole  of  the  eruptive  period,  and  shows  a 
continuous  type,  with  a  slight  morning  remission.  It  ceases  when  the 
eruption  disappears. 

Desquamation. — Desquamation  begins  from  the  sixth  to  the  tenth 
day,  sometimes  even  while  the  rash  is  still  out.  It  commences  on  the 
neck  and  the  chest,  and  finishes  on  the  palms  of  the  hands  and  the  soles  of 
the  feet.  It  never  assumes  the  branny  form  of  measles.  On  the  face  it 
takes  place  in  small  scales  ;  on  the  trunk  larger  scales  are  seen.  On  the 
arms  and  legs,  and  especially  on  the  feet,  where  the  epidermis  is  thicker, 
patches  of  large  size  may  peel  ofi.  On  the  fingers  the  epidermis  is  some- 
times shed  in  strips,  which  may  resemble  the  fingers  of  a  glove.  Shedding 
of  the  nails  has  also  been  seen  (Graves).  Desquamation  lasts,  on  an  average, 
from  eight  days  to  a  fortnight.  It  may,  however,  be  prolonged  to  thirty, 
fifty,  and  seventy  days  (Trousseau).  The  knowledge  of  these  facts  is  of 
the  highest  importance,  for  scarlatinal  desquamation  may  give  a  clue  to 
such  complications  as  albuminuria,  anasarca,  severe  angina,  endocar- 
ditis, etc. 

Slight  Forms. — Sydenham's  dictum  that  "  scarlatina  scarcely  merits 
the  name  of  a  disease  "  may  be  applied  to  these  forms.  After  fever  lasting 
for  some  hours  and  slight  sore  throat,  a  trifling  eruption  appears,  but  the 
patient  only  experiences  slight  malaise.     The  digestive  functions  are  not 


1623  TEXT-BOOK  OE  :\IEDICIXE 

afiected.  The  desquamation  is  very  slight,  and  in  a  few  days  the  disease  is 
at  an  end.  Every  intermediate  form  between  these  benign  and  the  serious 
cases  is  seen. 

Severe  Forms — Malignant  Scarlet  Fever.— I  hare  preserved  the 
epithet  malignant,  because  this  term,  given  to  the  disease  by  our  prede- 
cessors, is  most  applicable  to  the  forms  which  I  shaU  now  describe. 
Malignant  scarlet  fever  runs  the  following  course  : 

On  the  first  day,  says  Trousseau,  or  during  the  first  few  hours,  the 
disease  reaches  its  maxLtnum.  It  may  prove  fatal  within  twenty-four  hours. 
This  form  which  IdUs  patients,  like  a  superacute  intoxication,  is  character- 
ized by  extremely  rapid  pulse,  hyperpyrexia,  delirium,  restlessness,  con- 
"^-ulsions,  uncontrollable  vomiting,  diarrhcea,  dryness  of  the  skin,  cyanosis, 
suppression  of  urine,  and  attacks  of  sufiocation.  And  as  these  troubles 
may  be  fatal  before  the  appearance  of  the  rash,  the  diagnosis  would  be  very 
difficult  in  the  absence  of  an  epidemic. 

The  following  cases,  quoted  by  Trousseau,  will  show  better  than  any 
description  the  picture  of  malignant  scarlet  fever  : 

"  I  was  summoned,"  says  Trousseau,  "  by  my  friend  Dr.  Bigelow  to  a  boarding- 
school  in  Paris  to  see  a  young  American  girl.  Since  the  morning  she  had  been  a  prey 
to  frightful  delirium,  with  incessant  vomiting  and  high  fever  ;  the  pulse  was  so  rapid 
that  the  beats  could  not  be  counted,  and  there  was  extraordinary  dryness  of  the  skin. 
These  symptoms  caused  me  to  state,  on  seeing  the  patient,  that  the  case  was  one  of 
scarlet  fever,  and,  indeed,  although  no  other  symptoms  appeared,  my  diagnosis  was 
confirmed  by  the  presence  of  a  characteristic  rash  upon  another  young  lady  at  the 
same  school,  in  which  an  epidemic  was  raging.  The  patient  died  before  the  end  of  the  day. 

"  In  1824,  at  the  beginning  of  the  disastrous  epidemic  which  broke  out  at  Tours, 
and  of  which  I  have  spoken,  I  saw,  with  Bretonneau,  a  yoimg  girl  who  died  in  less  than 
eleven  hours  with  acute  deHrium,  excessive  restlessness,  and  extraordinary  frequency 
of  the  pulse.  Here  there  was  nothing  to  indicate  the  nature  of  the  disease,  except  that 
an  epidemic  of  scarlatina  was  raging,  and  that  in  the  girl's  family  several  persons  had 
been  attacked. 

"  Beware,  then,  under  such  circumstances,  of  nervous  complications  marking  the 
onset  of  illness  in  the  midst  of  an  epidemic  of  scarlatina  which  has  already  attacked 
members  of  the  same  family  as  the  patient  to  whom  you  are  called.  These  symptoms 
nearly  always  indicate  mahgnant  scarlet  fever,  which  almost  always  kills  with  astonishing 
rapidity  those  whom  it  attacks." 

Side  by  side  with  these  fulminant  forms  we  see  very  similar  cases,  which 
are,  however,  slower  in  their  evolution,  and  which  may  end  in  recovery. 
In  them,  too,  the  nervous  troubles  play  the  chief  part,  and  the  period  of 
invasion  is  characterized  by  extreme  frecjuency  of  the  pulse,  by  delirium,  and 
by  insomnia,  which  yields  to  no  remedies.  The  temperature,  which  is 
already  very  high,  continues  to  rise.  The  patient  complains  of  pra&cordia] 
distress,  and  the  dyspnoea  is  so  great  that  the  respiration-rate  may  be 
40  or  50  per  minute,  although  auscultation  does  not  reveal  any  broncho- 
pulmonary lesion.     This  dyspnoea  is  of  nervous  origin — or  sine  materia. 


ERirnVH  FKVERS  1G20 

as  tilt!  old  writers  were  wont  to  call  it.  It  is  often  of  evil  augury  in  the 
loxi-iiifectious  diseases.  Vomiting  and  diarrhuja  an;  rarely  absent,  and 
if  the  patient  succumbs,  he  is  usually  carried  off  during  the  eruptive 
period. 

In  some  cases  grave  complications  supervene,  not  so  much  at  the  onset 
of  the  disease,  as  during  its  course,  when  the  eruption  is  fully  out.  Lastly, 
there  are  cases  in  which  the  nervous  troubles  assume  an  adynamic  form, 
and  the  patient  dies  in  a  typhoid  state. 

These  terrible  forms,  exceptional  in  sporadic  scarlatina,  belong  to  the 
epidemic  form  of  the  disease,  and  are  more  or  less  frequent,  according  to  the 
particular  epidemic. 

Haemorrhagic  Scarlatina. — This  form  is  very  rare,  for  scarlatina  is 
much  less  prone  to  haemorrhagic  complications  than  variola  and  measles. 
The  haemorrhage  generally  appears  at  the  same  time  as  the  rash.  The 
patients  experience  some  serious  symptoms — the  skin  is  covered  with 
petechiae  ;  haematm-ia  and  epistaxis  are  common.  The  prognosis  in  haemor- 
rhagic scarlatina  is  bad. 

Defaced  Scarlatina. — The  word  '"  defaced,"  coined  by  Trousseau,  is 
an  excellent  one.  He  applied  the  term  defaced  to  those  cases  of  scarlatina 
in  which  the  eruption  is  wanting,  and  which  show  only  some  one  s}Tnptom 
by  which  the  diagnosis  can  be  reconstructed,  just  as  in  archseology  an 
inscription  is  called  defaced  when  a  more  or  less  considerable  part  is  blotted 
out,  and  some  words  alone  remain  by  which  we  can  reconstruct  the  entire 
inscription.  Defaced  scarlatina  is  chiefly  seen  in  epidemics  (Graves).  In 
one  patient  who  has  had  no  rash  the  only  prominent  symptom  of  the  disease 
is  angina.  In  another  patient  the  scarlatina  reveals  itself  by  desquamation, 
anasarca,  nephritis,  albuminuria,  or  haematuria,  which  may  or  may  not  be 
preceded  by  angina. 

I  quote  two  cases  of  defaced  scarlatina  reported  by  Trousseau  : 

"  In  1854,  at  Meaux,  I  saw,  ^-ith  my  friend  Blache,  a  case  of  defaced  scarlatina. 
In  the  same  house  a  young  girl,  fourteen  years  of  age,  had  been  taken  ill  with  severe 
scarlatina,  characterized  by  pultaceous  angina,  high  fever,  and  specific  rash.  A  few 
days  later  her  sister  was  also  taken  ill  with  the  same  symptoms ;  almost  at  the  same 
time  a  housemaid  fell  sick  ;  and,  two  or  three  days  later,  a  valet,  who  remained  during 
the  whole  day  in  the  house,  was  affected  by  severe  sore  throat,  viith  pultaceous  exudate 
on  the  tonsils,  redness,  and  then  cleaning  of  the  tongue  and  acute  fever,  although  no 
eruption  appeared  on  the  skin.  It  was  clear  that  all  these  patients  had  scarlatina, 
and  that  the  valet,  remaining  in  such  an  epidemic  centre,  had  contracted  it  just  as  the 
whole  family  did,  but  in  another  form,  so  that  in  his  case  the  inscription  was  defaced, 
wliile  in  the  others  the  scarlatinal  phase  had  been  complete.  There  was  also  a  young 
bpy,  six  years  of  age,  who  suddenly  became  swollen  up,  without  having  been  ill  for  a 
moment.  Blache  and  I  were  then  called  in  consultation,  and  recognized  scarlatinal 
anasarca,  which  had  been  the  first  sjinptom  to  appear  ;  it  was  considerable  in  amount, 
and  was  accompanied  by  haematuria.  The  father  and  mother,  who  were  very  careful 
about  their  son's  health,  declared  that  he  had  eaten  his  breakfast  as  usual  that  morning. 


1630  TEXT-BOOK  OF  MEDICINE 

and  Ms  schoolmaster  also  told  us  that  he  had  played  about  as  usual.  He  had  neither 
fever  nor  rash  ;  the  disease  was  indicated  in  his  case  by  the  single  comphcation  for  which 
we  were  called  in  consultation. 

"  In  December,  1860, 1  saw,  with  my  friend  Dr.  Gros,  a  youth,  fifteen  years  of  age,  who 
furnished  another  example  of  defaced  scarlatina,  and  in  whom  the  diagnosis  would  have 
been  impossible  if  we  had  not  had  assistance  from  the  accessory  conditions.  This  youth 
had  come  from  college  with  shght  fever  and  sore  throat.  The  ilhiess  was  so  sUght  that 
Dr.  Gros  was  not  called  in,  and  the  patient  recovered  after  two  days  of  trifling  indispo- 
sition. A  few  days  later  his  younger  sister  took  scarlatina,  and  when  she  was  conva- 
lescent her  brother  was  attacked  by  hsematuria,  which  lasted  more  than  a  month.  I 
did  not  doubt  for  a  moment  that  this  youth  had  given  scarlatina  to  his  sister,  and  that 
the  haematuria  was  the  result  of  the  pyrexia,  the  manifestation  of  which  had  been  so 

shght." 

I  have  several  times  witnessed  defaced  scarlatina.  In  a  family  in  which  five  persons 
were  attacked  by  true  scarlatina,  I  saw,  with  Jules  Simon,  a  remarkable  example  of 
defaced  scarlatina  in  a  child  four  years  old.  In  this  case  the  expected  rash  did  not 
appear,  but  the  sore  throat  which  had  marked  the  onset  of  the  disease  was  followed  by 
considerable  swelling  of  the  neck  and  glands ;  anasarca  and  pyehtis,  with  scanty  and 
muco-purulent  urine,  followed.     The  patient  finally  recovered. 

I  saw  a  dhild  in  the  Avenue  Montaigne  with  fever,  rapid  pulse,  and  sore  throat ; 
the  redness  of  the  soft  palate  and  of  the  tonsils  (enanthema)  was  so  marked  that  I  at 
once  diagnosed  scarlatina.  We  watched  closely  for  the  appearance  of  the  rash,  but 
it  did  not  appear  ;  in  short,  the  scarlatina  was  absolutely  defaced.  About  the  eighth 
day,  however,  characteristic  desquamation  supervened.  Desquamation  may  occur  in 
scarlet  fever  without  any  previously  appreciable  rash. 

I  saw  one  of  my  colleagues  from  the  provinces  who,  after  attending  a  child  with 
scarlet  fever,  was  himself  taken  Ul  with  fever  and  a  sore  throat  of  strawberry-hke 
appearance.  As  he  was  certain  that  he  had  scarlatina,  he  watched  closely  for  the  rash, 
but  it  did  not  appear.  Eight  days  after,  desquamation  began ;  and  nephritis,  which  was 
fortunately  shght,  appeared  some  days  later. 

In  epidemics  of  scarlet  fever  we  see  attenuated  forms,  comprising  a 
simple  sore  throat,  so  slightly  marked  tliat  the  disease  passes  unnoticed, 
and  also  apyretic  forms  which  are  not  free  from  complications. 

Complications  of  Scarlatina. 

The  conditions  which  we  call  "  complications,"  in  order  to  conform  to 
custom,  and  which  are  usually  the  result  of  secondary  infections,  may 
supervene  in  the  most  benign  cases  of  scarlatina.  They  appear  during  the 
course  of  the  disease,  or  during  the  period  of  defervescence. 

Scarlatinal  Angina. — Scarlatina  is  essentially  a  disease  accompanied 
by  sore  throat.  I  have  already  described  the  early  erythematous  angina, 
which  may  hamper  deglutition  and  respiration,  and  which  is  often  accom- 
panied by  marked  glandular  enlargement.  This  form,  usually  associated 
with  the  streptococcus  or  the  staphylococcus,  yields  rapidly. 

Membranous  angina,  a  condition  of  much  interest,  presents  quite  another 
picture.  Trousseau  was  the  first  to  admit  two  varieties  of  membranous 
angina  in  scarlatina.  The  one  which  is  not  diphtheritic  is  usually  early 
and  benign,  and  has  no  tendency  to  spread  to  the  larynx.     It  was  in  this 


RRTTPTIVK  FEVERS  ](\n 

connoctioii  witli  this  form  that  Troussoau  enunci.ilcd  the  celel)rate(l 
ai)liorism,  "  Scarhitina  does  not  like  the  larynx."  The  other  variety, 
di})htheritic  in  nature,  and  more  serious,  may  invade  the  respiratory  tract, 
or  run  the  course  of  malignant  di])htheria.  Bacteriology  has  demonstrated 
the  truth  of  Trousseau's  observation,  and  also  of  his  clinical  teaching. 
Bacteriological  research  has  clearly  elucidated  the  question  of  huffy  angina 
in  scarlatina,  which  was  formerly  so  confused. 

Early  and  late  membranous  buffy  angina  is  seen  in  scarlatina.  The 
early  cases  usually  appear  from  the  third  to  the  sixth  day  of  the  fever,  and 
are  hardly  ever  diphtheritic.  They  are  due  to  a  streptococcus,  with  which 
other  microbes,  including  the  Bacillus  coli  and  the  staphylococcus,  are 
associated.  These  cases  resemble  diphtheria,  by  reason  of  the  fibrinous 
false  membranes,  by  the  accompanjdng  glandular  enlargement,  and  by  the 
reproduction  of  the  membranes  ;  but  they  do  not  produce  croup,  are  not 
followed  by  paralysis,  and  are  generally  benign. 

Although  they  are  not  diphtheritic,  they  may  assume  a  certain  degree 
of  gra\aty.  They  resemble  the  form  described  by  Henoch  under  the  name 
of  "  necrotic  inflammation."  In  this  form  the  membranes  in  the  throat 
may  spread  to  the  mouth  and  lips,  and  are  very  adherent.  When  they  are 
removed,  the  mucosa  is  ulcerated  and  bleeding.  The  breath  is  foetid ;  the 
enlargement  of  the  glands  and  the  submaxillary  oedema  are  very  marked, 
and  the  fever  is  somewhat  high.  They  usually  terminate  in  recovery,  in 
spite  of  their  apparent  gravity. 

In  other  circumstances  these  cases  of  membranous  angina,  although  not 
diphtheritic  (I  am  stiU  speaking  of  the  early  form),  run  a  malignant  course. 
They  are  characterized  by  the  rapid  spread  of  the  membranes,  by  the 
marked  swelling  of  the  glands  (Bourges),  by  the  obstinate  character  of  the 
angina,  which  lasts  as  long  as  three  weeks,  and  by  the  persistence  of  the 
fever.  Hsemorrhages  and  gangrene  are  also  seen.  The  mucosa  of  the 
mouth  and  of  the  phar}Tix  is  oedematous,  ecchymosed,  bleeding,  and  necrotic 
(Henoch).  The  gangrene  eats  away  the  tonsils,  and  causes  ulceration  of 
the  base  of  the  tongue,  of  the  pillars  of  the  fauces,  and  of  the  uvrda.  The 
breath  is  excessively  foetid,  and  a  viscous  liquid  dribbles  from  the  mouth. 
This  process,  although  not  diphtheritic,  may  affect  the  nasal  fossae,  the 
eyelids,  the  conjimctivse,  and  the  larynx.  Buboes,  nephritis,  broncho- 
pneumonia, and  otitis  are  fairly  often  associated  with  it,  and  the  patient 
usually  dies  in  a  condition  of  adynamia. 

While  discussing  the  severe  non- diphtheritic  angina  of  scarlatina,  I 
remarked  that  the  Staphylococcus  aureus  is  often  associated  with  the  strepto- 
coccus. The  streptococcus  is  the  chief  factor  in  these  cases  of  angina,  just 
as  it  is  in  most  of  the  complications  of  scarlatina,  and  the  angina  may  assume 
the  membranous  or  the  malignant  type,  although  diphtheria  is  absent. 


1632  TEXT-BOOK  OF  MEDICINE 

Diplitlieritic  angina  appears  during  the  second,  third,  or  fourth  week 
of  scarlatina,  when  the  patient  is  on  the  road  to  recovery  or  is 
convalescent.  In  some  cases  the  disease  is  relatively  benign,  and  re- 
covery takes  place  ;  but  in  other  cases  croup  occurs  (four  times  in  ten 
cases  in  Bourges'  statistics).  Other  cases  run  a  malignant  course,  and  are 
always  fatal. 

It  would  be  weU  to  quote  as  a  whole  Trousseau's  admirable  accoimt  of 
malignant  diphtheria  in  scarlatina.  "  Individuals  are  taken  ill  with  scar- 
latina of  moderate  severity.  They  have  slight  delirium  at  night,  and  per- 
haps some  nervous  symptoms.  The  pulse  is  rather  quick,  and  the  pain  in 
the  throat  is  of  moderate  severity.  Recovery  appears  certain  about  the 
eighth  or  ninth  day.  The  fever  has  fallen  and  the  eruption  has  disappeared, 
so  that  the  physician  reassures  the  family.  Suddenly  considerable  swelling 
appears  at  the  angle  of  the  jaw,  and  is  not  confined  to  this  region,  but 
extends  to  the  neck,  and  sometimes  to  a  portion  of  the  face.  Very  abundant 
and  f cetid,  sanious  fluid  flows  from  the  nostrils  ;  the  tonsUs  are  much  swoUen  ; 
the  breath  is  foetid ;  the  pulse  suddenly  becomes  very  rapid  and  small ; 
the  delirium  reappears,  and  other  nervous  symptoms  set  in.  Then,  while 
the  delirium  is  persistent,  coma  appears,  and  at  the  same  time  the  skin 
becomes  cold,  the  pulse  more  and  more  feeble,  and  the  patient  dies  after 
three  or  four  days,  or  is  suddenly  carried  off  by  syncope.  How  can  we  ex- 
plain the  course  of  events  ?  These  phenomena  so  closely  resemble  the 
terrible  forms  of  diphtheria,  which  kill  patients  before  the  membrane  has 
had  time  to  spread  to  the  larynx,  and  are  so  like  in  character  to  these  ful- 
minant forms  of  malignant  diphtheria,  that  we  are  tempted  to  believe  that 
it  is  not  scarlatina,  but  rather  this  latter  and  deadly  aflection,  which  has 
carried  off  the  patient.  Indeed,  the  patients  succumb  with  every  symptom 
of  diphtheritic  poisoning — coldness  of  the  body,  smallness  of  the  pulse, 
foetor  of  the  breath,  and  universal  paUor  of  the  skin,  which  are  seen  in  no 
other  species  of  grave  disease." 

We  know  that  this  malignant  diphtheria  is  most  often  due  to  the  associa- 
tion of  the  diphtheria  bacillus  with  the  streptococcus.  This  angina  super- 
venes as  a  secondary  infection,  the  diphtheria  developing  on  a  soil  already 
prepared  by  the  scarlatinal  angina. 

I  must  now  say  a  word  about  suppurative  angina.  It  would  appear 
a  'priori  that  it  should  be  frequent  in  scarlatina,  seeing  that  the  virulent 
streptococcus  is  often  present  in  this  disease.  On  the  contrary,  however, 
suppurative  tonsillitis  and  retropharyngeal  abscess  are  very  rare. 

Purulent  rhinitis  is  a  very  grave  complication,  since  eighteen  patients 
out  of  thirty-nine  died.  It  may  be  early  and  characterized  by  profuse 
running  from  the  nose,  as  in  glanders.  This  is  the  most  severe  form.  Some- 
times it  does  not  appear  until  desquamation  has  begun.     Lastly,  it  may  be 


ERUPTIVE  FEVERS  1033 

pseudo-membrauous  (non-diphtheritic),  and  the  nasal  cavities  are  covered 

witli  mciiihranes,  duo  to  streptococci. 

Nephritis  and  Urinary  Troubles.  —  We  find  albuminuria,  nephritis, 
hseniaturia,  anuria,  and  pyelitis. 

Albuminuria  occurs  at  an  early  period  in  a  half,  or  at  least  in  a  third, 
of  the  patients  sufFerinfr  from  scarlatina.  This  early  albuminuria  is  usually 
febrile,  and  is  connected  with  very  transient  change  in  the  renal  epithelium. 
It  is  not  as  a  rule  accompanied  by  any  other  sjinptom  of  nephritis,  and 
disappears  during  the  course  of  the  second  week.  It  may,  indeed,  last  only 
a  few  days.  I  liave,  however,  seen  early  albuminuria  last  for  some  weeks, 
and  be  accompanied  by  puffiness  of  the  face — a  proof  that  we  cannot  make 
too  clear  a  distinction  between  the  early  albuminuria  of  scarlatina  and  the 
nephritis  which  appears  later.  In  both  cases  nephritis  is  present,  and  the 
severity  of  the  process  alone  distinguishes  them. 

Apart  from  the  cases  which  I  have  just  quoted,  it  may  be  said  that 
scarlatinal  nephritis  does  not,  as  a  rule,  appear  before  the  fifteenth  day — 
that  is  to  say,  when  the  fever  and  rash  are  no  longer  present.  It  may  assume 
every  form. 

Nephritis  of  moderate  intensity  is  the  most  common  form.  It  is  char- 
acterized by  albuminous  urine,  which  is  sometimes  smoky  or  bloodstained, 
and  by  more  or  less  general  oedema,  which  commences  in  the  face.  In  some 
cases,  indeed,  the  anasarca  is  the  first  symptom.  After  some  weeks,  re- 
covery, or  at  least  apparent  recovery,  takes  place,  and  yet  the  kidney  may 
carry  the  mark  of  the  lesion  for  a  long  time. 

In  exceptional  cases  the  nephritis  is  very  grave,  and  ends  in  a  few  days 
in  acute  uraemia.  Sometimes  gastro-intestinal  troubles,  with  vomiting  and 
diarrhoea,  are  the  first  symptoms  to  appear ;  but  at  other  times  dyspnoea, 
with  or  without  pleural  effusion,  and  oedema  of  the  lung  dominate  the 
scene.  In  other  cases  the  ursemia  sets  in  with  nervous  symptoms — head- 
ache, convulsions,  and  coma — which  prove  rapidly  fatal.  QEdema  of  the 
glottis  may  appear  as  the  initial  manifestation  of  scarlatinal  nephritis. 
Abundant  epistaxis  and  visual  troubles,  such  as  amblyopia  or  amaurosis, 
are  seen  in  some  patients. 

Scarlatinal  nephritis  may  appear  in  an  epidemic  state,  being  sometimes 
associated  with  typical  scarlatina  and  at  other  times  with  the  defaced  forms 
of  the  disease.  Fiessinger  has  published  an  interesting  paper,  in  which  he 
quotes  an  epidemic  of  acute  nephritis,  where  some  cases  were  independent  of 
scarlatina,  while  others  were  associated  with  it. 

Scarlatina  is  fairly  often  the  starting-point  of  Bright's  disease,  and  it 
cannot  easily  be  explained  how  an  opposite  opinion  (Bartels,  Charcot)  was 
upheld  a  few  years  ago.  Acut€  scarlatinal  nephritis  may  not  only  end  in 
chronic  nephritis,  but  in  some  cases  the  nephritis  seems  to  have  been  chronic 


1634  TEXT-BOOK  OF  IVIEDICINE 

from  the  first.  "We  see  adiilts  or  cMldren  in  whom  the  initial  phase  of 
scarlatinal  nephritis  is  so  slight  that  it  may  pass  practically  unnoticed. 
We  see  children  or  adults  in  whom  the  sjnnptoms  of  nephritis  are  reduced 
to  albuminuria,  with  slight  and  transient  oedema.  These  cases  are  too 
often  treated  lightly,  being  termed  "  early  albuminuria,"  and  no  further 
attention  is  paid  to  them.  And  yet  five  or  six  months  later  oedema  of  the 
eyelids  and  puffin  ess  of  the  face  are  seen,  and  the  albuminuria  reappears. 
This  subacute  process  may  pass  unnoticed  if  the  child  is  absent  from  home 
or  a  boarder  at  school,  and  the  disease  progresses  until  symptoms  of  greater 
importance  sound  a  warning. 

Scarlatina  is,  therefore,  a  frequent  cause  of  Bright's  disease,  as  the 
f ollo\\'ing  cases  show  : 

I  saw,  with  Chamer,  a  child  six  years  of  age.  He  had  suffered  two  years  before 
from  slight  scarlatinal  nephritis,  but  had  never  completely  recovered,  beiag  at  times 
troubled  with  albuminuria,  oedema  of  the  face,  dyspepsia,  and  vomiting.  In  this  case 
improvement  was  obtained  only  by  the  most  rigid  milk  diet.  Several  years  ago  I 
attended  a  youth  suffering  from  Bright's  disease,  consecutive  to  scarlatina  seven  years 
previously.  His  father,  who  was  head-master  of  one  of  our  colleges,  told  me  that  the 
nephritis  came  on  during  the  attack  of  scarlatina,  but  was  so  shght  that  no  attention 
was  paid  to  it ;  the  later  symptoms  ran  a  very  slow  course,  with  well-marked  periods  of 
arrest,  untU  uraemia  set  in.  I  receive  from  time  to  time  a  visit  from  a  young  man 
who  has  been  on  a  milk  diet  for  some  years :  he  caught  from  his  sister  a  very  benign 
scarlatina,  complicated  by  mild  nephritis,  albuminuria  being  the  only  symptom.  When 
the  scarlatina  got  better,  the  kidneys  were  not  attended  to  ;  later,  oedema  and  headache 
supervened,  and  finally  the  symptoms  of  uraemia  became  threatening. 

The  chronic  form  of  scarlatinal  nephritis  did  not  escape  the  notice  of 
Trousseau.  "  Scarlatinal  albuminuria  may  pass  into  the  chronic  state — 
that  is,  into  Bright's  disease."  Chronic  nephritis  of  scarlatinal  origin,  is 
now  admitted  by  nearly  all  authors,  and  Lecorche  and  Talamon  quote 
absolutely  characteristic  cases. 

Scarlatina  exercises  a  peculiarly  noxious  action  on  the  kidney,  and  in 
this  regard  I  do  not  know  any  other  disease  which  can  be  compared  with  it. 
Typhoid  fever,  influenza,  erysipelas,  etc.,  are  far  from  attacking  the  kidney 
with  the  same  frequency  and  severity.  The  scarlatinal  toxine  has  a  powerful 
and  lasting  efiect  on  the  renal  epithelium.  For  my  part,  I  consider  that  the 
greatest  danger  in  scarlatina,  aside  from  some  rare  complications,  is  to  be 
found  in  present  or  in  future  renal  trouble.  In  the  statistics  of  scarlatina 
at  the  Hopital  des  Enfants-Malades  in  1895,  Apert  found  nephritis  in 
20  per  cent,  of  the  cases,  and  in  6  per  cent,  the  disease  was  serious.  The 
clinical  records  of  a  hospital,  however,  give  us  no  information  as  to  the 
future  of  these  children  sufiering  from  scarlatinal  nephritis,  for  we  lose  sight 
of  them.  Many  leave  the  hospital,  although  albumin  is  still  present  in  the 
urine.  Their  kidneys  are  diseased,  and  many  of  these  children  are  likely 
to  develop  Bright's  disease.     The  renal  lesions  may  remain  dormant,  and 


ERUPTIVE  FEVERS  1(]35 

1)0  n'vi\c(l  1 1(  >r  hy  a  fresh  iufcclion,  sucli  as  tyjdioid  fever,  influenza, 
mum])8,  or  sy]>liilis  ;  but  in  any  case,  when  the  Icidncv  lias  been  damaged 
by  scarlatina,  it  dues  not  lose  the  taint  quickly. 

Few  lesions  have  been  as  much  discussed  as  scarlatinal  nephritis,  which 
has  been  in  turn  described  as  catarrhal,  interstitial,  glomerular  (Klebs' 
glomerulitis),  and  parenchymatous.  It  forms  part  of  the  group  of  acute 
diffuse  nephritis.  According  to  the  case,  the  inflammation  is  slight  or 
severe.  According  to  the  time  of  death  and  the  nature  of  the  process,  we 
find  post  mortem  the  large  white  kidney,  the  large  ha3morrhagic  kidney,  the 
red  hyperaemic  kidney,  the  soft,  white,  oedematous  kidney,  and  the  kidney 
undergoing  fibrous  atrophy ;  but  the  character  of  the  lesions  is  not  so 
clearly  marked  that  we  can  place  scarlatinal  nephritis  in  a  separate 
class. 

The  chief  lesions  in  scarlatinal  nephritis  comprise  glomerulitis,  glomerular 
and  tubular  h?emorrhages,  and  interstitial  oedema — that  is  to  say,  diapedesis 
of  a  large  number  of  white  corpuscles  into  Bowman's  capsule,  between  the 
glomeruli  and  the  tubules  (Wagner's  acute  lymphomatous  nephritis). 
Cloudy  swelling  of  the  epithelium,  necrosis,  and  granulo-fatty  degeneration 
in  the  epitheliimi  of  the  convoluted  tubes,  are  the  lesions  found,  according 
to  the  particular  case. 

Scarlatinal  nephritis  is  of  toxi-infectious  origin.  It  is  due  to  the  micro- 
organisms which  accompany  the  disease  as  a  secondary  infection,  and  which 
have  been  found  in  the  kidneys  (streptococci,  micrococci,  diplococci),  to 
toxines  elaborated  by  these  microbes,  and  especially  to  the  poison  of  scarla- 
tina, the  nature  of  which  is  as  yet  unknowTi  to  us. 

HoBmaturia. — Heematuria  is  a  frequent  symptom  during  the  decline 
of  scarlatina.  If  the  blood  is  in  fairly  large  quantity,  the  urine  is  of  a 
blackish  or  brownish  colour,  and  a  more  or  less  thick  deposit  of  blood  is 
seen  at  the  bottom  of  the  specimen-glass.  If  the  haemorrhage  is  trifling,  it 
may,  on  superficial  examination,  pass  unnoticed.  As  a  rule,  haematuria  is 
associated  with  other  s}TD.ptoms  of  acute  nephritis,  but  it  may  precede  or 
even  accompany  them,  whether  the  case  is  one  of  classical  or  of  defaced 
scarlatina,  and,  indeed,  the  frequency  of  haematuria  in  defaced  scarlatina 
is  very  remarkable.  The  haematuria,  which  may  be  severe  or  slight,  lasts 
several  days.  It  then  disappears,  lea\'ing  the  acute  nephritis  to  continue 
its  course,  which  may  be  transient  or  lasting.  A  patient  of  whom  Trousseau 
speaks  was  taken  ill  with  haematuria,  lasting  more  than  a  month,  and 
forming  the  prelude  of  nephritis,  lasting  nearly  a  year.  Scarlatinal 
haematuria  fairly  often  appears  at  the  same  time  as  does  the  oedema.  One 
child  of  whom  Trousseau  speaks  was  attacked  during  an  epidemic  with 
defaced  scarlatina,  characterized  by  considerable  dropsy  and  haematuria. 
The  attack  was  very  severe  and  affected  both  kidneys  in  the   form  of 


1636  TEXT-BOOK  OF  MEDICINE 

haemorrhage,  and  the  subcutaneous  cellular  tissue  at  the  same  time  in  the 
form  of  general  oedema. 

Scarlatinal  hsematuria,  however,  is  not  always  associated  with  nephritis. 
Blood  may  come  from  the  kidney  without  the  haematuria  being  neces- 
sarily the  prelude  of  nephritis. 

Blondeau  reports  the  case  of  a  little  boy,  eight  years  of  age,  suffering  from  defaced 
scarlatina.  Among  other  symptoms  he  had  hsematuria,  which  lasted  forty-eight  hours, 
but  which  was  not  followed  by  nephritis.  Some  days  later  the  urine  regained  its 
normal  character,  and  contained  no  albumin. 

Let  US  note,  lastly,  hsematuria  as  a  part  of  the  multiple  haemorrhages 
which  occur  in  the  haemorrhagic  form  of  scarlatina. 

Scarlatinal  Anuria. — Scarlatinal  anuria  has  several  origins.  Some- 
times, in  the  course  of  scarlatinal  nephritis,  the  urine  falls  to  a  few  ounces 
in  the  twenty-four  hours  (oliguria) — a  symptom  of  very  bad  augury.  In 
such  a  case,  however,  the  urine  is  that  of  acute  nephritis,  and  the  cause 
of  the  oliguria  is  revealed  by  analysis  of  the  urine,  which  is  rich  in  albumin 
and  cylindrical  casts,  while  the  oliguria  and  anuria  in  scarlatina  at  times 
supervene  apart  from  any  nephritis  ;  the  urine  contains  no  albumin,  and 
becomes  scanty,  or  may  be  suppressed  completely.  Uraemia  appears,  and 
the  prognosis  is  very  grave. 

Bartels  reports  two  cases  in  which  death  supervened  very  rapidly  (nine 
hours  in  one  and  twelve  hours  in  the  other  case).  The. anuria  came  on 
suddenly,  the  urine  having  been  normal  in  appearance,  without  the  least 
trace  of  albumin.  At  the  autopsy,  Leichtenstern  found  large  white 
oedematous  kidneys,  and  facts  such  as  these,  says  Bartels,  led  him  to  explain 
the  anuria,  not  by  glomerulo-nephritis,  as  Klebs  believed,  but  by  oedema 
of  the  kidney. 

In  1892 1  attended  a  child  for  scarlatinal  anuria,  which  had  lasted  twenty-four  hours 
without  other  symptoms.  The  scarlatina,  which  was  of  moderate  severity,  had  up 
till  then  run  a  normal  course.  The  child  was  put  on  milk  diet,  and  the  urine,  which  I 
examined  daily,  contained  neither  blood  nor  albumin,  when  the  secretion  of  urine, 
which  hitherto  had  been  abimdant,  suddenly  ceased.  My  satisfaction  when  the 
urinary  secretion  was  re-established  can  be  easily  understood. 

Anuria  and  oliguria  usually  supervene  during  the  decline  of  the  disease. 
Juhel-Renoy  has  described  anuria  in  the  early  stage  of  scarlatina.  The 
patient  of  whom  he  speaks  died  seven  days  after  the  appearance  of 
anuria,  and  the  autopsy  revealed  embolisms  and  infarcts  containing 
micro-organisms  in  the  vessels  of  the  glomeruli.  In  short,  the  mechanism 
of  scarlatinal  anuria  is  obscure ;  but  it  is  certain  that  the  scarlatinal 
poison  may  paralyze  the  renal  function,  affecting  the  secretion  of  urine, 
and  thus  provoking  uraemia. 

Pyelitis  is  also  seen  in  scarlatina.  The  urine  is  scanty  and  con- 
tains pus. 


ERUPTIVE  FEVERS  10:^.7 

Drvpny. — It  is  customary  to  consider  dropsy  in  scarlatina  as  being 
associated  with  nephritis,  and,  indeed,  droj)sy  and  all)urninuria  both  ariso 
from  tlie  nephritis  ;  but  in  some  cases  these  two  8ym])t()m8  are  dissociated. 
We  see  cases  of  scarlatina  in  which  the  albuminuria  is  transient  or  slight, 
while  the  dro])sy  assimies  unusual  proportions,  so  that  in  such  a  case  the 
droi)sy  appears  to  evolve  on  its  own  account.  Further,  even  though  scar- 
latinal dropsy  is  always  the  result  of  nephritis,  it  is  none  the  less  true  that 
the  soil  upon  which  it  develops  offers  conditions  that  do  not  exist  in  the 
case  of  non-scarlatinal  nephritis.  Dropsy  in  acute  or  chronic  nephritis 
does  not  set  in  so  suddenly,  and  does  not  become  general  with  such  rapidity'. 
Accordingly,  scarlatina  is  of  considerable  moment  in  the  pathogenesis  of 
this  dropsy.  Dropsy  is  seen  more  frequently  in  the  moderate  than  in  the 
severe  forms  of  scarlatina,  and  has  often  been  found  in  defaced  scarlatina. 
Thus,  a  child  during  an  epidemic  suffers  from  a  sore  throat,  without  any 
rash,  and  hematuria,  followed  by  dropsy,  or  dropsy  without  haematuria, 
appears  twelve  or  fourteen  days  later.  The  dropsy  is  nearly  always  a 
complication  of  convalescence,  rarely  appearing  during  the  first  week  of 
scarlatina,  and  more  rarely  still  after  the  fifth  week  (Tripp).  The  dropsy 
may  or  may  not  commence  with  fever.  The  swelling  generally  starts  in 
the  face,  and  invades  the  trunk  and  limbs  so  rapidly  that  it  becomes  general 
in  twenty-four  to  thirty-six  bours.  For  example,  a  cliUd  who  the  evening 
before  was  thin  and  miserable  appears  next  day  to  be  fat,  from  the  enor- 
mous swelling  which  has  occurred.  The  dropsy  disappears  gradually,  but  local 
oedema,  especially  that  of  the  face,  is  obstinate,  and  subject  to  recurrence. 

Although  dropsy  is  usually  a  benign  complication,  we  must  not  forget 
that  it  is  sometimes  accompanied  by  effusion  into  the  pleurae  or  the  peri- 
toneimi  and  by  oedema  of  the  larynx,  which  rapidly  endangers  life.  (Edema 
of  the  palato -pharyngeal  mucosa  is  the  more  easily  understood,  as  this 
mucous  membrane  has  been  prepared  by  the  scarlatinal  angina.  Trousseau 
reports  several  cases  of  pharyiigo-laryngeal  oedema  in  which  tracheotomy 
became  necessary. 

When  the  dropsy  appears  independently  of  the  renal  lesion  and  of  the 
albuminuria,  we  invoke,  without  sufficient  proof,  "  cold  as  a  cause.  Other- 
wise the  origin  remains  obscure,  and  we  can  only  suspect  the  changes  pro- 
duced in  the  cutaneous  capillaries  by  the  exanthem,  and  especially  by 
desquamation "  (Jaccoud).  These  facts  may  have  some  bearing  on  the 
oedema  studied  by  Potain,  which  supervenes  apart  from  any  cardiac  or  renal 
lesions,  and  appears  to  depend  on  the  rheumatic  diathesis.  However  this 
may  be,  we  see  on  closer  inspection  tbat  dropsy  in  scarlatinal  patients  is, 
above  all,  associated  with  nephritis. 

Pseudo-Rheumatism  in  Scarlatina.— Joint  troubles  are  fairly  frequent 
in  scarlatina — at  any  rate,  in  adults.     "  In  a  large  number  of  cases,"  says 
n.  104 


1638  TEXT-BOOK  OF  MEDICINE 

Graves,  "  I  have  found  articular  rheumatism  following  scarlatina."  This 
rheimiatism,  says  Trousseau,  is  generally  quite  slight.  It  must  be  looked 
for  by  pressure  over  the  wrist  or  over  the  instep,  where  it  is  most  often 
found.  This  pseudo-rheumatism  rarely  runs  the  same  course  as  acute 
rheumatism,  being  more  fixed,  less  subject  to  relapses,  and  not  as  a  rule 
returning  again  in  the  joints  which  it  has  left.  Sometimes,  however,  it 
may,  like  true  rheumatism,  attack  the  organs  in  the  chest,  without  first 
touching  the  joints.  It  may  also  become  general.  When  I  was  house- 
physician  to  Axenfeld,  I  remember  seeing  a  patient  who  was  attacked  by 
acute  articular  rheumatism,  with  endocarditis,  iritis,  and  cerebral  troubles, 
during  the  decline  of  scarlet  fever. 

Hiller,  Ashby,  and  Picot  also  quote  cases  of  general  articular  rheumatism, 
with  or  without  endocarditis,  occurring  during  convalescence  from  scarlet 
fever.  Chorea,  which  in  children  is  so  closely  related  to  rheumatism, 
sometimes  appears  two  or  three  months  after  scarlatina. 

Is  it  that  scarlatina  only  reawakens  the  rheumatic  diathesis,  as  Peter 
thinks  ?  We  might  be  tempted  to  think  so  when  we  see  cases  of  general 
rheumatism,  but  as  a  rule  they  are  cases  of  infective  pseudo-rheumatism, 
so  that  the  different  visceral  manifestations — namely,  endocarditis,  which 
may  be  infective,  pericarditis,  and  pleurisy — depend  less  upon  rheumatism 
than  upon  the  scarlatinal  infection. 

Suppuration. — Scarlatina  predisposes  to  suppuration,  and  this  fact  is 
not  surprising,  seeing  that  the  streptococcus  is  inseparable  from  most 
scarlatinal  manifestations  and  their  secondary  infections. 

Pleurisy,  which  is  of  rapid  course,  insidious,  and  variable  according  to 
the  particular  epidemic,  is  sometimes  sero -fibrinous,  sometimes  purulent. 
In  children  it  may  be  purulent  from  the  first,  and  may  end  in  vomica. 

Pericarditis  may  be  sero-fibrinous,  hsemorrhagic,  or  purulent,  and  may 
be  associated  with  endocarditis  and  with  pleurisy. 

The  suppurative  arthritis  shows  various  characters.  In  the  most  common 
form  the  arthritis  is  serous  at  first,  and  suppuration  does  not  occur  till  later, 
Henoch  quotes  cases  of  suppurative  coxalgia  and  gonalgia.  In  another 
form  the  inflammation,  which  affects  the  joints  and  tendon-sheaths,  is 
purulent  from  the  first,  and  forms  a  true  pyaemia,  accompanied  by  delirium 
and  coma.  This  pyaemia  may  result  from  septic  embolisms,  originating  in 
a  focus  of  suppuration,  such  as  an  abscess  in  the  neck. 

We  must  consider  at  some  length  adeno-phlegmon  of  the  neck. 
Even  the  simplest  scarlatinal  angina  is  always  accompanied  by  swelling 
of  the  glands  at  the  angle  of  the  jaw.  This  adenitis,  which  is  generally 
painful,  clears  up  in  a  few  days.  Sometimes  the  swelling  is  more  marked, 
and  the  neck  is  more  brawny ;  but  yet  resolution  occurs,  and  recovery 
follows.     In  other  cases  suppuration  occurs  and  buboes  form  in  the  neck. 


ERUPTIVE  FEVERS  1630 

They  appeared  quite  early  in  an  epidemic  of  scarlatina  observed  by  Gueretin  ; 
but  more  often  they  supervene  during  the  stationary  stage,  or  even  when 
convalescence  is  fully  established.  They  are  associated  with  pseudo- 
diphtheritic  angina,  and  the  streptococcus  is  the  pathogenic  agent.  The 
adeno-phlegmon  transforms  the  side  of  the  neck  into  a  stiff,  painful  area, 
and  all  movement  of  the  head  and  neck  becomes  impossible.  The  oedema 
may  reach  the  face,  and  may  involve  the  cervical  region  as  far  as  the  clavicle 
and  the  palato-laryngeal  cavity.  The  patient  is,  as  it  were,  fixed  in  a  yoke. 
The  pain  is  intense,  deglutition  is  impossible,  phonation  is  difficult,  the 
respiration  is  embarrassed,  and  oedema  of  the  glottis  may  cause  death. 

Suppuration  in  adeno-phlegmon  is  not  always  ushered  in  by  fluctuation. 
The  tissues  are  hard  and  brawny,  the  skin  is  pale  or  shiny,  and  the  pus 
from  the  abscess  is  blood-stained,  foul-smelling,  and  rarely  homogeneous. 
These  adeno-phlegmons  are  sometimes  accompanied  by  gangrene,  which 
lays  bare  the  vessels,  the  muscles,  and  the  aponeuroses.  The  internal 
jugular  vein  and  the  internal  and  external  carotid  arteries  are  sometimes 
involved  in  the  inflammatory  process,  and  fatal  haemorrhage  is  the  result, 
the  blood  coming  from  the  mouth  or  from  the  opening  in  the  phlegmon. 

The  adeno-phlegmon  just  described,  although  serious,  may  end  in 
recovery ;  but  the  diffuse  phlegmon,  which  appears  early  and  at  once 
invades  the  cellular  tissue  and  the  glands  of  the  neck,  does  not  recover. 

Abscesses  and  cellulitis  may  develop  in  different  regions — in  the  axilla, 
the  thigh,  or  the  leg.  They  are  complications  seen  during  the  decline  of 
the  disease. 

Inflammation  of  the  parotid  glands  is  very  rare. 

Otitis. — Otitis  is  frequent  in  scarlatina,  and  this  is  not  surprising  when 
we  consider  the  condition  of  the  throat  and  the  ease  with  which  infections 
spread  from  the  pharynx  to  the  middle  ear  through  the  Eustachian  tube. 
In  the  slight  and  common  form  of  otitis,  pain,  noises  in  the  ears,  and 
diminished  acuteness  of  hearing  are  the  only  appreciable  symptoms.  Reso- 
lution takes  place  in  a  few  days,  and  recovery  follows.  In  the  more  severe 
forms,  which  generally  supervene  towards  the  end  of  the  eruption,  the  pain 
is  very  acute,  the  temperature  is  high,  and  the  child  is  restless,  and  may 
suffer  from  delirium  and  convulsions.  We  find  here  infection  in  a  closed 
cavity,  which  I  have  discussed  under  the  Pathogenesis  of  Appendicitis.  If 
the  Eustachian  tube  recovers  its  permeability  in  time,  the  symptoms  dis- 
appear, but  the  infection  usually  ends  in  perforation  of  the  membrana 
tympani,  and  the  pus  escapes  through  the  external  auditory  meatus.  As 
a  general  rule,  the  perforation  puts  an  end  to  the  acute  symptoms.  The 
suppuration,  however,  is  slow  to  dry  up,  and  many  children  suffer  from 
otorrhoea  for  weeks  and  months.  The  otitis,  which  is  nearly  always  bilateral, 
may  expose  the  patient  to  the  most  terrible  complications,  such  as  menin- 

104—2 


1640  TEXT-BOOK  OF  MEDICINE 

gitis,  encephalitis,  cerebral  abscess,  caries  of  tbe  petrous  bone,  ulceration 
of  a  large  vessel,  or  facial  paralysis.     Deafness  may  foUow  scarlatinal  otitis. 

Streptococci  and  staphylococci  are  found  in  the  pus  from  a  case  of 
otitis,  just  as  in  the  pus  from  cases  of  suppurative  adenitis.  In  some  cases 
the  diphtheria  bacillus  and  the  tubercle  bacillus  are  also  found  as  a  secondary 
infection. 

Sequelce. — Scarlatina  may  leave  indelible  sequelse.  I  have  just  spoken 
of  deafness.  Hsemoplegia  consecutive  to  cerebral  arteritis  has  been  noted 
(Alexeff). 

In  some  patients  of  lymphatic  temperament  scarlatina  leaves  glandular 
tumours  in  the  neck  and  chronic  eczema  of  the  nose  and  ear  (Hardy). 
Endocarditis  may  pass  unnoticed  during  the  course  of  scarlatina.  Some- 
times it  supervenes  later,  at  the  same  time  as  the  pseudo -rheumatism  or 
the  chorea.  It  may  persist  in  the  chronic  form.  I  shall  not  refer  again  to 
Bright's  disease,  which  is  a  possible  sequela. 

Diagnosis. — The  eruption  may  be  confounded  with  the  scarlatiniform 
eruptions  which  appear  at  the  onset  of  variola,  but  the  general  symptoms 
give  more  assistance  in  diagnosis  than  the  eruption  does,  and  I  would 
say  the  same  of  scarlatiniform  eruptions  appearing  in  the  course  of  rheu- 
matism, diphtheria,  typhus,  and  cholera,  or  arising  from  the  use  of  drugs 
(antipyrin,  belladonna).  Scarlatinal  angina  should  not  be  confounded 
with  simple  tonsillitis.  jThe  defaced  forms  are  distinguished  in  that  they 
appear  during  an  epidemic.  In  eczema  rubrum  we  find  fever  and  diffuse 
redness  of  the  skin,  but  the  invaded  region  shows  vesicles  rapidly  replaced 
by  fine  branny  scales,  which  do  not  reappear  when  once  they  have  fallen 
off.  The  itching  and  smarting  caused  by  eczema  are  more  marked  than  the 
simple  pruritus  seen  in  scarlatina. 

Infective  scarlatiniform  erythema  may  resemble  scarlatina  so  closely 
that  the  diagnosis  is  difficult,  and,  among  other  examples,  I  may  mention 
a  patient  who  wa,s  under  my  care  at  the  Necker  Hospital. 

A  man  was  taken  ill  with  fever,  headache,  and  lassitude.  The  throat  was  red,  the 
tonsils  were  large,  and  covered  with  a  pulpy  exudate  ;  there  was  a  polymorphous 
eruption,  which  had  in  places  the  diffuse  redness  of  scarlatina.  We  thought  of  scarla- 
tina, but  fresh  crops  appeared,  although  desquamation  had  begim ;  these  crops  were 
erythematous,  morbiUiform,  urticarial,  and  scarlatiniform,  so  that  in  all  these  points 
the  case  did  not  look  Hke  one  of  scarlatina,  and  yet  it  was  necessary  to  await  the  poly- 
morphous character  of  the  eruption  and  its  successive  crops  in  order  to  ehminate  the 
hypothesis  of  scarlatina,  and  to  make  the  diagnosis  of  infectious  scarlatiniform 
erythema. 

Accordingly,  the  dermatoses,  which  are  general,  red  in  colour,  and 
accompanied  by  desquamation,  may  simulate  scarlatina  in  a  singular 
manner.  Brocq,  in  his  treatise  upon  the  treatment  of  diseases  of  the  skin, 
gives  the  following  description  of  desquamative  scarlatiniform  erythema, 


ERUPTIVE  FEVERS  ic.ll 

or  acute  exfoliative  dermatitis.  It  is,  says  he,  a  Iciiifl  of  pseudo-exanthera, 
charaftorized  by  a  febrile  onset,  simulatinf?  that  of  srarlatina.  After  a 
variable  period,  a  more  or  less  bright  red  rash  stipervciKis,  which  is  uniform, 
or  punctuated  by  petechia?,  especially  on  the  lower  limbs.  The  rash  tends 
to  become  general,  and  is  more  marked  in  the  articular  folds,  the  neck,  the 
lateral  parts  of  the  body,  and  the  palms  of  the  hands  or  the  soles  of  the  feet. 
Abundant  dr}-,  flaky  desquamation  occurs  three  or  four  days  after  the 
appearance  of  this  rash,  although  the  redness  is  still  persistent. 

Ehrlich's  diazo-reaction,  which  is  constant  in  scarlatina,  is  absent  in 
scarlatiniform  erythema. 

Puerperal  Scarlatina. — What  view  should  be  taken  of  puerperal  scar- 
latina ?  Docs  it  deserve  description  under  Scarlatina,  or  should  it  be  put 
under  the  Scarlatiniform  Erythemata  ?  A  woman  during  the  puerperal 
period  may  take  true  scarlatina,  just  as  she  may  take  measles  or  variola  ; 
but  this  is  not  the  question.  I  allude  to  those  epidemics  of  so-called  puer- 
peral scarlatina  which  formerly  caused  such  terrible  ravages  in  lying-in 
hospitals  or  in  different  localities  before  antiseptic  methods  were  practised, 
and  which,  as  a  rule,  coincided  with  erysipelas  in  new-born  children,  so 
happily  called  by  Trousseau  "  a  manifestation  of  puerperal  fever  in  the  new- 
born." Are  these  cases  of  so-called  puerperal  scarlatina,  whether  they  are 
epidemic  or  isolated,  true  or  pseudo  scarlatina  ? 

So-called  puerperal  scarlatina  usually  begins  suddenly  a  few  days  after 
delivery.  The  woman,  who  has  so  far  been  in  good  health,  is  -suddenly 
seized  with  slight  chill,  followed  by  fever,  nausea,  and  vomiting.  Oculo- 
nasal catarrh,  which  at  first  sight  simulates  measles,  may  be  seen.  After 
this  period  of  invasion,  which  may  last  only  a  few  hours,  the  eruption  comes 
out,  and  shows  all  the  characters  of  the  scarlatinal  rash.  The  angina  is 
perhaps  less  marked  or  less  inevitable  than  in  scarlatina,  and  perhaps, 
too,  the  inflammation  of  the  submaxillary  glands  is  slighter.  Desquama- 
tion follows  the  eruption,  large  shreds  of  the  epidermis  peeling  off.  The 
lochia  and  the  secretion  of  milk  are  suppressed  or  modified.  Patients 
sometimes  recover,  and  v,^hen  death  supervenes,  it  does  so  from  cholera-like 
complications  (diarrhoea,  coldness  of  the  body,  and  livid  colour  of  the  skin), 
collapse,  or  coma. 

It  is  quite  evident  that  there  is  here  material  for  discussion,  and  the 
dualists  and  unicists  have  not  yet  conie  to  an  agreement.  For  my  part, 
I  accept  the  conclusions  of  Wurtz,  which  I  have  found  very  sensible. 
"  There  is,"  says  he,  "  an  important  fact  which  throws  a  singular  light  on 
the  true  nature  of  puerperal  scarlatina — namely,  that,  since  the  application 
of  antiseptic  methods  in  obstetrics,  the  disease  has  become  practically 
unknown  in  maternity  hospitals  (Varnier).  It  is  therefore  rational  to 
admit  that  these  so-called  cases  of  scarlatina  were  only  cases  of  infec- 


1642  TEXT-BOOK  OF  MEDICINE 

tiOUS  erythema,  due  to  the  toxines  of  the  streptococcus."  In  my  opinion  a 
point  in  favour  of  this  view  is  that  so-called  puerperal  scarlatina,  which  is 
contagious  from  patient  to  patient  in  a  lying-in  ward,  does  not  attack 
those  who  come  in  contact  with  the  patients.  The  cases  are,  therefore, 
infectious  scarlatiniform  erythema. 

I  may  say  the  same  of  wound  or  surgical  scarlatina.  Our  bacteriological 
classifications  as  regards  the  streptococci  are  far  from  being  sufficiently 
advanced  to  decide  the  specificity  of  scarlatina,  because  these  different 
conditions  have  for  their  essential  agent  the  toxine  of  the  streptococcus, 
and  because  the  streptococcus  appears  to  be  an  important  agent  in  scar- 
latina. In  short,  we  find  scarlatina  on  the  one  hand,  and  on  the  other 
hand  scarlatiniform  erythema ta. 

Prognosis. — ^A  reserved  prognosis  must  always  be  given  in  scarlatina, 
even  in  apparently  benign  cases,  for  many  complications  may  supervene 
during  convalescence  (dropsy,  ursemia,  diphtheria,  empysema,  and  abscesses), 
or  appear  after  the  patient  seems  cured.  The  chronic  sequelae  of  the  disease, 
including  cardiac  lesions,  Bright's  disease,  chorea,  etc.,  must  also  be  reckoned. 
In  scarlatina,  just  as  in  all  epidemic  diseases,  the  severity  and  the  course  of 
the  disease  vary,  according  to  the  epidemic.  Sydenham,  who  saw  only  the 
most  benign  forms  of  scarlatina,  hesitated  to  give  it  the  name  of  a  disease. 
Graves  says  that  the  epidemics  of  1800  to  1804  in  Ireland  were  terrible, 
while  they  became  extremely  benign  for  a  period  of  thirty  years,  and  then 
reappeared  with  exceeding  severity  in  Dublin  in  1831  and  1834.  Bretonneau, 
who,  like  Sydenham,  considered  scarlatina  as  a  very  benign  disease,  because 
he  did  not  lose  a  single  patient  in  twenty  years,  changed  his  opinion  when 
a  terrible  epidemic  claimed  numerous  victims  at  Tours, 

Epidemics  of  scarlatina  may  not  only  severely  affect  an  entire  popula- 
tion, but  their  gravity  may  be  circumscribed  to  a  small  centre,  to  a  single 
house,  or  to  a  single  family,  as  the  writings  of  StoU  and  Graves  clearly  show. 
Whether  the  malignancy  depends  upon  the  nature  of  the  infective  agent,  or 
whether  it  is  some  inherent  peculiarity  of  the  constitution  of  the  indi- 
vidual, it  is  none  the  less  true  that  "  when  scarlatina  attacks  a  family  and 
kiUs  the  first  members  attacked,  it  must  be  feared,  because  it  will  probably 
claim  other  victims"  (Trousseau).  I  have  recognized  the  truth  of  this 
statement.  In  a  family  at  Amiens  three  persons — ^mother  and  two  chil- 
dren— ^were  taken  ill  with  scarlatina,  complicated  by  diphtheria,  and  all 
died  in  a  few  days. 

The  severity  of  scarlatina  in  the  Anglo-Saxon  race  has  been  often  recog- 
nized. While  in  France  it  is  responsible  for  only  one-third  of  the  deaths 
that  measles  causes,  in  Belgium  it  kills  more  than  the  latter  disease.  In 
England  it  figures  in  the  first  rank  among  the  causes  of  mortality  :  in  Paris 
it  shows  an  average  of  100  deaths  a  year  ;  in  London,  4,000  to  5,000.     Scar- 


ERUPTIVE  FEVERS  10  H 

latina  is  more  frequent  and  more  severe  in  I*]ii^lisli  ])eoj)le  living  on  the 
Continent  than  anionj;  the  natives. 

Ago  is  important  from  the  point  of  view  of  prognosis.  In  the  figures 
given  by  Marfan  and  Apert  we  find  that  among  children  in  the  hospitals 
of  Paris  the  mortality  is  greater  the  younger  the  patient  (50  per  cent,  below 
one  year,  11  per  cent,  between  one  and  two  years,  2  per  cent,  between  two 
and  ten  years,  and  nil  above  this  age).  Legendre  has  seen  a  mortality  of 
1*88  per  cent,  in  adult  patients  at  Aubervilliers. 

etiology. — Scarlatina  is  epidemic  and  contagious.  The  inoculation."? 
which  have  often  been  made  have  given  no  positive  result.  It  chiefly 
attacks  children  between  the  ages  of  six  and  ten  years,  and  usually  confers 
immunity.  There  are  some  cases  which  prove  that  the  foetus  may  receive 
the  contagion  from  the  mother. 

While  scarlatina  is  contagious  during  the  eruptive  period,  it  is  especially 
so  during  desquamation,  and  the  dust  from  the  epidermic  scales  is  very 
contagious.  Contagion  may  be  direct  or  indirect — direct  when  there  is 
contact  with  the  patient ;  indirect  when  the  disease  is  transmitted  by 
different  objects,  such  as  toys,  toilet  articles,  and  clothes  which  have 
belonged  to  a  patient  with  scarlatina.  Contagion  may  even  occur  at  a 
distance  through  articles  carrying  the  contagious  germs.  Books  and 
letters  have  rightly  been  held  guilty,  and  I  will  quote  some  undeniable 
cases. 

Sann6  reports  that  a  lady  and  her  daughter  Hving  in  Brittany  received  from  a  friend 
in  Germany  a  letter,  in  which  she  said  that  she  was  convalescent  from  scarlatina,  and 
was  peeling  so  freely  that  while  writing  the  letter  she  was  obhged  to  shake  the  paper 
several  times  in  order  to  get  rid  of  the  scales  which  fell  on  it.  The  mother  and  daughter 
who  received  this  letter  were  taken  ill  with  scarlatina,  and  the  former  died,  while  the 
latter  narrowly  escaped  death. 

Grasset,  of  Riom,  reports  a  similar  case :  The  parents  of  a  girl  who  was  suflfering 
from  scarlatina  collected  some  of  the  scales  of  skin,  and  sent  them,  as  a  curiosity, 
in  a  letter  to  her  little  brother,  who  took  scarlatina.  I  have  quoted  in  this  article  the 
case  of  a  yoimg  girl  suffering  from  a  chronic  scarlatinal  nephritis :  she,  too,  took  the 
disease  from  her  sister,  who  kept  on  sending  letters  which  evidently  contained  contagious 
particles  of  skin. 

How  does  the  contagion  enter  the  system  ?  Is  it  by  the  respiratory 
tracts,  or  does  not  the  tonsil  receive  the  virus  ?  The  question  is  still  a 
moot  point. 

Bacteriology. — Bacteriological  researches',  made  in  order  to  discover 
the  microbe  of  scarlatina,  are  not  as  yet  conclusive.  Klebs,  in  1875,  de- 
scribed certain  nomad  forms  in  scarlatina,  but  did  not  cultivate  them. 
Later,  Edington  noted  in  the  blood  and  the  scales  eight  kinds  of  bacteria, 
of  which  one,  in  the  form  of  a  rod  or  of  a  diplococcus,  was  capable  of 
producing  in  animals,  and  particularly  in  calves,  a  febrile  affection,  accom- 
panied by  a  cutaneous  rash  resembling  that  of  scarlatina.     The  Streyto- 


1644  TEXT-BOOK  OF  MEDICINE 

coccus  conglomerafus,  which  Kurth  considered  as  the  pathogenic  agent  of 
scarlatina,  has  no  specific  property. 

The  bovine  origin  of  scarlatina  has  been  upheld  for  several  years  by 
numerous  physicians  and  veterinary  surgeons  in  England,  and  the  con- 
tagion is  supposed  to  result  from  ulceration  of  the  udders  of  cows  and 
from  the  use  of  milk. 

In  short,  we  do  not  know  the  pathogenic  microbe  of  scarlatina,  but  we 
do  know  what  agents  cause  secondary  infections  in  patients  with  scarla- 
tina (Marie,  Kaskin,  Babes,  Wurtz,  Bourges).  I  must,  in  the  first  place, 
mention  the  streptococcus  which  is  present  in  nearly  all  the  lesions  (simple 
and  suppurative  arthritis,  ulcers  of  the  tonsils  and  pharynx,  adenitis  and 
adeno-phlegmon  in  the  neck,  diphtheroid  exudation  in  the  throat,  pus  in 
cases  of  otitis,  pleuritic  eSusion,  and  nephritis). 

Staphylococcus,  coli  bacillus,  pneumococci,  saprogenic  bacilli  (Babes), 
etc.,  are  often  found,  in  addition  to  the  streptococcus,  which  in  scarlatina 
assumes  special  virulence,  but  which  is  not  specific  fer  se.  It  produces 
suppuration  and  erysipelas  in  animals,  while  scarlatinal  angina  appears 
able  to  cause  erysipelas  by  contagion. 

Treatment. — Scarlatina,  when  slight  or  of  moderate  intensity,  requires 
only  careful  hygiene  ;  but  the  severe  forms,  with  very  high  temperature 
and  marked  nervous  symptoms,  should  be  treated  by  cold  sponging  or  by 
baths.  I  have  witnessed  the  good  eSect  of  this  treatment  in  Trousseau's 
clinic,  and  I  have  often  followed  his  practice. 

The  patient  is  placed  naked  in  an  empty  bath,  and  three  or  four  buckets 
of  water  at  70°  F.  are  poured  over  his  body,  the  affusion  lasting  half  a  minute. 
Instead,  he  may  be  placed  on  a  stretcher  and  sponged  by  two  attendants 
with  water  at  70"  F.  to  which  aromatic  vinegar  has  been  added.  In  either 
case,  after  the  bath  the  patient  is  placed,  still  wet,  in  a  cotton  sheet, 
and  given  an  infusion  of  camomile  tea,  or  peppermint- water ;  healthy 
reaction,  generally  followed  by  perspiration  and  reduction  of  the  tempera- 
ture, speedily  takes  place.  The  affusions  may  be  repeated  several  times 
in  the  twenty-four  hours.  In  some  cases  the  patient  may  be  placed 
in  a  cold  bath,  the  method  described  under  Typhoid  Fever  being 
employed. 

Acetate  of  ammonia,  musk,  syrup  of  ether,  and  bromide  of  potassium, 
are  of  service  in  the  severe  nervous  forms. 

At  the  onset  of  scarlatina  the  patient  should  be  put  on  milk  diet 
(Jaccoud),  in  order  to  prevent  possible  nephritis,  and  tliis  principle  is 
absolutely  essential.  Not  only  do  I  prescribe  exclusive  milk  diet  during 
the  disease  itself,  but  I  continue  it  for  three  or  four  weeks  after  recovery. 
We  thus  avoid — or,  I  believe,  at  least  lessen — the  likelihood  of  renal 
complications. 


ERITPTIVK  FRVF-mS  1G45 

The  treatment  of  scarlatinal  angina  differs  aecording  as  the  disease  is 
or  is  not  diphtheritic.  In  every  case  antiseptics  shoiiM  he  applied  1o  the 
pharynx,  and  for  this  purpose  moutli-wasiies  of  a  solution  of  chh)riiiiit('(l 
soda  may  be  employed  (Roux),  and  the  throat  may  be  painted  with 
equal  parts  of  menthol  and  camphor,  as  extolled  by  Roux. 

When  diphtheria  (complicates  the  scarlatinal  angina,  injections  of  anti- 
diphtheritic  serum  must  be  given  ;  but  in  these  cases  the  combination  of  the 
streptococcus  with  the,  diplitheria  bacillus  produces  an  increase  of  virulence, 
and  it  is  especially  in  such  cases  that  the  injection  of  serum  produces  morbilli- 
form eruptions,  which  Sevestre  attributes  principally  to  streptococcal 
infection.  This  fact  agrees  \vith  the  statistics  of  Marfan  and  Apert,  who 
found  that  in  scarlatinal  patients  suffering  from  non-diphtheritic  mem- 
branous angina,  and  treated  with  injections  of  antidiphtheritic  serum,  the 
frequency  of  post-serotherapic  eruptions  is  28  per  cent.,  while  it  is  only 
from  10  to  15  per  cent,  if  the  angina  is  diphtheritic. 

As  the  streptococcus  plays  the  chief  part  in  non-diphtheritic  angina, 
ought  we  to  make  use  of  antistreptococcic  serum  ?  The  following  con- 
clusions are  given  in  an  article  which  appeared  on  this  subject  in  the 
Gazette  Hehdomadairc,  July  19,  1896  :  Marmorek  was  the  first  to  publish 
a  series  of  cases  favourable  to  the  employment  of  his  serum  in  scarlatina, 
and  Dubois,  who  has  devoted  much  time  to  researches  with  this  serum  and 
speaks  in  its  favour,  reports  four  cases  in  which  it  is  said  to  have  produced 
beneficial  results.  All  authorities,  however,  are  far  from  sharing  this 
enthusiasm.  Baginski  did  not  obtain  conclusive  results  from  his  experi- 
ments, and  Josias  considers  that  the  serum  has  no  marked  influence  on  the 
course  of  scarlatina.  The  cases  published  by  Marfan  and  Apert  and  by 
Comby  are  far  from  being  encouraging. 

Prophylactic  treatment  consists  in  isolating  the  patient  during  the 
whole  period  of  the  disease,  and  we  must  not  forget  that  the  shreds  of 
epidermis  detached  during  desquamation  are  endowed  with  contagious 
properties,  which  they  preserve  for  a  long  while. 

V.  MEASLES. 

The  old  writers  often  described  measles  under  the  name  of  morbillus 
fever,  morbilli,  or  the  small  plague.  The  whole  subject  was  in  confusion 
until  Sydenham,  between  1760  and  1764  (London  epidemics),  clearly  dis- 
tinguished measles  from  scarlatina  and  variola. 

Description. — I  shall  choose  for  my  descriptive  type  an  ordinary  case  of 
measles  of  moderate  severity,  and  I  shall  consider  later  the  less  common  forms 
of  abnormal  and  haemorrhagic  measles.  The  course  of  measles  is  generally 
divided  into  four  periods — incubation,  invasion,  eruption,  and  desquamation 


1646  TEXT-BOOK  OF  MEDICINE 

1.  Incubation. — The  incubation  is  generally  latent,  wliile  the  economy 
hatches  the  morbid  seed.  In  some  cases,  however,  we  see  during  this  period 
elevation  of  temperature,  malaise,  cough,  and  coryza.  In  children  the  weight 
rapidly  falls,  and  there  is  already  an  outline  of  the  symptoms  which  appear 
during  the  next  period.     The  incubation  lasts  from  eight  to  eleven  days. 

2.  Invasion. — The  invasion  of  measles  is  not  as  sudden  as  that  of 
variola  and  scarlatina.  The  course  of  the  fever  is  worthy  of  study,  for  it 
is  sometimes  slight,  and  at  other  times  reaches  104°  F.,  with  chills,  head- 
ache, and  sneezing.  The  fever  often  falls  during  the  next  day,  and  reappears 
with  the  eruption. 

At  the  commencement  of  the  disease  the  mucous  membranes  of  the 
nose  and  eyes,  and  sometimes  those  of  the  Eustachian  tubes,  larynx,  and 
bronchi,  are  attacked  by  catarrh.  The  eyes  are  red,  swoUen,  and  weeping. 
The  nasal  catarrh  causes  sneezing  and  abundant  secretion.  The  laryngeal 
catarrh  is  accompanied  by  frequent  obstinate  cough,  hoarseness,  and  some- 
times by  complete  aphonia.  Otitis  appears  later,  and  is  accompanied  by 
sharp  pain.  In  some  cases  the  catarrh  affects  one  or  other  organ  to  such 
an  extent  that  an  error  in  diagnosis  may  result.  Some  children  appear  to 
have  only  simple  or  stridulous  laryngitis,  when  the  eruption  appears  four 
or  five  days  later.  Other  children,  again,  are  treated  for  several  days  for 
bronchitis  or  for  intestinal  catarrh,  and  then  the  eruption  appears,  giving 
the  lie  to  the  diagnosis.  In  consultation  with  Waltelet  I  saw  a  young  child 
in  whom  otitis  preceded  the  eruption,  and  caused  us  to  suspend  our  judg- 
ment. During  the  period  of  invasion  the  laryngeal  sjnnptoms  are  the  most 
frequent  and  the  most  important.  Laryngitis  (frequent  spasmodic  cough, 
hoarse  and  muffled  voice)  is  a  valuable  factor  in  making  an  early  diagnosis. 

Epistaxis  is  frequently  seen  at  this  period,  and  young  children  are 
sometimes  seized  with  convulsions.  If  the  patient's  throat  is  carefully 
examined  in  a  good  Hght,  we  see  that  the  eruption  (enanthem)  is  already 
out  on  the  mucous  membrane  of  the  roof  of  the  palate,  on  the  anterior  pillars 
of  the  fauces,  and  on  the  pharynx,  in  the  form  of  a  red  stippling,  which 
usually  shows  neither  swelling  nor  pulpy  deposits.  The  enanthem  may 
precede  the  eruption  on  the  skin  by  one  or  two  days,  marked  dyspnoea 
resulting. 

I  have  often  seen  a  submaxillary  adenitis,  which  I  think  might  be 
included  among  the  symptoms  of  invasion  of  measles,  and  which  is  not 
absolutely  special  to  this  disease. 

The  duration  of  the  period  of  invasion  is  long,  since  it  may  last  from 
four  to  seven  days,  while  it  is 'very  short  in  scarlatina,  in  which  disease  it 
may  last  only  a  few  hours.  The  fever  is  not  continuous,  and  falls  on  the 
second  or  on  the  third  day,  but  reappears  with  the  rash.  In  some  very  mild 
cases  fever  may  be   practically   absent.      The  different  symptoms  just 


ERUPTIVE  FEVERS  1647 

described  are  trifling,  and  the  eruption  is  practicall}'  the  first  symptom  of 
the  disease. 

3.  Eruption. — At  the  time  of  the  eruption  the  symptoms  of  invasion 
do  not  disappear,  as  in  the  cases  of  discrete  variola,  but,  on  the  contrary, 
they  return  with  fresh  severity.  Tlie  cough  is  frequent,  paroxysmal,  and 
painful.  The  voice  becomes  hoarse,  and  is  sometimes  lost,  and  the  fever 
reaches  its  maximum,  decreasing  later  when  the  eruption  disappears.  The 
eruption  may  appear  on  the  fourth,  fifth,  sixth,  or  seventh  day  of  the 
disease.  It  commences  on  the  face,  around  the  lips,  and  on  the  forehead.  It 
then  invades  the  neck,  trunk,  and  limbs.  In  its  usual  form,  when  we  examine 
the  rash  on  the  chest  or  on  the  abdomen,  we  see  that  it  is  composed  of 
little  red,  velvety  projections,  which  are  not  as  rough  as  those  of  scarlatina. 
The  spots  in  measles  are  about  as  large  as  a  grain  of  rice,  imeven,  fade  for  a 
moment  on  pressure,  and  are  grouped  in  irregular  patches  of  a  crescentic 
shape,  separated  by  intervals  of  healthy  sldn.  In  some  cases,  however,  the 
eruption  is  confluent,  and  the  redness  of  the  skin  becomes  diffuse  and 
uniform.  In  exceptional  instances  the  erythema  of  measles  may  show  the 
greatest  analogy  with  the  rash  of  scarlatina  (Sanne,  Renon,  and  Follet). 

The  eruption  becomes  general  in  twenty-four  to  forty-eight  hours.  It 
fades  in  the  same  order  as  it  appeared,  commencing  on  the  face,  which 
becomes  pale,  while  it  is  stiU  fully  out  upon  the  limbs. 

When  the  inflammatory  exudate  forming  the  morbillous  spot  is  associated 
with  the  presence  of  colloid  deposits  in  the  Malpighian  cells,  the  projection 
formed  by  the  papule  gives  to  the  eruption  the  appearance  known  as  pimply 
measles. 

During  this  period  the  catarrh  reaches  its  maximum.  The  cough  is  less 
dry ;  the  sputum  in  adults  (children  do  not  expectorate)  becomes  thick 
and  nummular,  like  that  of  phthisis,  and  bronchitic  rales  are  heard. 

Diarrhoea  is  common  in  children  when  the  rash  comes  out.  This 
intestinal  catarrh  may  last  twenty-four  hours,  and  is  sometimes  accom- 
panied by  true  colitis,  with  haemorrhage  and  mucous  diarrhoea. 

4.  Desquamation. — The  fever  falls  about  the  eighth  day  of  the  disease, 
and  the  rash  tends  to  disappear  first  from  the  face.  Desquamation  begins 
from  the  fourth  to  the  seventh  day  of  the  eruption.  It  is  so  slight  that 
there  is  not  really  a  period  of  desquamation,  although  some  desquamation 
in  the  form  of  branny  scales  usually  occurs  on  the  skin  of  the  face  and  forehead. 

The  nervous  form  of  measles  is  more  frequent  at  an  early  age,  and  is 
characterized  during  the  period  of  invasion  by  convulsions,  with  delirium, 
vomiting  and  very  high  temperature.  The  eruption  is  late  and  incomplete, 
or  unrecognisable ;  the  fever  is  persistent ;  the  skin  is  livid  and  dry ;  the 
pulse  is  smaU  and  very  quick  ;  the  urine  is  scanty ;  and  death  by  coma  ends 
the  scene. 


1648  TEXT-BOOK  OF  MEDICINE 

In  exceptional  cases  abnormal  complications  supervene  in  the  course  of 

typical  measles.     I  have  seen  the  following  case  : 

A  young  girl  was  taken  ill  with  measles  ;  invasion  and  eruption  were  classical.  All 
went  weU  until  the  second  day  of  the  disease,  and  then  the  menses  appeared ;  the 
patient  experienced  some  nausea  at  this  time.  Next  morning  paraphasia  appeared ; 
her  mind  was  less  clear,  and  the  temperature  suddenly  fell  from  102°  P.  to  97°  P.  ;  a 
series  of  epileptiform  attacks,  with  loss  of  consciousness  and  coma,  followed.  In  a  few 
hours  the  temperature  rose  from  97°  P.  to  106°  P.  ;  the  attacks  succeeded  one  another 
without  interruption,  and  the  patient  died  the  same  day  in  convulsions. 

Writers  have  described,  and  I  myself  have  witnessed,  malignant  cases 
with  dyspnoea  or  delirium,  the  severe  symptoms  coming  on  in  the  course  or 
during  the  decline  of  the  eruption.  Measles  only  becomes  malignant  at  a 
later  stage  during  the  eruption,  in  contradistinction  to  scarlatina,  which 
assumes  the  malignant  type  from  the  very  onset, 

Hsemorrhagic  measles  is  characterized  by  cutaneous  ecchymoses  and 
purpuric  spots,  which  do  not  disappear  on  pressure,  and  may  last  eight  or 
ten  days  after  the  eruption.  This  form  is  obviously  more  grave  than  normal 
measles,  but  as  long  as  the  haemorrhage  remains  limited  to  the  skin,  it  does 
not  imply  a  fatal  prognosis.  The  case,  however,  is  quite  difierent  when  the 
haemorrhage  becomes  general.  If  epistaxis,  haematuria,  metrorrhagia,  and 
haemorrhages  from  the  mouth  and  bowels  appear,  the  patient  dies  with 
adynamic  and  typhoid  symptoms. 

Complications  of  Measles. 

I  have  just  described  the  normal  form  and  also  the  anomalous  varieties 
of  measles  ;  but  at  any  period  of  the  disease  we  may  witness  the  onset  of 
complications  which  are  in  some  cases  an  exaggeration  of  the  ordinary 
symptoms,  but  in  other  cases  comprise  unusual  signs.  These  complications 
are  sometimes  due  to  the  excessive  virulence  of  the  pathogenic  agent ;  at 
other  times  they  result  from  secondary  infection  or  from  the  association  of 
other  microbes  (diphtheria,  gangrene,  tuberculosis),  and  vary  in  difierent 
individuals,  surroundings,  and  epidemics. 

Convulsions,  epistaxis,  and  false  croup  belong  to  the  period  of  invasion. 
The  convulsions  special  to  infancy  are  not  of  fatal  omen  if  they  are  transient 
and  solitary,  though  the  case  is  not  the  same  if  they  occur  in  the  so-called 
nervous  forms.  Epistaxis  is  a  common  symptom  of  the  disease.  It  may 
become  so  profuse  as  to  threaten  the  life  of  the  patient. 

Laryngeal  Complications. — Measles  shows  a  predilection  for  the  larynx, 
and  even  in  the  period  of  invasion  the  laryngeal  symptoms  are  prominent, 
cough  and  vocal  troubles  being,  so  to  say,  constant.  This  larjnigitis  in 
measles  comprises  both  erythema  and  catarrh.  Laryngoscopic  examination 
reveals  discrete  or  confluent  erythema,  with  exudation,  papules,  and  erosion 
of  the  vocal  cords. 


i<:rinp'rivK  kkvers  1640 

This  catarrliul  laryngitis  in  children  between  the  ages  of  two  and  five 
years  may  run  the  eourse  of  false  croup,  but  it  is  not  a  serious  accident,  and 
it  sometimes  announces  the  onset  of  measles. 

In  short,  laryngitis  in  measles  is,  as  a  ruh^,  a  transient  and  harmless 
phenomenon.  At  other  times  it  Ixjcomes  a  formidajjle  complication,  and 
ends  either  in  very  severe  catarrhal  laryngitis  or  in  an  ulc(!rativc  form. 

The  severe  form  is  not  simply  a  catarrhal  inflammation.  The  mucosa  is 
profoundly  affected,  as  has  been  shown  by  Coyne.  The  chorion  is  infiltrated 
with  leucocytes,  the  mucous  glands  are  much  swollen,  and  the  mucous  mem- 
brane of  the  larynx  is  cedematous,  so  that  we  can  understand  how  in  chil- 
dren these  lesions,  with  spasm  of  the  glottis,  may  cause  as])hyxia.  The 
little  patients  in  the  epidemic  of  1809,  reported  in  Campaignac's  thesis, 
died  from  this  cause.  The  mucous  membrane  was  found  to  be  swollen 
and  infiltrated,  but  there  were  neither  ulcers  nor  false  membranes  on  post- 
mortem examination.  This  form  is  the  severe  er}i;hematous  laryngitis 
described  by  Rillet  and  Barthez. 

In  another  form  the  laryngitis  is  ulcerative,  and  the  ulcers  are  superficial, 
erosive,  and  anfractuous,  or  sometimes  serpiginous  and  deep,  so  as  to  lay 
bare  the  cricoid  and  arytenoid  cartilages.  The  ulcerations  may  be  situated 
at  the  free  border  or  at  the  posterior  extremity  of  the  vocal  cords,  but  they 
are  principally  seen  in  the  neighbourhood  of  the  arytenoids.  Clinically, 
this  ulcerative  laryngitis  appears  during  or  after  the  eruption  of  measles, 
and  produces  symptoms  like  those  of  croup  ;  but  yet  it  differs  from  croup 
in  pain  localized  to  the  larynx,  in  the  slower  evolution  of  the  symptoms, 
in  the  absence  of  false  membranes,  and  in  the  lesions  of  the  larynx,  which 
are  readily  recognized  with  the  laryngoscope.  An  interesting  case  of  this 
kind  has  been  noticed  by  Cardier  in  Barbier's  monograph,  and  I  have  had 
a  similar  one  under  my  care.  This  form  of  laryngitis  is  much  less  serious 
in  adults  than  in  children,  in  whom  it  may  necessitate  tracheotomy. 

Membranous  laryngitis  may  occur  in  measles,  and  the  false  membrane 
may  or  may  not  be  diphtheritic.  In  the  latter  event  the  laryngitis  was  pseudo- 
diphtheritic,  and  due  to  the  streptococcus  and  the  staphylococcus.  It  is, 
however,  exceptional,  and  the  croup  seen  in  measles  is  usually  diphtheritic. 

Speaking  generally,  measles  lends  itself  admirably  to  the  generalization 
of  the  diphtheria  baciUus,  which  may  be  found  in  the  pharynx,  bronchi, 
nasal  fossae,  mouth,  and  skin,  but  the  larynx  is  its  favourite  seat.  This 
primary  croup,  so  rare  in  primary  diphtheria,  is  fairly  frequent  in  the 
secondary  diphtheria  of  measles.  It  is  a  complication  special  to  childhood, 
and  may  supervene  either  during  or  after  the  eruption.  From  the  local 
point  of  view  this  croup  is  attenuated,  in  the  sense  that  it  provokes  less 
dyspnoea  than  primary  croup  ;  but  from  the  general  point  of  view  it  is 
formidable,  because  it  assumes  the  toxic  character  of  malignant  diphtheria. 


1650  TEXT-BOOK  OF  MEDICINE 

For  tliis  reason  Trousseau  advised  against  operation  in  children  suffering 
from  croup  in  measles.  It  is  often  difl&cult  to  diagnose  diplitlieria  in  a 
l&iynx  already  affected  by  measles.  The  coexistence  of  pharyngeal 
diphtheria,  rejection  of  membranes  from  the  larynx,  and  bacteriological 
examination,  wiU  establish  the  diagnosis. 

Sometimes,  indeed,  although  the  pharynx  seems  to  be  free  from  diph- 
theria, it  is  suflS.cient  to  cultivate  a  particle  of  mucus  from  the  tonsil 
of  a  chUd  supposed  to  be  suffering  from  croup,  in  order  to  obtain  cultures 
of  the  diphtheria  bacillus. 

Broneho-Pulmonary  Complications.— Ca'pillary  hronchitis  and  Idbidar 
pneumonia  are  in  adults  and  children,  but  especially  in  children,  the  most 
formidable  complication  of  measles.  This  complication  may  appear  as 
early  as  the  third  or  the  fourth  day  of  the  disease — that  is  to  say,  before  the 
eruption.  It  may  not  show  itself  till  later,  during  convalescence.  As  a 
rule,  this  complication  appears  about  the  sixth  or  the  seventh  day  of  the 
disease — that  is  to  say,  when  the  rash  is  fully  out.  It  is  ushered  in  by  a 
return  of  the  fever  and  by  increasing  dyspncea.  In  addition,  if  about  the 
eighth  day  of  the  disease  the  fever,  which  should  have  fallen,  persists  or 
becomes  severe,  and  if  the  bronchitic  rales  become  finer  and  more  numerous, 
we  should  fear  the  invasion  of  capillary  bronchitis  and  lobular  pneumonia, 
to  which  children  so  often  succumb.  The  frequency  of  these  broncho- 
pulmonary complications  varies  according  to  the  particular  epidemic. 
They  are  chiefly  seen  in  children's  hospitals  and  in  the  army. 

Capillary  bronchitis  and  broncho-pneumonia  are  not  only  attributable 
to  the  poison  of  measles ;  they  are  especially  the  result  of  secondary  infec- 
tions caused  by  the  pneumococcus,  streptococcus,  staphylococcus,  and 
diphtheria  bacillus. 

In  some  cases,  especially  in  adults,  the  chief  lesion  is  capUlary  bronchitis  ; 
but  it  does  not  end  in  broncho-pneumonia,  for  it  has  not  had  time  to  do 
so,  the  patients  being  carried  off  in  a  few  days  by  this  suffocative  catarrh, 
which  may  appear  during  the  invasion  and  before  the  rash.  It  might  be 
said  that  the  entire  exanthem  is  confined  to  the  bronchi,  while  the  rash 
upon  the  skin  is  absent  or  much  delayed.  The  production  of  pus  charac- 
terizes this  capillary  bronchitis.  In  adults  the  sputum  is  purulent, 
"  phlegmorrhagic  "  (Trousseau)  by  the  first  or  by  the  second  day.  Indeed, 
it  may  be  said  that  the  patient  coughs  up  the  pus  from  an  abscess  and  fills 
the  sputum  mug,  and,  as  in  the  last  hours  of  life  expectoration  no  longer 
takes  place,  the  pus  accumulates  in  the  bronchi,  the  trachea,  and  the  nasal 
fossse,  so  that  after  death  it  is  sufl&cient  to  lower  the  head  of  the  corpse  for 
the  pus  to  flow  out  freely  ( Joffroy). 

Pleurisy  is  more  frequent  in  adults  than  in  children.  It  sometimes 
assumes  the  purulent  or  the  putrid  form. 


KllUrTlVE  KEVKIi.S  1651 

Tuberculosis. — Tlie  broncho-pulmonary  compliciitions  of  measles  are 
formidable,  because  they  are  often  associated  with  other  infections,  such 
as  diphtheria,  gangrene,  suppuration,  and  tuberculosis. 

Tuberculosis  associated  with  measles  may  assume  various  forms.  In 
young  children  and  babies  the  l)roncho-pneumonia  of  measles  is  often 
tubercular,  and,  post  mortem,  rarely  presents  the  nodular  forms  seen  in  tuber- 
culosis of  the  adult  lung ;  but  the  tubercle  bacillus  is  frequently  found  by 
curetting  or  by  examination  of  cut  sections  after  hardening.  Hypertrophy 
of  the  spleen  and  of  Peyer's  patches  and  fatty  degeneration  of  the  heart 
are  lesions  which  accompany  this  double  infection. 

Babes  has  described  a  form  of  morbillo-tubercular  pneumonia,  which  he 
has  met  with  in  a  certain  number  of  autopsies.  The  lesion  seems  to  begin 
in  the  softened  peribronchial  glands,  which  contain  both  tubercle  bacilli 
and  streptococci.  He  foimd  around  the  glands  pneumonic  infiltration, 
which  was  hard,  whitish  and  uniform,  slightly  granular,  and  of  a  sarco- 
matous appearance.  Bacilli  were  found  in  this  tissue,  which  was  infiltrated 
with  embryonic  cells. 

Acute  miliary  tuberculosis  may  occur  during  the  course  or  during  the 
convalescence  of  measles.  In  children  tubercular  meningitis  is  not  rare 
after  measles.  Lastly,  some  patients  only  experience  at  a  late  date  the 
first  symptoms  of  tuberculosis  which  has  commenced  during  measles. 

Enlargement  of  the  bronchial  glands,  which  is  sometimes  tubercular,  is 
almost  constant  in  children  suffering  from  measles.  It  may  pass  unnoticed, 
or  it  may  assume  a  clearly  marked  character,  and  last  for  several  months, 
with  the  general  symptoms  of  dyspncea  and  of  spasmodic  cough  (Gueneau 
de  Mussy). 

Digestive  System. — We  must  note  the  following  complications  in  the 
digestive  system  : 

Stomatitis.  —  The  stomatitis  of  measles,  really  an  enanthem  of  the 

'  mouth,  is  often  followed  by  desquamation  of  the  tongue,  which  bears  some 

resemblance  to  the  strawberry  tongue  of  scarlatina.     This  stomatitis  is 

comparable  to  the  erythema  and  catarrh  of  the  throat  and  larynx,  and  opens 

the  door  to  the  following  secondary  infections  : 

Aphthous  stomatitis,  in  which  the  ulcers  are  very  painful,  and  occur 
on  the  tongue,  the  lips,  and  the  inner  surfaces  of  the  cheeks. 

Ulcero-membranous  stomatitis,  which  usually  appears  during  the  decline 
of  the  disease  or  during  convalescence. 

Diphtheritic  stomatitis,  or  buccal  diphtheria,  affecting  the  gums,  tongue, 
cheeks,  and  lips,  and  forming  in  some  cases  the  starting-point  of  pharyngo- 
laryngeal  diphtheria. 

Thrush,  which  is  often  seen  towards  the  end  of  severe  cases  of 
measles. 


1652  TEXT-BOOK  OF  MEDICINE 

Gangrene  of  the  mouth  (noma)  has  become  infinitely  more  rare  since 
antiseptic  and  prophylactic  measures  have  been  rigorously  employed. 
Noma  is  often  a  late  complication,  which  appears  about  the  twentieth  or 
about  the  thirtieth  day.  It  is  not,  as  might  be  supposed,  the  appanage  of 
severe  cases,  since  it  may  appear  in  very  benign  ones.  Its  course  is  so  rapid 
that  a  gangrenous  cavity  may  be  produced  in  two  days.  The  gravity  of 
noma  in  measles  is  the  greater  in  that  it  often  coincides  with  gangrene  of  the 
lung,  vulva,  and  pharynx. 

Enteritis. — Diarrhoea  is  the  natural  result  of  the  intestinal  catarrh  in 
measles.  It  may  form  a  serious  complication  in  children  when  it  runs  the 
course  of  cholera  infantum.  It  may  be  asked  if  there  is  not  in  such  cases  a 
bacterial  association  analogous  to  that  described  by  Baginsky  at  the 
Medical  Society  of  Berlin. 

The  entero-colitis  of  measles  may  be  dysenteriform,  the  patient  suffering 
from  tenesmus,  and  passing  blood  in  the  stools.  In  adults  I  have  often 
seen  this  form  of  entero-colitis. 

Organs  of  the  Senses. — Measles  may  cause  ocular  and  aural  corn- 
phcations. 

Ocvlar  Comflications. — Conjunctivitis  is  one  of  the  benign  and  con- 
stant symptoms  of  the  period  of  invasion,  but  several  ocular  complications 
may  occur  in  measles.  Phlyctenular  conjunctivitis  and  kerato-conjuncti- 
vitis  are  seen,  and  are  characterized  by  the  appearance  of  isolated  or 
confluent  vesicles.  This  complication,  which  generally  supervenes  during 
convalescence,  may  occur  dming  the  onset  of  the  disease.  It  may  be  the 
only  manifestation  of  defaced  measles. 

These  ocular  complications  are  in  some  children  the  origin  of  grave  and 
persistent  lesions  :  Chronic  blepharitis,  which  is  obstinate  and  rebellious 
to  treatment,  and  causes  the  eyelashes  to  fall  out ;  opaline  spots,  or  leucoma 
of  the  cornea  (KevKoco,  to  whiten) ;  inflammation  of  the  lachrymal  sac,  or 
dacryocystitis  {SaKpvov,  tear ;  and  kvo-tl^,  sac) ;  ulcer  and  abscess  of  the 
cornea ;  effusion  of  pus  in  the  anterior  chamber,  or  h}'3)opyon  {viro,  under  ; 
and  TTvov,  pus) ;  perforation  of  the  cornea,  staphyloma,  and  loss  of  sight ; 
disorders  of  refraction,  strabismus,  and  asthenopia. 

Otitis. — Otitis  in  measles  especially  affects  the  middle  ear.  It  is  nearly 
always  double,  and  is  so  common  that  in  twenty-three  autopsies  on  patients 
who  had  died  from  various  complications  in  measles  Cordier  found  otitis 
media  in  twenty.  Out  of  sixteen  autopsies  in  children  who  had  succumbed 
to  the  complications  of  measles,  Miinchen  found  otitis  in  every  case,  even 
when  death  supervened  on  the  third  day  of  the  disease.  This  frequency 
is  explained  by  the  fact  that  the  Eustachian  tube  establishes  a  communica- 
tion between  the  middle  ear  and  the  naso-pharynx,  which  is  always  invaded 
bv  catarrh.     Miinchen,  however,  does  not  consider  that  the  otitis  is  always 


ERUPTIVE  FEVERS  1G53 

due  to  the  s])ri"ii(l  (»f  infection  from  the  pharynx,  lie  thinlcs  that  the 
middle  ear  is  infected  on  its  own  account.  The  otitis  would,  therefore,  be 
coni|)iiral)le  to  the  conjunctivitis,  bronchitis,  and  enteritis,  and  would 
result  from  an  cnanthem,  like  that  of  the  mucosa). 

Slight  otitis  is  characterized  by  muco-purulent  catarrh  of  the  tympanum, 
with  exudation  and  vascularization  of  the  raucous  membrane.  In  a  more 
advanced  degree  the  catarrh  is  purulent,  affects  the  tympanum  and  Eus- 
tachian tube,  and,  according  to  the  age  of  the  patient,  invades  the  pre- 
mastoid  or  the  mastoid  cells.     In  some  cases  the  chain  of  ossicles  is  affected. 

This  otitis  in  its  slight  forms  may  pass  almost  unnoticed,  because  there 
is  little  or  no  pain.  No  auditory  troubles  are  present,  and  the  muco- 
purulent fluid  often  flows  through  the  Eustachian  tube,  which  has  again 
become  permeable.  The  severe  forms  are  accompanied  by  sharp  pain, 
auditory  troubles,  and  painful  swelling  in  the  mastoid  region.  There 
is,  however,  less  pain  in  the  otitis  of  measles  than  in  the  other  forms  of 
infective  otitis.  The  speculum  shows  that  the  membrana  tympani  has  lost 
its  pearly  grey  tint,  and  is  of  a  rosy  colour,  while  it  bulges  outwards  instead 
of  being  flat,  especially  in  its  subumbUical  segment.  This  otitis  often  ends 
in  perforation  of  the  membrane,  in  which  case  the  patient  obtains  very 
great  and  instant  relief. 

The  otitis  of  measles,  when  properly  treated,  can  nearly  always  be 
cured,  without  lea\'ing  any  trace  of  deafness  ;  but  it  is  sometimes  followed 
by  chronic  otorrhoea,  which  ends  in  irremediable  lesions  of  the  tjTnpanum 
(thickening,  vegetations,  adhesions,  and  necrosis  of  the  ossicles).  The 
power  of  hearing  is  impaired  or  abolished. 

In  some  cases  very  grave  complications  arise — suppuration  in  the 
mastoid  cells,  calling  for  operation  ;  invasion  of  the  meninges  (otitic  menin- 
gitis) ;  general  purulent  infection,  with  abscesses,  jaundice  (Trousseau), 
gangrenous  broncho-pnemnonia,  and  pleurisy  (Netter).  These  various 
complications  may  supervene  during  the  decline  of  measles,  or  even  during 
convalescence. 

Complete  deafness  is  one  of  the  saddest  sequelse  of  measles.  In  children 
under  the  age  of  three  years  it  results  in  deaf -mutism.  It  may  be  said  that 
of  a  hundred  deaf-mutes  in  twenty-five  the  condition  is  due  to  otitis  follow- 
ing the  eruptive  fevers,  such  as  scarlet  fever,  measles,  or  typhoid ;  and 
of  these  figures  measles  claims  the  largest  share. 

In  the  autopsies  reported  by  Miinchen  the  exudation  in  the  tympanum 
was  nearly  always  purulent  or  sero-purulent,  but  in  four  cases  fibrinous 
exudate  was  also  present.  Bacteriological  examination  of  the  exudate  has 
sometimes  shown  the  presence  of  streptococci  alone,  and  at  other  times  the 
presence  of  staphylococci.  The  exudate  from  the  ear  after  puncture  of  the 
membrana  tympani  has  given  the  same  result, 
n.  1U5 


1654  TEXT-BOOK  OF  IMEDICINE 

Other  Complications. — Gangrene  of  the  lung,  of  the  vnJ.va,  and  of  the 
mouth  {noma)  may  supervene  after  measles,  especially  in  children's  hos- 
pitals. It  must  be  said  that  these  troubles  are  far  less  common  since  the 
rules  of  antisepsis  have  been  rigorously  observed. 

DipMheria,  whether  pharyngeal,  laryngeal, •cutaneous,  or  malignant, 
is  a  terrible  complication  that  has  become  much  less  frequent,  on 
account  of  prophylactic  measures  and  of  antiseptic  treatment. 

Associated  Eruptive  Fevers. — Measles  and  scarlatina  may  occur  at  the 
same  time  in  the  same  patient.  It  appears  to  me  that  the  association 
of  these  two  eruptive  fevers  in  the  same  subject  may  be  classified  in  the 
following  manner : 

The  two  fevers  succeed  one  another — ^that  is  to  say,  the  one  commences 
when  the  other  ends.  They  are  sometimes  simultaneous.  The  clinical 
picture  difiers  according  to  the  particular  type.  Whooping-cough  is  often 
associated  with  measles. 

Diagnosis. — The  diagnosis  of  measles  is  often  difficult  in  the  period  of 
invasion.  If  aU  the  symptoms  are  present,  no  hesitation  can  be  possible ; 
but  if  one  of  them  is  predominant,  we  may  look  upon  the  case  as  laryngitis, 
false  croup,  bronchitis,  enteritis,  or  influenza,  until  the  appearance  of  the 
eruption  some  days  later  corrects  our  error. 

Koplik's  sign  (white  and  bluish  spots  on  the  mucous  membranes  of 
the  lips  and  cheeks  during  the  pre-eruptive  period)  is  not  of  great  value  in 
the  early  diagnosis  of  measles,  for  it  is  sometimes  absent,  and,  on  the  other 
hand,  it  may  be  found  in  other  diseases  (Widowitz),  I  may  say  the  same  of 
Bolognini's  sign  (peritoneal  friction  perceived  by  repeated  pressure  over  the 
patient's  abdomen),  which  is  absent  in  half  of  the  cases  (Koppen). 

Morbilliform  eruptions  simulate  the  rash  of  measles,  as,  for  instance, 
that  of  variola  (rash),  diphtheria,  malaria,  German  measles,  and  roseola ; 
but  in  measles  the  period  of  invasion  is  characterized  by  catarrh,  and  I 
have  constantly  made  this  remark  to  my  class  :  In  an  eruptive  fever  the 
symptoms  of  the  period  of  invasion  rather  than  the  eruption  give  the  disease 
its  specific  character.  Difficult  cases  may,  however,  occur,  and  I  shall 
therefore  mention  them. 

Syphilitic  Roseola. — At  first  sight  the  diagnosis  between  measles  and 
the  roseola  of  syphihs  appears  quite  simple.  The  latter  appears  from  six 
weeks  to  three  months  after  the  contagion.  It  is  the  earliest  and 
commonest  of  the  manifestations  of  syphilis.  It  is  usually  apyretic  and 
discrete.  Itching  is  completely  absent,  and  when  the  eruption  occm's  in 
successive  crops,  their  various  colours  give  the  skin  a  peculiar  appearance, 
which  Petit  called  the  trout's  skin.  S}^hilitic  roseola  shows  two  chief 
forms,  which  are  often  associated.  The  former  is  macular,  and  character- 
ized by  flat  rose-coloured  spots,  which  disappear  on  pressure,  while  the 


ERUPTIVE  FEVEKS  1655 

other  is  papular,  and  composed  of  projecting  spots.  The  spots  are  scanty 
on  the  limbs  and  face,  and  are  not  seen  on  tlio  feet  and  hands.  De8([uama- 
tion  does  not  occur.  These  characters  appear  sullicient  to  establish  the 
diagnosis,  but  the  roseola  sometimes  assumes  a  slightly  different  character. 
It  may  be  coulliient,  morbilliform  (Bazin),  and  acconipaiiied  by  fever, 
erythema,  and  phar}^ngo-laryngeal  catarrh,  so  that  the  diagnosis  from 
measles  then  requires  careful  attention. 

Roseola  from  Bnujs. — Copaiba,  cubebs,  antipyrin,  and  iron  sometimes 
produce  morbilliform  eruptions,  which  do  not,  as  a  rule,  commence  on  the 
face,  and  are  usually  accompanied  by  itching.  In  a  case  of  real  difficulty 
inquiry  as  to  the  cause  will  clear  up  the  diagnosis.  Subacute  poisoning  by 
arsenic  deserves  notice,  because  it  has  many  points  in  common  with  measles. 
This  poisoning,  as  may  be  seen  from  numerous  cases,  may  cause  not  only 
a  morbilliform  eruption,  but  also  catarrh  of  the  eyes,  nose,  larynx,  and 
bronchi,  simulating  the  catarrh  seen  in  measles.  Accordingly,  in  cases  of 
doubt  the  nervous  symptoms  of  arsenical  poisoning  (paresis,  anaesthesia, 
and  hypersesthesia)  must  be  carefully  looked  for,  and  the  m-ine  and  the 
hair  of  the  patient  tested  for  arsenic. 

Other  Diseases. — The  diagnosis  of  measles  from  miliaria,  roseola,  and 
rubeola  will  be  discussed  in  the  description  of  these  diseases. 

Prognosis — Sequelae. — Measles  is  per  se  a  benign  disease,  but  the 
numerous  complications  which  I  have  enumerated  show  how  serious  it 
may  be.  Measles  may  leave  sequelse,  of  which  some  constitute  an  infir- 
mity, while  others  are  dangerous.  Among  these  sequelae  I  will  mention 
deaf-mutism,  chronic  otitis,  visual  troubles,  blindness,  inflammation  of  the 
mediastinal  glands,  and  pulmonary  tuberculosis.  In  predisposed  and 
lymphatic  subjects  measles  leaves  behind  it  blepharitis,  ophthalmia,  and 
chronic  eczema,  by  reason  of  the  local  lesions  in  the  eyes,  nose,  and  ears. 

I  have  twice  seen  in  an  adult,  as  a  sequel  of  measles,  chronic  bronchial 
catarrh,  with  cough,  night-sweats,  wasting,  and  rales  in  both  lungs,  simu- 
lating tuberculosis.  The  bacteriological  examination  showed  that  the 
case  was  one  of  false  tuberculosis,  Koch's  bacilli  and  elastic  fibres  being 
absent.  The  microbic  flora  was  made  up  of  micrococci  grouped  in  masses, 
in  short  chains,  tetrads,  and  short  and  thick-set  rods,  which  did  not  stain 
with  Gram. 

^Etiology.  —  Although  measles    may  appear  at  any  age,  it  is   more 

common  in  infancy.     Cases   of   congenital   measles,   transmitted  to   the 

foetus  by  the  mother,  have  been  quoted.     Measles  is  rare  during  the  first 

year,  and  reaches  its  maximum  in  children  between  three  and  five  years  of 

age.     It  is  epidemic  and  extremely  contagious,  and  one  case  of  measles 

among  a  number  of  children  may  cause  the  disease  in  ten,  twenty,  or  thirty 

of  them. 

105—2 


1656  TEXT-BOOK  OF  MEDICINE 

The  contagiousness  of  measles  commences  dm-ing  the  period  of  invasion, 
and  lasts  rnitil  the  end  of  the  eruption.  The  fact  that  measles  is  chiefly 
contagious  during  the  period  of  invasion  proves  that  the  germ  in  measles 
comes  less  from  the  skin  than  from  the  respiratory  tracks  (mucus  from  the 
nose,  the  larynx,  or  the  bronchi).  The  germ  shows  little  tendency  to  spread 
to  a  distance,  and  measles  is  no  longer  contagious  a  few  yards  away.  On 
the  other  hand,  indirect  contagion  is  much  more  frequent  than  was  formerly 
thought,  and  the  germ  may  be  carried  by  an  intermediary  (third  person, 
clothes,  utensil,  etc.)  to  a  distance  of  several  miles  in  a  very  short 
time.  The  agent  in  measles  rapidly  loses  its  pathogenic  properties,  and 
if  a  child  with  measles  has  left  its  room,  other  children  may  enter  by 
the  next  day  without  fear.  A  child  suffering  from  another  infectious 
disease,  such  as  enteric  fever,  diphtheria,  or  scarlatina,  is  not,  as  was 
supposed,  immune  to  measles.  These  afEections  may  develop  simul- 
taneously. 

The  first  attack  of  measles  generally  confers  immunity.  The  disease 
may,  however,  appear  several  years  apart,  and  may  show  relapses,  as 
in  a  typical  case  reported  by  Vergely.  The  question  of  recurrences  and 
relapses  in  measles  is  stUl  obscure,  because  writers  have  not  given  sufficient 
details.  Nevertheless,  they  are  not  frequent,  and  recurrence  is  much  less 
common  than  a  relapse  (Vergely). 

The  infectious  agent  in  measles  has  yet  to  be  discovered.  Klebs 
described  in  1875  certain  monad  forms  in  measles,  but  was  unable  to 
cultivate  them.  Babes  found  small  micrococci — single,  in  pairs,  or  in  chains — 
in  the  products  of  secretion  and  in  the  pulmonary  alveoli  of  a  patient  who 
died  from  measles.  Lesage  has  met  with  an  extremely  small  micrococcus, 
agglomerated  into  a  zoogloea  and  decolorized  by  Gram,  in  mucus  from  the 
throat  and  nose  during  the  eruptive  period  of  measles.  Culture  on  simple 
agar  yields  a  very  fine  sand,  which  is  transparent  and  analogous  to  the  small 
cultures  of  the  streptococcus  or  of  Pfeifier's  bacillus.  In  the  rabbit  sub- 
cutaneous or  intravenous  injection  causes  hsemorrhagic  septicaemia,  which 
lasts  from  two  to  twenty  days.  It  is  possible  to  produce  the  same  septi- 
caemia by  placing  the  mucus  from  a  case  of  measles  in  the  nasal  fossae  of 
the  rabbit.  Blood  taken  from  an  infant  during  an  attack  of  measles  and 
injected  in  a  rabbit  also  causes  septicaemia.  This  microbe  must  not  be 
confounded  with  the  bacillus  of  Pfeifier,  nor  with  that  of  Wilks.  It  is, 
however,  impossible  to  say  whether  the  microbes  are  indifierent  or  pathogenic. 
Inoculation  experiments  have  given  positive  results  only  ia  the  monkey. 
Josias  was  able  to  give  measles  to  Sajou  monkeys,  while  the  macaques 
were  refractory.  In  the  ape  the  disease  runs  its  course  in  five  days,  with 
coryza,  lachrymation,  and  fever.  Measles,  it  is  said,  may  appear  in  the 
monkey  when  it  is  living  amidst  infected  surroundings. 


ERUPTIVE  FEVERS  1C57 

Treatment. — In  an  ordinary  case  of  measles  the  treatment  consists 
in  hygienic  measures — antiseptic  irrigation  of  the  nose,  throat,  eyes,  and 
vulva  ;  milk  diet  (with  the  addition  of  lime-water  in  cases  of  diarrh(jea)  ; 
soothing  drinks,  with  a  few  drops  of  aconite  or  of  syrup  of  opium  for  the 
cough.  Otitis  must  be  carefully  looked  for.  As  measles  is  very  contagious, 
strict  isolation  and  disinfection,  as  recommended  in  all  contagious  diseases, 
must  be  carried  out.  Grancher  has  formulated  rules  for  isolation  which 
have  given  remarkable  results  in  his  practice ;  and  L.  Martin,  at  the  Pasteur 
Hospital,  has  instituted  a  system  of  isolation  and  hygiene  which  has  reduced 
the  contagion  and  the  mortality  (measles,  scarlatina,  variola,  diphtheria, 
etc.)  to  a  degree  previously  unknown. 

When  measles  assumes  a  malignant  form,  with  the  t}'phoid  stat€, 
delirium,  or  hypertoxic  symptoms,  I  have  successfully  used  the  cold-bath 
treatment.  The  reader  will  find  in  the  Bulletins  de  la  Societe  Medicale  des 
Hopitaux,  Seances  du  9  Mai  et  20  Juin,  1890,  an  account  of  two  young  girls 
sufEering  from  measles,  which  threatened  to  be  speedily  fatal.  They  were 
certainly  cured  by  the  cold  baths  which  I  ordered. 

In  one  of  these  cases  the  patient  was  a  girl  sixteen  years  of  age.  The  attack  had 
run  a  regular  course  until  the  sixth  day,  when  the  temperature  rose  to  105°  F.  ;  the 
pulse-rate  reached  140  ;  the  tongue  became  dry  and  red,  the  urine  scanty,  and  deUrium 
appeared  on  the  scene.  Dyspnoea  and  prostration  were  also  marked.  I  then  ordered 
cold  baths,  six  being  given  in  the  twenty-four  hours,  and  the  result,  which  was  excellent, 
was  soon  evident.  In  the  other  case,  a  child  ten  years  of  age,  whom  I  saw  with  Blache, 
was  suffering  from  measles  of  a  malignant  character.  The  symptoms  were  restlessness, 
dyspncea,  the  respiration-rate  being  80  a  minute,  temperature  of  104°  F.,  pulse  of  140, 
and  almost  total  suppression  of  urine.  In  spite  of  severe  bronchial  catarrh,  I  recom- 
mended cold  baths,  and  the  treatment,  which  was  rigorously  carried  out,  gave  a 
very  favourable  result.  I  think,  therefore,  that  I  may  state  the  following  con- 
clusions : 

1.  As,  in  spite  of  cold  baths,  the  eruption  continues  its  normal  course, 
we  need  not  be  afraid  of  driving  in  the  rash.  In  my  second  patient,  who 
took  seven  cold  baths  on  the  second  day  of  a  general  and  almost  confluent 
eruption,  the  rash  became  slightly  pale  during  the  bath ;  but  a  quarter  of 
an  hour  later  it  reappeared,  and  desquamation  took  place  in  a  classical 
manner  on  the  proper  day. 

2.  The  secretion  of  urine  tends  to  return  under  the  influence  of  cold 
baths,  so  that  it  is  customary  to  treat  by  cold  baths  infectious  diseases  of  a 
severe  type,  such  as  scarlatina,  enteric  fever,  or  pneumonia,  in  which  the 
urinary  secretion  is  scanty. 

3.  The  cold  baths  do  not  show  any  bad  efiect  on  bronchitis  or  on  pneu- 
monia in  measles,  since  capillary  bronchitis  and  broncho-pneumonia,  which 
threatened  in  my  second  patient,  yielded,  in  spite  of  the  continuation  of  the 
cold  baths,  and  perhaps  as  the  result  of  them.  The  same  remark  applies 
to  bronchitis  and  to  pneumonia  in  typhoid  fever,  which  do  not  form  a  contra- 


1658  TEXT-BOOK  OF  MEDICINE 

indication  to  cold  batlis.  It  is  injurious  to  apply  a  blister  to  a  patient  in 
whom  the  secretion  of  urine  is  already  below  the  normal,  and  a  blister  should 
not  be  used  in  a  case  of  primary  or  secondary  pneumonia,  especially  when 
the  urinary  function  is  afiected,  with  or  without  albuminuria.  A  severe 
case  of  pneumonia,  of  the  ataxo-dynamic  form,  which  I  treated  successfully 
by  cold  baths  and  without  drugs,  induces  me  to  refrain  from  the  use  of 
blisters  in  such  cases. 

In  short,  every  infectious  disease  which  assumes  the  severe  type  known 
as  malignant,  ataxo-adynamic,  etc.,  whether  it  is  a  question  of  measles, 
scarlatina,  or  pneumonia,  should  (unless  there  is  some  contra-indication) 
be  treated  with  cold  baths.  This  treatment,  which  has  been  almost  ex- 
clusively reserved  for  enteric  fever,  should  be  generally  employed  in  in- 
fectious diseases  in  which  the  infection  assumes  certain  characters  and 
marked  intensity.  Drugs  and  other  means  of  treatment,  useful  though 
they  may  be,  appear  to  me  of  secondary  importance,  and  cold  baths  in 
such  conditions  form  the  best  method  of  treatment. 

The  temperature  of  the  bath  should  be  regulated  according  to  the  nature 
and  severity  of  the  disease.  In  any  case,  we  must  not  be  content  with 
tepid  baths,  but  must  give  them  cold — that  is  to  say,  baths  in  which  the 
temperature  varies  from  68°  to  72°  F.  We  may  place  the  patient  in  a  bath 
at  72°  F.,  and  gradually  cool  the  water  to  68°  F.,  according  to  the  principles 
stated  under  Typhoid  Fever. 

By  means  of  phototherapy,  similar  to  the  method  employed  by  Finsen 
in  variola — ^that  is  to  say,  by  placing  the  patient  in  a  room  lighted  with 
red  glass — Chatiniere  has  been  able  to  modify  many  of  the  symptoms  in 
measles.  The  eruption,  the  hyperthermia,  and  the  bronchitis  have  made 
progressive  improvement, 

VI.  RUBELLA. 

Rubella  is  an  eruptive  fever  which  is  more  frequent  in  Germany  than 
in  France.  It  is  contagious,  and  sometimes  breaks  out  in  epidemics,  distinct 
from  those  of  scarlatina  and  measles.  It  may  also  attack  individuals  who 
have  or  have  not  had  scarlatina  and  measles,  and  confers  upon  them  no 
immunity  against  these  two  diseases.  These  characters  compel  us  to 
admit  that  rubella  is  a  distinct  morbid  entity. 

Description. — RubeUa  is  a  disease  of  early  life,  and  is  extremely  rare 
in  adults.  Its  incubation  period  is  imperfectly  known,  but  a  period  of 
invasion  is  absent,  and  the  disease  appears  to  begin  with  the  eruption. 
The  eruption  is  sometimes  preceded  by  injection  of  the  conjunctiva,  hoarse- 
ness, slight  dry  cough  (as  in  measles),  and  enlargement  of  the  jugular  and 
subauricular  glands,  which  has  been  given  as  a  characteristic  sign  of  rubeUa, 


ERUPTIVE  FEVERS  1C59 

but  which  T  \uivo  also  seen  in  meuslea.  The  <rijj.ii(>n  invades  the  face, 
trunk,  and  limbs  in  succession.  It  is  polymorphous,  being  morbilliform 
an,d  scarlatiniform,  macular  and  papular,  discrete  or  confluent,  and  scanty 
on  the  hands,  feet,  and  forehead,  but  well  marked  on  the  cheeks  and  around 
the  mouth.  The  eruption  disappears  after  a  duration  of  one  to  five  days. 
It  is  sometimes  followed  by  alight  branny  desquamation.  Relapses  are 
not  rare.  Although  the  prognosis  is  good,  severe  cases  and  complications 
have  been  noticed.  Broncho  -  pneumonia,  albuminuria,  and  oedema  have 
been  seen. 

From  this  description  we  see  that  rubella  somewhat  resembles  attenuated 
measles,  or  measles  associated  with  scarlatina.  Is  it  identical  with  the 
roseole  sais&nniere  described  by  Trousseau  ?  This  roseola,  says  Trous- 
seau, is  an  eruptive  fever,  sometimes  epidemic,  and  probably  contagious. 
It  is  really  modified  measles,  which  is  not  accompanied  by  ocular,  nasal, 
or  bronchial  catarrh,  and  which  does  not  expose  the  patient  to  the  compli- 
cations of  morbillous  fever.  The  period  of  invasion  lasts  from  two  to  three 
days  (chills,  headache).  The  eruption  difiers  from  that  of  measles,  the 
spots  being  paler  and  more  distinct  from  one  another.  They  give  rise  to 
acute  itching  (Vogel),  do  not  fonn  papules,  and  are  of  short  duration. 

I  think  that  there  is  a  roseole  saisonniere,  as  Frank,  Vogel,  and  Trousseau 
have  described  ;  but  there  is  also  rubella,  the  distinctive  characters  of  which 
are  not  yet  clearly  defined.  And,  lastly,  there  are  combined  forms  of  the 
eruptive  fevers  (scarlatina  and  measles),  which  must  not  be  confounded  with 
roseola  and  rubella. 

VII.  MILIARY  FEVER. 

etiology. — Miliary  fever  is  an  infectious,  endemic,  and  epidemic  disease, 
probably  of  microbic  origin,  which  appears  with  abundant  sweats,  accom- 
panied by  a  rash  and  nervous  symptoms.  It  is  not  inoculable  ;  it  is  con- 
tagious. It  confers  no  immunity  ;  it  may  pass  from  the  mother  to  the  f  cetus, 
which  may  or  may  not  be  born  alive.  In  the  three  cases  so  far  observed  the 
foetus  suffered  from  the  disease. 

Miliary  fever  occurs  at  every  age  and  at  any  season  of  the  year,  in  the 
form  of  epidemics,  preceded  by  sporadic  cases,  which  are,  as  it  were,  the 
seeds  of  the  epidemic.  The  epidemic,  therefore,  arises  from  an  endemic 
focus  which  is  sometimes  nearly  latent,  and  invades  countries  which  it  has 
never  before  visited.  When  the  disease  breaks  out  in  virgin  soil,  the  power 
of  diffusion  is  so  extraordinary  that  hundreds  of  individuals  are  taken  ill 
at  once.  The  epidemic  reaches  its  height  in  eight  days,  and  then  decreases. 
The  extension  of  the  epidemic  follows  no  rule.  In  some  cases  the  epidemic 
centre  is  localized  to  one  region ;  in  others  it  becomes  scattered,  somewhat 


1660  TEXT-BOOK  OF  MEDICINE 

like  influenza.  Miliary  fever  has  broken  out  several  times  in  France,  the 
last  epidemics  being  at  I'Herault  (1865),  and  Poitou  (1888),  Charente  and 
Deux-Sevres  (1907). 

Description. — The  duration  of  the  incubation  may  be  less  than  twenty-four 
hours.     Three  periods  are  described — invasion,  eruption,  and  desquamation. 

Invasion. — The  disease  sometimes  begins  with  prodromata,  such  as 
malaise,  headache,  chills,  heat,  dyspnoea,  vomiting,  epistaxis,  and  cough ; 
but  as  a  rule  the  sweats  form  the  initial  symptom  of  the  disease.  These 
sweats  are  so  abundant  that  the  disease  is  called  "  sweating  sickness."  The 
bedclothes  and  the  mattresses  are  soaked.  They  have  neither  special  odoui 
nor  critical  characters,  and  bring  the  patient  no  relief.  The  thirst  is  ex- 
cessive, the  urine  is  scanty  and  thick,  and  constipation  is  the  rule. 

The  sweats  are  often  paroxysmal,  and  the  attacks  are  especially  frequent 
at  night.  An  attack  is  ushered  in  by  a  feeling  of  angina  or  of  dyspnoea, 
with  tightness  in  the  epigastrium  and  pharynx,  palpitation,  tendency  to 
fainting,  or  a  terrible  sensation  of  approaching  death.  The  end  of  the 
attack  gives  only  a  relative  relief,  because  the  other  symptoms — headache, 
cramp,  and  subsultus  tendinum — persist  apart  from  the  attacks.  The  day 
is  relatively  more  restful,  but  at  night  the  whole  train  of  severe  symptoms 
reappears.  Insomnia,  nightmare,  or  delirium  may  also  be  present.  The 
period  of  invasion  lasts  from  two  to  four  days.  The  temperature  may  rise 
above  105°  F. 

Eruption. — Between  the  second  and  fourth  days  of  the  disease  the 
eruption  appears,  with  pricking,  formication,  and  recrudescence  of  the 
nervous  symptoms.  The  eruption  is  composed  of  two  elements — the 
exanthem  and  the  miliary  rash.  When  the  exanthem  is  absent,  the  miliary 
rash  is  white,  like  the  vesicles  of  sudamina.  The  exanthem,  however, 
makes  the  miliary  rash  red.  The  exanthem  may  be  morbilliform,  scarla- 
tiriiform,  hsemorrhagic,  or  purpuric.  It  varies  in  different  epidemics.  The 
miliary  rash  is  composed  of  very  smaU  transparent  vesicles,  which  ia  some 
cases  imite  and  form  blebs  (bullous  miliaria). 

The  miliary  eruption  commences  on  the  neck  and  the  front  of  the  body, 
and  then  spreads  to  the  back  and  the  limbs,  especially  to  the  wrists  (miliary 
bracelet).  It  generally  spares  the  face.  It  comes  out  in  several  crops,  and 
lasts  on  an  average  from  five  to  seven  days.  During  this  period  the  general 
symptoms  become  less  severe,  the  fever  falls,  and  the  period  of  desquamation 
begins. 

Desquamation. — Desquamation  ia  sweating  sickness  may  assume  several 
forms.  It  may  be  furfuraceous,  or  it  may  take  the  form  of  a  coUarette 
around  the  dried  -  up  vesicles.  In  some  cases  it  is  scarlatinif  orm,  large 
shreds  of  epidermis  being  thrown  off.  It  lasts  three  or  four  weeks. 
Polyuria,  which  is  a  sign  of  recovery,  then  appears. 


ERUPTIVE  FEVERS  ir.Gl 

The  disease  lasts  from  seven  to  fourteen  days.  Convalescence  is  usually 
Ions;  jiiid  painful,  even  in  the  benign  forms  of  the  di.sfuse.  The  gravity  of 
miliary  fever  varies  in  different  epidemics  and  in  different  patients,  but 
here,  as  in  all  epidemic  diseases,  benign  and  severe  cases  occur.  In  some 
cases  the  disease  is  from  the  first  so  acute  that  death  may  supervene  early 
from  cerebral  troubles,  such  as  delirium  and  coma  (early  malignant  form), 
or  at  a  later  period  (late  malignant  form).  In  some  cases  haemorrhages 
appear,  and  are  of  evil  augun-.  Miliary  fever  may  be  associated  with 
malaria,  with  the  eruptive  fevers,  and  with  t}^hus. 

The  epidemics  of  miliary  fever  are  often  preceded  or  accompanied  by 
those  of  measles  or  of  scarlatina.  In  some  instances,  indeed,  measles  and 
miliary  fever  appear  to  be  associated.  I  say  "  appear,"  for  in  the  majority 
of  cases  it  is  not  so  much  an  association  of  the  two  diseases,  but  rather  that 
the  miliary  fever  takes  on  a  morbillous  form. 

We  must  not  confound  miliary  fever,  which  is  a  definite  morbid  entity, 
with  the  sudamina  which  appear  as  an  epiphenomenon  in  the  course  of 
other  affections. 

Tonic  treatment  has  given  the  best  results,  and  the  use  of  quinine  is 
indicated  if  the  fever  assumes  a  periodic  type. 

I  shall  now  give  a  summary  of  the  important  communications  made  by 
Chantemesse  to  the  Academy  of  Medicine  in  1907.  It  deals  with  the 
epidemic  of  1907  in  Charente,  Charente-Inferieure,  and  Deux-Se%T:es. 
Within  forty-five  days  the  disease  attacked  6,000  people.  From  the  patho- 
genic point  of  view,  microscopical  examination,  attempts  at  making  cultures 
from  the  blood  and  from  the  cerebro- spinal  fluid,  and  inoculation  of  macaque 
monkeys  and  other  animals,  gave  no  results.  The  epidemic  was  remarkable 
for  its  rural  localization.  The  towns  in  the  affected  districts  were  not 
attacked. 

The  epidemic  furnished  no  evidence  that  miliary  fever  is  directly  conta- 
gious. Thus,  at  the  fair  of  RouiUac,  226  people  from  Angouleme  remained 
all  day  in  an  infected  centre,  and  yet  they  did  not  take  the  disease  back  to 
Angouleme.  The  virus  of  the  nuliary  fever  especially  attacked  those  who 
lay  on  the  ground,  and  houses  without  floors  furnished  most  of  the  cases. 

Chantemesse  believes  that  the  disease  may  be  communicated  to  man  by 
fleas  from  the  field-rat.  The  arguments  for  this  view  are  :  the  area  invaded 
in  1907  by  sweating  sickness  had  been  overrun  two  years  pre\'iously  by  field- 
lats.  "  ^Yhen  we  visited  the  houses  in  Genac,  where  the  fever  first  appeared, 
we  found  innumerable  flea-bites  on  the  bodies  of  the  inhabitants.  Many 
of  them  had  noticed  the  increase  in  the  number  of  fleas,  which  they  attri- 
buted to  the  invasion  of  their  houses  by  water-rats  driven  away  from  a 
stream  in  flood."  If  this  theory  is  proved,  the  destruction  of  field-rats  is 
essential  as  a  prophylactic  measure  in  miliary  fever. 


1662  TEXT-BOOK  OF  MEDICINE 


VIII.  DENGUE. 

etiology. — "  Dengue  is  a  contagious  or  transmissible  epidemic  febrile 
disease,  characterized  by  a  polymorphous  and  diffuse  cutaneous  eruption, 
severe  pains  in  the  joints  and  muscles,  and  a  cyclical  course,  comprising 
four  periods,  of  which  the  last,  or  convalescent,  is  often  tedious  "  (Mahe). 

This  affection  arises  in  the  tropics,  and  affects  two  chief  centres — the 
former,  in  America,  bounded  on  the  one  side  by  a  line  passing  through  the 
United  States  to  the  south  of  Boston,  and,  on  the  other  hand,  by  a  line 
through  Brazil  and  Peru.  The  second  is  on  the  shores  of  the  Indian  Ocean 
and  the  Eed  Sea  (India,  Southern  China,  Tonkin,  Mozambique,  Arabia,  and 
Egypt).  Apart  from  these  two  centres,  dengue  has  existed  in  an  endemic 
or  epidemic  condition  since  1845  in  Tripoli,  and  since  1861  in  Syria  (De 
Brun).  In  1889  the  whole  of  Asia  Minor,  Turkey,  and  G-reece  were  visited 
by  the  disease.  Each  of  these  epidemics  is  remarkable  for  the  large  number 
of  persons  affected,  for  the  suddenness  of  its  appearance,  and  the  ease  with 
which  the  disease  has  assumed  an  endemic  form  in  a  country  recently 
invaded. 

Dengue  shows  no  distinction  of  sex,  race,  age,  or  of  social  condition. 
Animals  also  are  said  to  suffer  from  it.  The  contagion  is  spread  by  the 
air,  but  the  micro-organism  which  gives  rise  to  it  is  at  present  unknown. 
Laughlin  has  found  in  the  blood  small  spherical  elements  to  which  he 
assigns  a  pathogenic  influence,  but  the  benign  nature  of  this  disease  has  not 
given  us  an  opportunity  to  examine  the  viscera. 

Symptoms. — In  tropical  countries  dengue  has  often  a  sudden  onset, 
which  roots  the  patient  to  the  spot  where  he  is,  and  compels  him  to  be 
carried  home.  In  the  Temperate  Zone  the  onset  is  less  sudden.  For  some 
hours  the  patient  feels  out  of  sorts,  complains  of  headache  or  of  insomnia, 
and  is  unwUling  to  move  about.  Then  the  characteristic  pains  of  the 
disease  appear.  They  are  unbearable,  and  affect  the  head,  the  trunk,  and 
the  limbs,  either  separately  or  together.  The  headache,  which  is  often  the 
chief  symptom,  occupies  the  forehead,  the  superciliary  ridges,  and  the 
temples.  It  is  sometimes  accompanied  by  painful  aching  of  the  scalp,  and 
pains  in  the  orbit  or  in  the  motor  muscles  of  the  eye,  and  in  the  levatores 
palpebrarum.  The  lumbar  pains  are  increased  by  walking,  and  diminished 
by  rest  in  bed.  The  pain  in  the  limbs  chiefly  affects  the  knees.  It  may 
affect  the  muscles  more  than  the  joints  (De  Brun). 

These  muscular  pains  may  invade  every  part  of  the  body,  and  form  the 
chief  symptom  in  some  epidemics.  In  others  the  chief  symptom  is  swelling 
of  the  joints,  of  the  tendon-sheaths,  of  the  hands,  and  of  the  feet. 

As  regards  the  digestive  system,  we  find  loss  of  appetite,  nausea,  vomiting, 
and  unquenchable  thirst.     The  belly  is  slightly  distended,  but  supple ; 


ERUPTIVE  FEVERS  1663 

constipation  is  the  rule ;  the  spleen  is  not  swollen,  but  the  liver  is  BOmetimes 

consrested,  and  the  skin  then  assumes  a  subicteric  tinge. 

The  helplessness  is  very  pronounced,  and  compels  the  patient  to  take  U> 
his  bed  on  the  first  day.  Any  movement  or  mental  effort  is  painful  or 
impossible. 

At  the  end  of  from  twenty-four  to  forty-eight  hours,  sometimes  earlier, 
the  eruption,  which  varies  in  appearance  and  in  distribution,  comes  out.  It 
may  resemble  that  of  measles,  rubella,  scarlatina,  or  urticaria,  or  it  may 
be  papular.  The  eruption,  while  often  of  a  vivid  red,  is  never  ecchymotic. 
It  usually  lasts  three  or  four  days,  but  it  may  disappear  at  the  end  of 
twenty-four  hours.  It  rarely  lasts  a  week.  At  the  onset  of  some  cases 
writers  have  seen  a  vegetative  eruption,  followed  after  a  few  days  by  the 
characteristic  rash.  These  eruptions  give  place  to  desquamation,  which 
may  resemble  that  seen  in  measles  or  in  scarlatina,  and  which  is  accom- 
panied by  sharp  itching. 

Fever  is  practically  constant  (the  thermometer  registers  about  104°  F.), 
but  falls  at  the  end  of  two  or  three  days,  and  this  fall  is  often  accompanied 
by  crises  (diaphoresis,  diarrhcea,  epistaxis).  Apart  from  boils  and  abscesses 
and  delirium  or  convulsions  in  children,  the  complications  of  dengue,  such 
as  epistaxis,  adenitis,  or  orchitis,  are  exceptional  and  transient.  De  Brun 
rejects  the  cardiac  forms  which  are  said  to  occur  by  Zuelzer,  Dunkby,  etc. 

This  affection  is  essentially  proteiform  (gastric,  rheumatic,  cerebral, 
eruptive,  febrile,  or  apyretic),  and  is  followed  by  convalescence,  which  is 
always  very  long,  and  at  variance  with  the  shortness  of  the  febrile  period. 
Moreover,  it  may  be  interrupted  by  relapses.  Recurrences  are  not 
uncommon  in  dengue. 

Diagnosis. — The  many  forms  of  dengue  explain  the  large  number  of 
diseases  with  which  it  may  be  confounded.  Influenza  forms  the  most 
frequent  source  of  error.  The  absence  of  respiratory  symptoms,  the  fre- 
quency of  eruptions  compared  with  their  rarity  in  influenza,  the  desqua- 
mation and  the  subsequent  itching,  and  the  bem'gn  character  of  the  disease, 
will,  as  a  rule,  prevent  errors. 

The  epidemic  character,  the  marked  contagiousness,  the  suddeimess  of 
onset,  and  the  rapid  recovery  in  dengue,  are  features  found  neither  in 
typhoid  fever  nor  in  febrile  gastritis. 

The  pains  in  the  muscles,  joints,  and  lumbar  region  may  suggest  rheu- 
matic trouble  (lumbago,  sciatica,  or  acute  rheimaatism),  and  yet  the  rapid 
helplessness,  the  eruptions,  the  desquamation,  and  the  other  symptoms 
present  in  dengue,  are  not  f  oimd  in  these  diseases. 

The  intense  headache  may  suggest  acute  meningitis,  especially  if  fever, 
constipation,  and  vomiting  are  also  present ;  but  the  eruption  and  the  rapid 
recovery  quickly  decide  the  point. 


1664  TEXT-BOOK  OF  MEDICINE 

The  febrile  form  is  distinguisiied  from  scarlatina  by  the  absence  or  by 
the  slight  importance  of  the  palato -pharyngeal  symptoms  ;  from  measles 
by  the  sudden  onset  and  absence  of  symptoms  in  the  chest ;  from  rubella 
by  the  absence  of  enlargement  in  the  jugular  and  subauricular  glands,  and 
by  the  infrequency  of  angina.  The  error  of  mistaking  the  disease  for  variola 
may  be  committed  at  first,  but  it  is,  in  general,  of  short  duration,  and  the 
same  holds  good  in  the  case  of  typhus. 

Treatment. — Eest  in  bed,  diet,  and  purgatives  are  generally  sufficient 
in  a  slight  case.  If  the  disease  is  severe,  we  should  prescribe  acidulated 
and  effervescing  drinks,  or  hot  toddy,  and  if  vomiting  occurs,  ice.  Sulphate 
of  quinine  does  not  reduce  the  temperature,  and  has  the  further  inconveni- 
ence of  causing  noises  in  the  ears.  For  the  insomnia  chloral  should  be  pre- 
scribed, and  during  convalescence  bitters,  quinine,  and  iron  will  assist  in 
promoting  recovery. 


CHAPTER  II 
TYPHOID    DISEASES 

I.  TYPHOID  FEVER. 

History.— At  the  present  time  we  include  under  the  term  typhoid  re?er  the  various 
forms  of  a  disease  which  the  old  writers  had  described  under  the  name  of  putrid  fever 
(Stoll),  malignant  nervous  fever  (Huxham),  putrid  hjemorrhagic  fever,  ataxic  and 
ataxo-advnamic  fever. 

The  progress  of  pathological  anatomy  at  the  commencement  of  the  century  has 
united  imder  one  heading  these  different  varieties,  which  were  previously  considered  as 
distinct  species.  Since  that  period  the  classification  of  fevers  has  entered  upon  a 
new  path. 

In  1804  Prost,  in  a  work  entitled  "  Medecine  Eclairee  par  I'Ouverture  des  Corps," 
had  noted  the  inflammation  and  the  ulcers  foxmd  post  mortem  in  those  who  had  died 
with  ataxic,  putrid,  or  maUgnant  fever  ;  but  he  thought  that  these  fevers  were  only  an 
excess  of  intestinal  phlogosis,  causing  death.  Broussais'  teaching  arose  from  this 
false  interpretation. 

In  1811  Petit  and  Serres,  in  their  treatise  on  "  Fievre  Entero-mesenterique,"  came 
nearer  the  truth  by  estabhshing  the  specific  nature  of  the  intestinal  lesions,  but  they 
committed  two  errors ;  firstly,  in  thinking  that  there  were  three  varieties  of  entero- 
mesenteric  fever — namely,  simple,  granular,  and  ulcerative — without  seeing  that  the 
appearance  of  the  lesion  varied  with  the  stage  of  the  disease  ;  secondly,  they  also  thought 
that  the  intestinal  lesion  comprised  the  whole  malady. 

Bretonneau,  in  1820,  first  described  the  intestinal  lesion,  and  clearly  estabhshed 
the  relations  existing  between  the  disease  and  the  lesion.  He  settled  the  question  of  its 
specific  nature,  and  united  in  one  morbid  species,  which  he  called  dothlenenterie 
(SoTi^v,  button  ;  ivrepov,  intestine),  all  the  scattered  varieties  previously  described. 
Next,  appeared  the  work  of  Trousseau,  Andral,  and  Bouillaud,  who  threw  such  a  vivid 
light  on  medicine  in  France,  and  typhoid  fever  definitely  took  the  place  which  it  now 
occupies  in  medical  nosology. 

The  discovery  of  the  typhoid  bacillus  (Eberth)  has  proved  the  specific  nature  of 
this  disease,  and  has  given  a  striking  confirmation  of  the  teaching  of  Bretonneau  and 
of  Trousseau. 

Symptoms. — I  shall  first  describe  a  typical  case  of  typhoid  fever,  and 
I  shall  then  discuss  the  special  forms  and  the  many  complications  of  this 
disease. 

1.  Onset  —  Period  of  Ascension. — As  a  rule,  the  invasion  of  typhoid 
fever  is  preceded  by  a  period  which  lasts  from  a  few  days  to  two  weeks,  and 
which  some  authors  describe  as  being  prodromal.  The  patient  complains 
of  lassitude,  muscular  pains,  loss  of  appetite,  giddiness,  and  sometimes  of 

1665 


1666  TEXT-BOOK  OF  MEDICINE 

epistaxis.  In  other  cases,  however,  this  prodromal  period  is  absent,  and 
the  disease  commences  suddenly  with  rigors  and  high  temperature.  In  some 
cases  the  morbid  localization  is  marked  at  a  particular  point,  even  from  the 
outset,  and  therefore  in  rare  instances  typhoid  fever  has  begun  with  lobar 
pneumonia.  "  These  cases  of  initial  pneumonia,  which  run  the  course  of 
simple  primary  inflammation,  mark,  however,  the  invasion  of  enteric 
fever.  During  the  first  week,  while  the  symptoms  proper  to  pneumonia 
improve,  the  signs  of  typhoid  fever  (swelling  of  the  spleen,  rose-spots,  and 
pain  in  the  iliac  region)  show  themselves.  In  certain  patients  dyspeptic 
or  intestinal  troubles  open  the  scene,  so  we  may  take  the  onset  of  enteric 
fever  for  appendicitis,  if  due  care  is  not  exercised.  In  other  cases  a  catarrhal 
angina  especially  attracts  our  attention. 

Normal  typhoid  fever  shows  three  stages — ascending,  stationary,  and 
descending.  The  first  two  stages  have  been  included  by  Jaccoud  under  the 
term  "  period  of  invasion,"  while  the  descending  stage,  in  his  opinion, 
coincides  with  the  period  of  repair.  The  course  of  the  fever  is  practically 
parallel  with  these  three  stages,  and  is  represented  on  the  temperature  chart 
by  oscillations  which  in  succession  ascend,  remain  stationary,  and  descend 
(Jaccoud).  These  divisions,  though  convenient  for  descriptive  purposes, 
are  clinically  not  so  clearly  marked,  and  the  periods  often  follow  one  another 
by  such  an  insensible  transition  that  it  is  difficult  to  say  where  the  one 
begins  and  the  other  ends. 

The  onset  of  the  period  of  ascent  cannot  be  always  defined,  for  the 
symptoms  are  blended  with  the  prodromata,  and  in  a  patient  seen  for  the 
first  time  some  days  after  the  invasion  of  the  fever  we  are  often  much 
embarrassed  in  stating  on  the  chart  the  exact  onset  of  the  disease. 

The  first  period  is  characterized  by  an  increase  in  the  prodromal  symp- 
toms or  by  the  appearance  of  fresh  ones.  Headache  is  severe,  and  may  be 
the  chief  symptom  for  some  days.  It  is  present  day  and  night,  and  some- 
times assumes  a  neuralgic  form,  with  painful  points  in  the  course  of  the 
suborbital  and  occipital  nerves.  Insomnia  is  practically  constant,  and 
is  also  a  symptom  of  great  value.  The  patient  complains  of  pains  in  the 
neck,  vertigo,  and  of  buzzing  in  the  ears,  which  increase  as  soon  as  he  raises 
himself  or  sits  up  in  bed.  Epistaxis  is  frequent,  but  not  profuse.  The 
tongue  is  coated  ;  the  loss  of  appetite  is  complete,  and  diarrhoea  commences. 
Some  patients  by  this  time  show  considerable  prostration.  Bronchial 
congestion  is  frequent,  and  revealed  on  auscultation  by  scattered  sibilant 
rales.  During  this  period,  which  lasts  from  four  to  six  days,  the  fever  is 
continuous,  the  evening  reading  being  always  higher  than  the  morning  one. 
The  temperature  rises  until  it  reaches  104°  E.  at  night.  The  acceleration  of 
the  pulse  is  not  always  in  proportion  to  the  elevation  of  temperature.  The 
cause  of  this  discrepancy  is  discussed  under  the  Pathological  Physiology. 


TYPHOID  DISEASES  1667 

2.  Stationary  Stage. — This  stage,  so  called  because  of  the  stationary 
character  of  the  fever,  does  not  deserve  this  name  as  far  as  the  symptoms 
arc  concerned,  hocanse  they  •generally  become  worse  during  this  stage. 
The  eruption  of  lenticular  rose  spots  usually  appears  on  the  abdomen 
about  the  seventh  day  of  the  disease — that  is,  at  the  commencement  of 
this  stage.  The  spots  are  from  2  to  5  millimetres  in  circumference,  papular, 
slightly  prominent,  appreciable  to  the  touch,  and  fade  on  pressure.  Each 
spot  lasts  from  three  to  six  days.  It  then  becomes  pale,  and  disappears 
without  leaving  any  trace.  The  whole  eruption  may  last  two  or  three 
weeks.  It  is  generally  discrete,  and  is  sometimes  limited  to  a  few  spots  ; 
but  in  other  cases  it  is  so  confluent  as  to  simulate  a  papular,  morbilliform 
eruption.  The  rose  spots  are  usually  seen  on  the  belly  and  chest.  They 
sometimes  spread  over  the  back  and  the  limbs.  Although  they  are  not 
absolutely  constant,  they  are  of  considerable  diagnostic  value. 

During  this  period  the  nervous  symptoms  become  gradually  more  severe, 
with  the  exception  of  the  headache,  which  improves  or  disappears.  The 
buzzing  noises  in  the  ears  are  followed  by  dullness  of  hearing,  which  may 
end  in  deafness.  In  addition  to  the  insomnia  and  disturbed  dreams,  quiet 
delirium  may  occur  at  night,  and  may  be  accompanied  by  restlessness  and 
incoherent  speech.  During  the  day  the  patient  is  quite  indifEerent  to  what 
is  going  on  around  him,  and  lies  in  a  state  of  somnolence,  which  in  some 
cases  borders  on  stupor  (tu^09).  He  lies  in  the  dorsal  decubitus,  with 
vacant  look,  wasted  face,  and  mouth  half  open.  His  lips  are  tremulous,  and 
his  nostrils  work  rapidly,  and  at  times  he  appears  to  grasp  imaginary  objects 
(carphologia,  from  Kap<^o<;,  flake  ;  XiyeLv,  to  pluck).  We  shall  see  later 
how  severe  these  sjniiptoms  become  in  the  ataxo-ad}Tiamic  forms. 

The  digestive  disturbances  are  chiefly  seen  in  this  period.  The  tongue 
is  dry,  cracked,  red,  tremulous,  and  covered  by  dry  mucus,  blackened  by 
traces  of  blood.  Sordes  are  seen  on  the  teeth,  and  the  throat  is  covered  with 
mucus  or  with  pulpy  exudate.  Vomiting  is  rare.  The  diarrhoea  is  charac- 
terized by  frequent,  offensive,  liquid  stools  of  a  yellow-ochre  colour.  They 
are  sometimes  passed  without  the  patient's  knowledge,  and  contain,  among 
other  microbes,  Eberth's  bacillus.  In  some  cases  diarrhoea  is  absent,  and 
there  may  even  be  constipation. 

As  soon  as  diarrhoea  has  set  in,  we  find  in  the  right  iliac  fossa  gurgling, 
which,  however,  is  of  no  value  in  diagnosis ;  but  this  region,  and  also  the 
epigastric  hollow,  are  usually  tender  on  pressure.  Meteorism,  due  to  intes- 
tinal paresis  and  accumulation  of  gas,  sometimes  becomes  so  marked  as  to 
push  up  the  diaphragm  and  embarrass  respiration. 

The  troubles  in  the  respiratory  system  are  of  moderate  severity. 
Although  the  patient  coughs  but  Kttle,  numerous  sonorous  and  mucous 
rales    are    heard    on    auscultation.     The  broncho-pulmonary  congestion 


1668  TEXT-BOOK  OF  MEDICINE 

causes  fairly  acute  dyspncea,  and  may  be  tke  origin  of  serious  compli- 
cations. 

TLie  urine  is  scanty,  highly  coloured,  rich  in  extractives,  and  often 
contains  albumin,  whUe  the  amount  of  urea  varies  inversely  to  the  severity 
of  the  disease.  Albuminuria  does  not  appear,  as  a  rule,  until  the  beginning 
of  the  second  week,  and  disappears  in  the  course  of  the  third  week  (Gubler). 
Retention  of  urine  is  fairly  common,  and  it  is  therefore  necessary  to  watch 
the  bladder,  in  order  to  perform  catheterism  if  needed. 

The  spleen  is  enlarged,  and  the  swelling  is  marked  from  the  commence- 
ment of  the  case,  especially  in  young  patients.  The  pulse  is  sometimes 
dicrotic  {bis  feriens) — ^that  is  to  say,  the  beat  appears  to  be  doubled — and 
the  rate  varies  from  100  to  110  beats  a  minute.  A  pulse  of  120  in  an  adult 
indicates  a  grave  condition,  especially  if  this  frequency  is  maintained 
(Hardy).  Softness  and  irregularity  of  the  pulse  are  also  unfavourable 
signs,  and  are  often  associated  with  lesions  in  the  cardiac  muscle,  which,  in 
the  grave  forms,  favour  collapse. 

During  this  period  the  evening  temperature  may  exceed  104°  F.,  while 
the  morning  temperature  shows,  as  a  rule,  only  a  slight  remission  (stationary 
oscillation),  and  the  prognosis  becomes  graver  the  less  marked  the  morning 
remission. 

Other  eruptions,  including  blue  spots  and  sweat  rashes,  are  seen,  in 
addition  to  the  rose  spots.  The  blue  or  dusky  spots  which  are  found  in 
many  other  diseases  would  present  little  interest  if  the  question  of  their 
pathogenesis  had  not  aroused  curiosity.  Mourson  has  shown  that  these 
blue  spots  are  due  to  the  presence  of  pediculi.  This  opinion  has  been  con- 
firmed by  Duguet's  experiments,  in  which  colouring  matter  from  the 
pediculi  introduced  under  the  skin  gives  rise  to  blue  spots. 

The  sudamina  met  with  in  different  stages  of  typhoid  fever  are  only  of 
moderate  interest. 

3.  Period  of  Decline. — ^Between  the  fifteenth  and  the  thirtieth  day  of 
the  disease — rarely  earlier,  and  sometimes  later — the  patient  enters  on  the 
period  of  defervescence.  The  evening  temperature,  although  it  falls  some- 
what, remains  higher  than  the  morning  temperature  ;  but  the  morning 
remissions  are  well  marked,  and  the  temperature  curve  falls  progressively. 
This  slow  defervescence  by  lysis  {'\.vat<;,  solution)  occurs  in  most  cases.  In 
some  cases,  however,  the  defervescence  is  as  sudden  as  in  pneumonia. 
Jaccoud  has  carefully  studied  this  sudden  defervescence,  and  has  found  it 
seventy-three  times  in  261  cases.  It  takes  place  in  a  space  of  time  which  varies 
from  twelve  to  thirty-six  hours,  and  the  fall  of  temperature  varies  from  1  J° 
to  3° ;  but  it  does  not  end  in  hypothermia.  It  may  be  seen  in  all  the 
varieties  of  typhoid  fever.  We  shall  find  later  a  curve  showing  sudden 
defervescence  in  one  of  my  cases. 


TVIMIOID  DISKASKS  1669 

During  this  period  the  symptoms  gradually  diminish  in  severity.  The 
insomnia  is  rej)hi((>(l  by  sK^ep  ;  the  tongue  is  moist ;  and  the  patient^  who 
now  takt's  some  interest  in  his  surroundings,  has  not  the  previous  appear- 
ance of  prostration  and  stupor.  The  diarrhoea  and  meteorism  disappear ; 
the  pulse  is  loss  frequent,  and  tends  to  regain  its  normal  characters,  and 
the  patient,  although  much  wasted  and  anaemic,  enters  on  convalescence. 

4.  Convalescence. — In  this  stage  the  wasting  stops  and  the  appetite 
returns,  but  convalescence  in  typhoid  fever  presents  this  peculiarity  :  that, 
without  appreciable  cause,  the  fever,  which  had  completely  disappeared, 
may  return,  last  three  or  four  days,  and  disappear,  in  order  to  return  again. 
This  fever  of  convalescence  does  not  indicate  a  relapse,  and  has  nothing 
in  common  with  the  febrile  condition  which  sometimes  follows  an  increase 
in  the  diet.  Moreover,  it  is  not  associated  with  any  inflammatory  lesion, 
and  presents  no  danger,  although  it  may  delay  recovery. 

If  the  attack  has  been  severe,  and  no  complication  interrupts  the  natural 
course  of  convalescence,  the  patient  requires  months  to  recover.  In  the 
convalescent  patient  the  temperature  is  subnormal,  the  pulse  is  often  slow, 
the  reflexes  are  exaggerated,  and  vertigo  and  palpitation  are  frequent 
symptoms.  The  first  attempts  at  feeding  are  sometimes  followed  by 
vomiting.  The  muscular  system  remains  weak  for  a  long  while ;  the 
patient  has  not  the  same  aptitude  for  work,  and  in  some  cases  the 
memory  is  very  slow  to  return. 

Typhoid  fever  often  causes  temporary  alopecia,  and  sometimes  leaves 
scars  on  the  skin  of  the  thighs  and  of  the  abdomen  (Bouchard).  In  young 
subjects  growth  is  quickened. 

Clinical  Forms  of  Typhoid  Fever. 

Mild  Typhoid  Fever.^ — Mild  or  defaced  forms  occur  in  typhoid  fever, 
just  as  in  aU  the  eruptive  fevers.  In  the  slight  forms  improperly  grouped 
under  the  name  of  "  mucous  fever,"  the  symptoms  are  mild.  This  term 
must  be  abandoned,  and  we  must  remember  that  these  cases,  although 
usually  quite  benign,  are  not  exempt  from  such  dread  complications  as 
hsemorrhage,  perforation,  and  peritonitis. 

Abortive  Typhoid  Fever.— The  term  abortive  typhus,  coined  by 
Lebert,  corresponds  to  the  disease  named  by  other  authors  as  t}'phus  levis- 
simus.  As  Griesinger  has  remarked,  the  word  levissimus  should  not  be 
applied  to  the  benign  nature  of  the  s}Tnptoms,  but  rather  to  the  short 
duration  of  the  disease.  In  this  form  the  invasion  is  acute  and  febrile,  and 
the  symptoms  (epistaxis,  diarrhoea,  swelling  of  the  spleen,  and  rose-rash) 
somewhat  resemble  those  of  mild  enteric  fever ;  but  in  the  second  week 
"  the  disease  stops  short,  beha\'ing  with  regard  to  abdominal  typhus  just 
as  varioloid  does  with  regard  to  variola  "  (Jaccoud).  The  fall  of  tempera- 
n.  106 


1670  TEXT-BOOK  OF  MEDICINE 

ture  is  usually  accompanied  by  critical  sweats.  It  is  possible,  adds  Jaccoud, 
thougb  not  proven,  that  in  the  abortive  forms  the  intestinal  changes  may 
be  limited  to  infiltration  of  the  glands,  and  that  resolution  replaces  necrosis 
and  consequent  sloughing. 

Ambulatory  Form. — The  preceding  or  abortive  form  was  characterized 
by  its  short  duration  and  by  its  well-marked,  though  benign,  symptoms. 
The  ambulatory  form,  so  called  because  patients  feel  such  slight  malaise 
that  they  continue  to  go  about,  is  latent.  Fever  is  absent  or  very  slight. 
The  malaise,  headache,  insomnia,  and  diarrhoea,  which  are  usually  so  marked 
in  typhoid  fever,  are  here  but  little  in  evidence.  Nevertheless,  we  may  find 
swelling  of  the  spleen,  rose  spots,  and  bronchitic  rales ;  but  the  patient, 
who  does  not  consider  himseK  ill,  and  has  not  lost  his  appetite,  goes  about 
and  tries  to  attend  to  business.  In  spite  of  the  apparently  benign  nature 
of  the  disease,  the  patient  runs  the  risk  of  haemorrhage,  perforation,  and 
peritonitis,  and  at  the  autopsy  the  typical  lesions  of  typhoid  fever  are 
found. 

Adynamic  Form. — This  term  does  not  apply  to  the  secondary  symptoms 
of  adynamia  which  supervene  in  severe  cases.  It  is  reserved  for  those 
cases  which  assume  an  adjmamic  character  during  the  invasion.  General 
feebleness  and  prostration,  compressible  pulse,  profound  and  lasting  stupor, 
quiet  delirium,  deafness,  paralysis  of  the  bladder,  abundant  diarrhoea,  con- 
siderable meteorism,  foetor  of  the  sweat  and  of  the  breath,  and  a  tendency 
to  haemorrhage  and  gangrene,  are  the  symptoms,  of  the  adynamic  form, 
which  corresponds  to  the  old  putrid  and  malignant  fever.  The  prognosis 
is  usually  grave. 

Ataxic  Form. — "  Prostration  and  enfeeblement  of  the  animal  functions 
are  not  present,  as  in  the  preceding  form.  It  is  their  want  of  harmony 
that  strikes  us  "  (Trousseau).  The  ataxic  form  begins  with  very  high 
temperature.  Cramps  and  lumbar  pain  occur.  The  delirium,  which  appears 
early  and  is  sometimes  violent,  may  be  accompanied  by  loquacity  and 
hallucinations.  Squint,  chewing  movements  of  the  jaws,  tremors  of  the 
face,  of  the  lips,  of  the  hands,  and  of  the  fingers,  carphologia,  subsultus 
tendinum,  and  convulsions  are  seen.  This  variety  of  enteric  fever  is  most 
fatal,  and  carries  the  patients  off  in  five  or  six  days.  In  some  cases  symp- 
toms of  adynamia  appear,  and  we  then  have  the  mixed  Ataxo-adynamic 
variety.  We  must  always  feel  anxious  in  these  ataxic  cases,  even  when  the 
symptoms  are  trifling. 

Sudoral  Form. — The  form  called  sudoral  by  Jaccoud  presents  special 
characters.  Apart  from  the  headache,  which  is  severe,  there  are  neither 
cerebral  symptoms,  delirium,  nor  stupor.  Abdominal  symptoms  are  almost 
absent — no  diarrhoea,  no  meteorism ;  the  tongue  remains  moist' ;  the 
broncho-pulmonary  system  is  less  affected  than  in  ordinary  typhoid  fever. 


TYPHOID  DJSEASKS  H)71 

/ 
and  albuminuria  is  extremely  rare.     The  rose  spots  are  not  presout  in  all 

the  cases,  but  their  complete  absence,  says  Jaccoud,  is  excej)tional.     Hajmor- 

rhage  from  the  bowels  is  fairly  frequent.     Fever  and  sweats  are  the  constant 

and  prominent  symptoms  in  this  form.     The  fever,  though  continuous, 

shows   well-marked   paroxysms,    which  may  occur  several  times   in   the 

twenty-four   hours,   and   are   followed   by   "  profuse,   drenching   sweats." 

This  form  is  common  in  Italy,  especially  in  Naples  (Borelli),  and  is  also  seen 

in  Paris. 

Haemorrhagic  Form. — This  form,  called  haemorrhagic  putrid  fever 
by  old  writers,  is  marked  by  cutaneous  haemorrhages,  purpuric  ecchymoses, 
bleeding  from  the  nose  and  gums,  hsematuria,  and  metrorrhagia.  It  is 
more  frequent  in  certain  epidemics.  It  is  usually  associated  with  changes 
in  the  liver,  and  with  symptoms  of  ataxia  or  of  ataxo-adynamia.  It  is 
always  fatal. 

Typhoid  Fever  in  Children  and  Elderly  People.— Typhoid  fever  in 
children  differs  anatomicaUy  and  clinically  from  the  disease  as  seen  in 
the  adult.  The  infiltration  of  Peyer's  patches  almost  always  takes  the 
form  of  soft  plaques,  which  rarely  ulcerate.  Perforation,  peritonitis,  and 
haemorrhage  are  very  rare  in  infancy.  The  disease  is  especially  frequent 
after  the  fifth  year,  but  yet  cases  have  been  seen  as  early  as  the  fiist  year, 
and  even  at  the  age  of  six  months.  The  tongue  remains  moist ;  vomiting 
is  frequent ;  diarrhoea  is  rare  ;  ballooning  of  the  belly  is  exceptional ;  con- 
vulsions, with  slight  deHrium,  may  be  seen ;  the  eruption  of  rose  spots  is 
discrete;  the  wasting  is  rapid;  and  the  disease  often  ends  with  critical  sweats. 
The  ataxo-adynamic  symptoms  which  are  seen  in  youths  about  the  age 
of  puberty  are  extremely  rare  in  young  children.  Pulmonary  manifesta- 
tions, especially  lobular  pneumonia,  are  formidable  in  early  life,  and  relapses 
are  more  frequent  than  in  adults ;  and  yet  the  prognosis  of  typhoid  fever 
in  the  child  is  much  less  grave  than  at  a  more  advanced  age.  In  children's 
hospitals  diphtheria,  the  eruptive  fevers,  and  whooping-cough  form  the 
common  complications. 

Typhoid  fever  in  elderly  people  presents  some  peculiarities.  The 
temperature  is  not  very  high,  the  swelling  of  the  spleen  is  slight,  the  rose 
spots  are  few  in  number ;  and  yet,  in  spite  of  the  apparently  trifling  nature 
of  the  symptoms,  the  disease  rapidly  ends  in  prostration.  The  course  of  the 
disease  is  slow,  and  the  broncho-pulmonary  troubles  add  much  to  the 
gravity  of  the  prognosis. 

Complications  of  Typhoid  Fever. 

Digestive  System. — Numerous  complications  affect  the  digestive  system. 
As  regards  the  bucco-pharyngeal  cavity,  there  is  little  to  be  said  ;  but 
membranous  angina,   due  to  staphylococci   or  to  streptococci,  may   be 

106—2 


1672  TEXT-BOOK  OF  MEDICINE 

seen.  Diphtheria  is  only  present  in  very  rare  cases.  We  may  see  on  the 
pillars  of  the  fauces,  on  the  tonsils,  and  on  the  pharynx  ulcers,  which  at  first 
sight  resemble  those  of  herpes  and  of  tuberculosis.  They  are  really  due  to 
Eberth's  bacillus.     Thrush  is  fairly  frequent  in  the  pharynx. 

Violent  spasmodic  dyspnoea  is  at  times  seen  during  the  course  or  during 
the  decline  of  typhoid  fever.  It  may  be  the  only  nervous  symptom  of  the 
disease  or  the  prelude  of  grave  nervous  troubles  in  convalescence  (Vergely). 

Gastric  Troubles.— The  anatomical  study  of  the  gastric  lesions  in  typhoid 
fever  (lymphatic  infiltration,  thrombosis,  miliary  abscesses,  and  ulcers) 
explains  the  symptoms  present  in  some  cases  (Chauffard).  I  refer  here  to 
the  repeated  and  obstinate  vomiting  sometimes  seen  in  the  course  of  the 
second  or  of  the  third  week,  or  even  during  convalescence  (Trousseau).  It 
appears  probable  that  this  vomiting,  which  is  accompanied  by  pain  and  a 
rise  of  temperature  in  the  epigastric  angle  (Peter),  is  associated  with  infective 
and  ulcerating  lesions  of  the  stomach.  Hsematemesis  may  be  seen.  If 
the  reader  will  turn  to  the  section  on  Appendicular  Vomito  Negro,  he  will 
see  that  in  one  of  the  cases  the  haematemesis  (Millard's  case)  was  due  to 
changes  in  the  stomach  following  upon  paratyphoid  appendicitis. 

Hcemorrhage  from  the  Bowel. — Haemorrhage  is  seen  in  6  per  cent, 
of  cases,  and  its  frequency  varies  according  to  the  epidemic.  In  some 
cases  the  blood  remains  in  the  bowel,  where  it  is  found  at  the  autopsy. 
As  a  rule,  it  is  passed  (melaena),  either  in  the  form  of  pure  blood  (this  is 
rare),  or  in  the  form  of  clots,  and  of  brownish  or  blackish  foetid  fluid,  like 
soot  and  water,  or  sticky,  like  tar.  Haemorrhage  may  occur  several  times 
in  the  same  day,  or  on  several  days  following.  It  usually  occurs  at  the 
beginning  or  during  the  course  of  the  third  week,  and  is  due  to  ulceration 
of  the  intestine,  to  degeneration  and  perforation  of  the  vessels,  and  to  the 
formation  of  fleshy,  perivascular  granulations.  When,  however,  the 
bleeding  appears  in  the  early  part  of  the  second  week,  before  ulceration 
has  taken  place,  we  must  rather  admit  that  it  is  due  to  congestion  of  the 
gut,  with  or  without  changes  in  the  vessel  wall.  The  more  abundant  and 
the  more  frequent  the  haemorrhage,  the  more  serious  the  outlook.  In  some 
exceptional  cases  the  bleeding  is  fulminating  at  the  first  onset.  Thus,  one 
of  Trousseau's  patients  was  carried  off  in  an  hour,  and  a  patient  whose  case 
is  reported  by  Leymarie  was  seized  with  such  severe  haemorrhage  from  the 
bowel  that  he  died  in  less  than  an  hour,  and  at  the  autopsy  the  haemorrhage 
was  found  to  proceed  from  a  smaU  artery  opening  into  an  ulcer.  Several 
authors  regard  haemorrhage  from  the  bowel  as  relatively  benign.  Graves 
called  it  an  almost  critical  phenomenon,  and  Trousseau  did  not  consider  it 
to  be  very  formidable.  Griesinger  says  that  it  is  fatal  in  only  33  per  cent, 
of  the  cases. 

Some  authors  have  distorted  Trousseau's  statement,  making  him  say 


TYPHOID  DISP:ASES  1G73 

that  he  consiiU'rod  intestinal  haemorrhage  as  absohitely  benign.  Trousseau, 
after  giving  his  opinion  that  these  haemorrhages  "  are  far  from  having  the 
gravity  usually  attrihutcd  to  thom,"  took  care  to  add  :  "  I  would  not  have 
it  said  that  I  regard  these  complications,  which  are  usually  considered  to  he 
serious  in  every  case,  as  being  absolutely  harmless."  For  my  part,  I  con- 
sider haemorrhage  as  formidable  to  a  moderate  degree.  Most  of  the  patients 
in  whom  I  have  seen  haemorrhage  have  recovered,  and  I  am  therefore  quite 
ready  to  regard  them  as  being  benign  in  most  cases  ;  and  yet  we  must  reserve 
our  prognosis,  because  haemorrhage  sometimes  heralds  perforation  of 
the  gut,  and,  on  the  other  hand,  it  is  particularly  formidable  when  it  forms 
part  of  a  general  haemorrhagic  process  (haemorrhagic  putrid  fever). 

When  the  haemorrhage  is  abundant,  it  usually,  but  not  always,  causes 
a  sudden  fall  of  temperature.  This  fall,  however,  is  transient,  and  in  some 
cases  in  one  or  two  hours  the  temperature  may  exceed  the  point  at  which 
it  stood  before  the  bleeding.  Such  a  course  is  not  seen  after  the  fall  pro- 
voked by  perforation  of  the  bowel. 

Peritonitis. — Two  varieties  of  peritonitis — one  by  perforation,  the  other 
by  propagation — are  usually  described.  The  former  is  more  serious,  and 
is  generally  due  to  perforation  of  Peyer's  patches,  or  of  the  ulcerated  closed 
iollicles.  The  latter,  less  serious  and  more  limited,  is  said  to  be  due  to  the 
propagation  of  the  infecting  process  through  the  intestine  which  is  ulcer- 
ated, but  not  perforated. 

The  perforation  is  usually  found  in  the  lower  portion  of  the  ileum — that 
is  to  say,  in  the  region  where  the  ulcerative  process  is  most  severe.  A  per- 
foration of  the  ileum  is  rarely  found  more  than  2  feet  above  the  ileo-caecal 
valve,  but  it  is  not  uncommon  to  find  perforation  below  the  valve  in  the 
caecum,  the  appendix,  or  the  colon.  In  Nacke's  statistics,  comprising 
127  autopsies,  perforations  were  found  106  times  in  the  end  of  the  ileum, 
15  times  in  the  appendix,  and  12  times  in  the  colon.  Care  must  be  exer- 
cised when  making  an  autopsy  not  to  mistake  an  artificial  tear  made 
during  the  examination  for  a  perforation  of  the  gut.  The  perforation  is 
usually  very  small,  being  about  as  large  as  a  pin's  head,  a  hemp-seed,  or  a 
lentil.  It  is  rounded,  forming  the  apex  of  a  kind  of  crater,  which  results 
from  the  ulceration  of  the  agminated  or  isolated  follicles.  In  some  cases 
the  ulcer  may  be  as  large  as  a  florin  ;  in  others  it  takes  the  form  of  a  slit.  As 
a  rule,  only  one  perforation  is  found,  but  it  is  by  no  means  rare  to  find  two, 
three,  or  even  several,  which  have  occurred  simultaneously  or  in  succession. 

Perforation  of  the  gut  takes  place  at  different  times,  but  most  frequently 
during  the  course  of  the  third  or  at  the  beginning  of  the  fourth  week,  when 
the  ulcerative  process  is  at  its  maximum.  Writers  have,  however,  quoted 
very  early  perforations,  occurring  between  the  eighth  and  twelfth  days  of 
the  disease  ;  but  it  may  then  be  asked  whether  the  date  of  the  onset  was 


1674  TEXT-BOOK  OF  MEDICINE 

correctly  determined.  Tliey  have  also  quoted  very  late  perforations, 
supervening  during  convalescence  or  after  recovery.  We  shaU  see  later 
the  meaning  of  these  facts.  Perforations  are  far  from  being  rare  during 
relapses. 

The  frequency  of  perforation  varies  in  different  epidemics  and  countries. 
As  a  general  rule,  perforation  is  one  of  the  most  formidable  complications 
of  t3rphoid  fever.  It  is  not  as  common  in  children  as  in  adults.  It  appears 
to  be  more  frequent  among  the  Anglo-Saxon  race.  Murchison  has  col- 
lected some  interesting  statistics,  which  show  the  large  proportion  of  eighty 
perforations  in  412  autopsies  (19  per  cent.)  in  English  hospitals.  In  the 
French  and  German  hospitals  the  proportion  is  116  perforations  in  1,300 
deaths  (10  per  cent.). 

Perforation  of  the  gut  is  the  result  of  an  ulcerative  process.  Drastic 
purgatives,  large  enemata,  the  strain  of  vomiting,  and  departure  from 
careful  treatment,  have  been  suggested  as  favouring  perforation.  There 
is  some  truth  in  these  statements.  Perforation  occurs  more  readily  in 
severe  ataxo- adynamic  cases,  but  cases  of  perforation  supervening  in  the 
course  of  very  mild  attacks  have  also  been  reported  (typhus  levissimus, 
typhus  ambulatorius).  In  the  latter  case  peritonitis  sets  in  suddenly,  just 
as  pneumothorax  may  do  in  the  course  of  an  almost  latent  tuberculosis. 
The  cold-bath  treatment  should  not  be  blamed.  I  think,  on  the  other 
hand,  that  hydrotherapy  lessens  the  virulence  of  the  disease,  and  eUminates 
to  some  extent  the  danger  caused  by  the  ulcerative  process. 

Intestinal  haemorrhage  fairly  often  precedes  peritonitis  by  perforation, 
and  the  fact  need  cause  no  surprise,  for  the  same  ulcerative  process  is  at 
work  in  both  these  complications.  HomoUe  gives  the  following  conclusive 
statistics  on  this  point :  In  the  cases  collected  by  Murchison,  11  out  of 
69  patients  who  suffered  from  perforative  peritonitis  had  haemorrhage  from 
the  bowel.  Goldhamer  has  observed  the  same  course  of  events :  in 
13  patients  suffering  from  peritonitis  3  had  intestinal  haemorrhage.  One 
of  Grasset's  patients  died  from  perforation  after  iatestinal  haemorrhage, 
and  one  of  Buhl's  patients,  who  had  escaped  the  complication  of  perforation, 
died  later  from  bleeding.  The  association  and  the  succession  of  these 
complications  had  arrested  my  attention,  and  of  the  numerous  patients 
whom  I  saw  die  from  peritonitis  by  perforation  many  had  previously  had 
haemorrhage  from  the  gut.  The  most  alarming  feature  of  haemorrhage  is, 
in  my  opinion,  that  it  is  often  a  forerunner  of  perforation. 

We  are  too  prone  to  think  that  peritonitis  in  the  course  of  typhoid  fever 
is  ushered  in  with  severe  symptoms.  In  some  instances  this  is  true,  but 
often  such  is  by  no  means  the  case.  In  typhoid  fever  peritonitis  is  often 
insidious  in  its  appearance.  It  is  somewhat  rare,  I  repeat,  for  peritonitis 
in  typhoid  fever  to  assume  the  severe  type,  with  intense  pain  and  porraceous 


TYPHOID  DISEASES  1075 

vomiting,  so  frequent  in  peritonitis  following  perforating  ulcer  of  (he 
stomach  or  of  the  duodenum.  1'here  are  several  reasons  for  this.  In  the 
first  place,  typhoid  peritonitis  often  supervenes  in  patients  whose  sensations 
are  more  or  less  blunted  by  the  infection ;  and,  further,  the  perforation  of  the 
howt'l  i.s  usually  so  small  and  so  limited  that  the  infecting  agents — intestinal 
iluid,  microbes,  and  toxines — reach  the  peritoneum  very  slowly  and  in  small 
doses.  Thus  in  some  cases,  as  I  have  often  seen,  the  onset  of  peritonitis 
would  pass  almost  unnoticed  if  the  patient  were  not  carefully  watched. 
He  has  pain,  it  is  true,  but  it  is  only  slight.  He  may  vomit ;  but  do  not 
patients  with  enteric  fever  vomit,  apart  from  peritonitis  ?  Tympanites 
may  be  present ;  but  is  not  the  belly  usually  t}Tnpanitic  in  typhoid  fever  ? 
There  may  be  pain  in  the  right  iliac  fossa ;  but  is  not  this  often  the  case 
in  the  course  of  this  disease,  without  any  reason  for  suspecting  perito- 
nitis ?  Accordingly,  nausea,  vomiting,  pain,  and  tympanites,  which 
may  be  more  or  less  marked,  leave  us  sometimes  in  doubt  as  to  the 
occurrence  of  perforation  and  the  appearance  of  peritonitis. 

Hiccough  is  a  sign  of  considerable  importance  in  my  opinion.  Peri- 
tonitis is  probably  present  when  a  patient  in  the  third  week  of  typhoid 
fever  suffers  from  abdominal  pain,  nausea,  and  vomiting,  while  the  abdomen 
is  more  distended  than  usual,  especially  if  hiccough  is  added  to  these  symp- 
toms. Hiccough  may,  however,  exist  in  typhoid  fever  as  a  consecutive 
complication,  independent  of  peritonitis.  Graves  many  years  ago  noticed 
this  fact,  and  I  have  seen  it  in  two  of  my  cases,  one  of  whom  came  under 
my  care  during  the  second  week  of  an  attack  of  typhoid  fever,  with  in- 
cessant hiccough  day  and  night.  After  the  first  few  cold  baths  had  been 
given,  the  hiccough  disappeared.  We  should  be  wrong,  therefore,  in  con- 
sidering hiccough  as  a  certain  sign  of  peritonitis. 

In  my  opinion  the  temperature  curve  is  the  most  important  symptom 
of  insidious  peritonitis  by  perforation.  Perforation  of  the  bowel  in  the 
course  of  typhoid  fever  shows  itself  in  a  large  number  of  cases  by  a  sudden 
fall  of  temperature.  This  fall  may  be  as  much  as  5°  or  6°  F.  in  a  few  hours. 
The  fall  nearly  always  results  in  hypothermia.  It  is  not  accompanied  by 
rigors,  and  may  be  almost  unnoticed  by  the  patient.  Most  writers  place 
this  sudden  fall  of  temperature  among  the  signs  of  perforation.  The 
following  cases  will  illustrate  this  point : 

The  temperature  fell  in  a  few  hours  from  lOS-S"  to  96°  F.  in  one  of  Netter's 
patients  suffering  from  severe  typhoid  fever,  which  had  nm  a  normal  course  imtU  the 
twentieth  day.  The  patient  did  not  vomit  or  complain  of  abdominal  pain,  because  his 
senses  were  much  duUed.  The  autopsy  revealed  fairly  circumscribed  peritonitis,  due 
to  perforation  of  a  Peyer's  patch.  In  a  case  reported  by  Dillay  sharp  pain,  with 
vomiting,  appeared  during  the  decline  of  a  case  of  typhoid  fever,  and  the  temperature 
fell  to  96"  F.  on  the  morning  after  the  patient's  admission  to  hospital.  The  man  died 
some  days  later,  and  the  autopsy  revealed  peritonitis,  conseoutive  to  two  intestinal 


1676 


TEXT-BOOK  OF  MEDICINE 


perforations  ini  ulcerated  Peyer's  patches.  These  perforations  were  situated  in  the 
Qeum,  6  and  8  inches  above  the  ileo-caecal  valve.  Peritonitis  supervened  on  the  fifteenth 
day  in  a  case  of  adynamic  fever  reported  by  Laboulbene ;  the  abdomen  was  much 
distended ;  the  patient  was  delirious.  He  did  not  vomit,  but  he  had  diarrhoea,  and  the 
temperature  suddenly  fell  from  103°  to  98°  F.  At  the  autopsy  peritonitis,  resulting 
from  a  perforation  of  a  Peyer's  patch  near  the  end  of  the  ileum,  was  found. 

Martineau  has  related  three  cases  of  peritonitis  by  perforation  in  the  course  of 
typhoid  fever,  and  all  three  showed  a  fall  of  temperature,  which  at  the  time  of  death 
was  only  96°  P. 

In  a  work  pubhshed  in  1889  by  Reunert  on  peritonitis  in  typhoid  fever  by  perforation 
of  the  bowel,  I  find  three  cases  in  which  it  is  said  that  in  the  first  patient  the  temperature 
fell  to  96°  F.,  m  the  second  to  97°  F.,  and  in  the  third  to  95°  F. 


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77. — TypHoro  Fevke:  Fall  of  Temperatdiie  after  iNTESTrNAL 
Perforation  in  a  Patient  of  Mine. 


a,  104-2°  F.  on  the  evening  of  the  seventeenth  day ;  b,  96-5°  F.  on  the  morning  of  the 
eighteenth  day  ;  c,  death  on  the  twenty -fourth  day. 


I  have  quoted  these  cases  because  sudden  hypothermia  is  a  valuable 
sign  of  insidious  perforation  in  the  course  of  typhoid  fever,  and  this  sign 
is  the  more  precious  because  the  other  sjnnptoms  of  acute  peritonitis — 
namely,  pain,  vomiting,  and  hiccough — are  sometimes  almost  absent.  In 
such  cases,  therefore,  our  best  guide  as  regards  surgical  intervention  is 
sudden  hjrpothermia  ;  but  I  do  not  say,  of  course,  that  this  h}^othermia 
always  follows  in  intestinal  perforation  of  typhoid  origin,  for  there  are 
cases  in  which  peritonitis  is  accompanied  by  severe  pain,  vomiting,  and  a 
rise  of  temperature  to  103°  or  104°  F. ;  but  whether  the  fall  of  temperature 


TYPHOID  DISEASES  1077 

be  due  to  the  hypothermic  action  of  the  coli  bacillus  and  its  toxim-,*  with 
or  without  tlie  assistance  of  Eberth's  bacillus,  or  whotlKT  it  is  due  to  sidora- 
tion  of  the  abdominal  sympathetic,  it  is  none  the  less  true  that  this  fall  is 
a  sign  of  undoubted  value.  Nevertheless,  it  must  not  be  thought  that 
sudden  falls  of  temperature  in  the  course  of  typhoid  fever  always  indicate 
a  perforation.  In  some  rare  cases  the  defervescence  in  typhoid  fever  is  as 
sudden  as  in  pneumonia.  In  the  evening  the  temperature  may  be  104°  F., 
and  on  the  next  morning  only  98°  F.,  this  fall  indicating  recovery.  T  have 
seen  an  instance  of  this  kind  in  one  of  my  patients.  A  young  woman  was 
suflFering  from  typhoid  fever  of  a  fairly  severe  type,  and  recovery  took  place 
by  sudden  defervescence,  as  the  chart  on  p.  167<S  shows. 

There  is  a  difference,  however,  between  the  sudden  defervescence  of 
recovery  and  that  of  perforation.  The  former  coincides  with  an  improve- 
'ment  in  all  the  symptoms,  and  the  temperature  does  not  fall  below  normal ; 
the  fall  which  announces  perforation  sometimes  leads  rapidly  to  hypothermia, 
and  coincides  with  aggravation  of  the  general  symptoms,  or  with  the 
appearance  of  fresh  ones. 

A  sudden  fall  of  temperature,  with  or  without  hypothermia,  may  also 
supervene  in  the  course  of  typhoid  fever  as  the  result  of  profuse  haemorrhage 
from  the  bowels,  and  consequently  simulate  the  sudden  hypothermia  of 
perforation  ;  in  the  latter  case  the  temperature  rises  slowly,  while  as  a  rule 
a  rapid  rise  follows  in  the  former,  so  that  the  temperature  in  a  few  hours 
is  as  high  as  it  was  before  the  fall. 

I  have  never  seen  a  better  proof  of  this  assertion  than  in  the  case  of  one  of  my 
patients,  whose  chart  is  given  (Fig.  79).  The  patient  was  taken  ill  on  the  twelfth  day 
of  very  severe  ataxo-adynamic  fever,  with  two  very  copious  haemorrhages  at  an  interval 
of  a  quarter  of  an  hour.  Just  before  the  haemorrhage  the  temperature  was  105°  F., 
but  it  at  once  feU  as  low  as  97-5°  F.  This  was  indeed  a  case  of  sudden  hypothermia, 
counterfeiting  that  of  perforation,  but  two  hours  after  the  haemorrhage  the  temperature 
had  already  gone  up  to  103-6°  F.  The  patient  died  four  days  later,  and  it  was  easy  to 
see  that  she  had  neither  perforation  nor  the  least  trace  of  peritonitis,  although  several 
Peyer's  patches  were  ulcerated  down  to  the  serous  coat. 

Peritonitis  from  perforation  is  fatal  in  the  great  majority  of  cases.  It 
has  a  duration  varying  from  two  to  eight  days,  sometimes  interrupted  by 

*  Sanarelli,  in  his  experimental  researches  on  typhoid  fever,  comes  to  the  following 
conclusions  :  He  injects  a  culture  of  the  Bacillus  coli  and  BaciUu-s  typhosus  into  the 
peritoneum  of  the  guinea-pig ;  he  then  injects  in  another  guinea-pig  the  peritoneal 
exudate  of  the  first  guinea-pig  which  has  succumbed,  and  so  on.  He  thus  succeeds  in 
obtaining  a  Bacillus  typhosus  of  much  increased  virulence.  Injection  of  two  drops  of 
this  virus  in  the  peritoneum  of  the  guinea-pig  kills  the  animal  in  fifteen  hours,  and 
produces  in  one  houra  fall  of  temperature  from  37o°  to  34°  C.  (Ann.  de  VInst.  Pasteur, 
Avril,  1894).  On  the  other  hand,  Roux  and  Rodet  arrive  at  the  same  result  with  a 
culture  of  coli  bacillus  of  increased  virulence  {Arch,  de  Med.  E.vp''rim.,  Mai,  1892). 
Boix.  in  a  work  on  the  pathogenesis  of  icterus  gravis,  has  analyzed  the  h^'pothermio 
properties  of  the  coh  bacillus  {Arch,  de  Med.,  Juillet  et  Aotit,  189G). 


1678 


TEXT-BOOK  OF  MEDICINE 


remissions  or  fictitious  improvement,  and  the  peritoneal  symptoms  are 
fairly  often  masked  by  the  typhoid  symptoms.  In  a  few  days  the  face 
becomes  pinched,  the  eyes  hollow,  the  pulse  miserable  and  very  rapid ;  the 
patient  is  cold  and  covered  with  clammy  sweat,  and  death  supervenes  in 
collapse  or  in  coma. 

Nevertheless,  peritonitis  from  perforation  is  not  always  fatal,  for 
adhesions  may  be  established  in  time,  in  which  case  the  peritonitis  becomes 
circumscribed,   and  after  two,   three,   or  four  days,   during   which    the 


18     19     20    21     2a    2Z 


Fia.  78.— TypHon)  Fever:  Recovery  on  Nineteenth  Day,  with  Sudden 

Deeervescence. 

Temperature  falling  from  104-2°  to  1005°  F. 

symptoms  of  peritonitis  from  perforation  have  been  evident,  improvement 
sets  in,  and  the  patient  recovers. 

Reunert's  cases,  to  ■which  I  alluded  above,  are  types  of  this  peritonitis  ending  in 
recovery,  and  in  them  sudden  fall  of  temperature,  vomiting,  hiccough,  tympanites, 
dyspnoea,  thready  pulse,  and  collapse  were  aU  present.  I  have  seen  a  case  of  this  kind. 
The  peritonitis  commenced  with  a  sudden  fall  of  temperature,  while  the  distension  of 
the  abdomen,  the  pain,  the  vomiting,  and  the  hiccough  caused  me  to  give  an  exceedingly 
grave  prognosis ;  but  the  patient  fortunately  recovered. 

In  these  cases  some  authors  maintain  that  the  peritonitis  is  caused  by 
propagation,  and  not  by  perforation.  It  appears  a  'priori,  that  peritonitis 
from  perforation  cannot  be  curable,  and  yet  it  may  if  adhesions  limit  the 


TYPHOID  DISEASES 


16V9 


perforation,  and  lessen  or  destroy  its  noxious  effects, 
kind  have  been  published. 


Positive  cases  of  this 


A  piitiont  of  Biic;quo3''8  with  typhoid  fovor  was  doiiif^  woll,  but  he  was  hardly 
oonvai(>3oont  when  a  relapse  occurred,  and  proved  rapidly  fatal.  At  the  autopsy 
Buc(|ii()y  found,  among  other  lesions,  a  largo  ulcer  at  the  termination  of  the  ileum,  with 
a  perforation  which  was  closed  by  old  adhesions,  and  which  dated  from  the  first 
attack  of  the  fever.  He  adds,  very  justly  :  "  This  is  a  well-marked  case  of  perforation 
causing  circumscribed  peritonitis,  which  had  escaped  notice,  and  which  would  not  have 
liindered  recovery  if  a  relapse  of  the  typhoid  fever  had  not  caused  the  patient's  death. 
Widal  tells  me  that  he  has  seen  a  similar  case  in  which  the  perforation  was  situated  in  the 
caecum ;  the  peritoneum  had  been  protected  by  the  timely  formation  of  adhesions. 


41° 


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-97' 
-96° 


95* 


Fig.  79. — Fall  of  Temperature  due  to  Intestestal  H.smorrhaoe. 

a.  Morning  of  twelfth  day  ;  b,  evening,  5  p.m.,  two  htemorrhages  ;  c,  two  hours  after 
the  second  haemorrhage ;  d,  death  on  sixteenth  day. 


We  must  now  consider  peritonitis  by  propagation,  in  which  case  the 
infective  process  is  supposed  to  traverse  the  ulcerated  but  non-perforated 
intestine.     The  term  "  peritonitis  by  propagation  "  was  coined  by  Trousseau. 

All  authorities  have  since  admitted  peritonitis  by  propagation,  and  they 
consider  it  more  limited,  circumscribed,  and  more  favourable  than  peritonitis 
by  perforation.  It  has  been  described  by  Jaccoud  and  by  Homolle,  who 
have  called  attention  to  Thirial's  monograph.*  Chantemesse  reserves  special 
mention  for  it  in  his  "  Treatise  on  Medicine,"  while  Brouardel  and  Thoinot 
*  Thirial,  Union  Med.,  1853,  Nos.  83,  84,  and  85. 


1680  TEXT-BOOK  OF  MEDICINE 

give  it  a  special  place  in  their  "  Treatise  on  Medicine  and  Therapeutics."  I 
shall  try  to  show  that  this  peritonitis  by  propagation  in  the  form  described 
by  Thirial  and  others  does  not  exist.  The  present  discussion  is  the  resume 
of  the  lectures  I  have  given  in  my  "  Course  of  Pathology  "  and  of  my  com- 
munication to  the  Academic  in  1896. 

I  said  then  that  there  is  no  longer  a  place  for  peritonitis  by  propagation 
as  understood  by  Thirial.  In  the  first  place,  if  the  reader  will  consult 
Thirial' s  monograph  he  will  see  that  in  the  four  cases  which  form  the  basis 
of  this  monograph  it  is  not  possible  to  find  in  any  case  a  process  of  peritonitis 
by  propagation.  The  information  furnished  by  the  autopsies  is  very  in- 
complete ;  we  find  that  four  patients  died  from  acute  peritonitis,  and  that 
peritonitis  supervened  during  convalescence  in  three  who  were  suffering 
from  typhoid  fever.  At  the  autopsy,  says  Thirial,  Peyer's  patches  were 
found  to  be  cicatrized.  I  cannot  therefore  admit  that  the  repaired  intestinal 
lesion  provoked  the  so-caUed  peritonitis  by  propagation.  Moreover,  I 
repeat,  the  process  of  propagation  was  not  found  in  any  of  the  autopsies. 
The  demonstrators  contented  themselves  with  opening  the  intestine  from 
above  downwards,  in  order  to  search  for  the  supposed  perforation,  which 
they  did  not  find ;  they  recognized  with  surprise  that  the  intestinal  lesions 
were  healed,  and  were  content  with  this  somewhat  too  summary  examina- 
tion. My  first  idea  on  reading  these  observations  is  that  the  patients  in 
question  died  from  appendicular  peritonitis.  The  tendency  of  the  peritoneal 
lesions  to  predominate  in  the  right  iliac  fossa  and  in  the  pelvis  leads  to  a 
suspicion  of  typhoid  appendicitis  ;  but  attention  had  not  been  drawn  to 
appendicular  peritonitis  in  Thirial's  time,  and  there  is  no  mention  made  of 
the  appendix  in  the  account  of  the  autopsies. 

I  will  quote  a  case  of  Letulle  in  opposition  to  those  of  Thirial.  A  patient  died  from 
typhoid  peritonitis,  and  the  most  minute  examination  of  the  intestine  revealed  typhoid 
ulcerations,  but  no  perforation.  In  this  case  peritonitis  by  propagation  might  have 
been  suspected,  but  the  anatomical  examination  was  complete,  and  showed  a  perforation 
of  the  appendix  as  the  cause  of  the  peritonitis.  The  lesion  is  thus  described :  "  The 
appendix  shows,  5  centimetres  from  its  tip,  a  perforation  extending  tlirough  the  anterior 
half  of  its  circumference.  After  opening  the  appendix,  the  mucous  membrane  is  seen 
to  be  swollen,  and  presents  two  ulcers  and  one  large  closed  foUicle  which  is  not 
ulcerated."  We  have,  therefore,  a  type  of  the  lesion  which  I  shall  describe  later  aa 
paratyphoid  appendicitis.  I  would  make  the  same  remark  regarding  JVIillard's  very 
interesting  case,  in  which  again  typhoid  peritonitis,  without  perforation,  was  found, 
and  the  intestinal  lesions  were  completely  cicatrized.  Peritonitis  "  by  propagation  " 
might  have  been  suspected,  but  MiUard  discovered,  on  careful  search,  appendicitis 
as  the  cause  of  the  peritoneal  infection  (paratyphoid  appendicitis). 

We  must  therefore  cut  out  "  peritonitis  by  propagation."  And,  more- 
over, if  it  reaUy  existed  many  persons  suffering  from  typhoid  fever  would 
die  of  peritonitis.  Very  often,  indeed,  the  autopsy  in  cases  of  typhoid  fever, 
in  which  death  has  been  due  to  other  causes  than  peritonitis,  shows  the 


TV n loll)  DISKASKS  1081 

intostinal  wall  to  bo  so  thin  in  tho  no.ifi;hl)(»iirlH)<)fl  of  tin-  IVycr's  patrhoa, 
which  are  so  ulcerated  and  transparent  that  we  wonder  how  the  tissue  could 
have  resisted  the  ulcerative  process,  and  how  such  a  fragile  barrier  was 
sufficient  to  prevent  peritonitis.  And  yet  it  does  so.  This  view  of  the 
question  was  well  borne  out  in  the  autopsy  on  a  woman  who  died  from  ataxo- 
adynamic  typhoid,  and  of  whom  I  spoke  above  with  reference  to  the  fall  of 
temperature  following  intestinal  hajraorrhage.  I  pointed  out  to  my  class 
how  excessively  thin  the  wall  of  the  intestine  was  in  the  neighbourhood  of 
several  of  the  ulcerated  Peyer's  patches,  and  yet  no  peritonitis  and  no 
adhesions  were  present. 

I  know  that  two  or  three  well-known  cases  (Chantemesse,  Veron,  and 
Bosquet)  may  be  quoted  in  favour  of  peritonitis  by  propagation,  a  perfora- 
tion being  absent.  What  is  there  to  prove  to  us  that  in  these  cases  the 
peritoneal  infection  came  from  the  bowel  ?  If  the  intestine  had  indeed  been 
the  origin  of  the  peritoneal  infection,  we  should  have  found  in  the  peritoneum 
not  only  Eberth's  bacillus,  but  other  intestinal  microbes,  including  the 
Bacillus  coli.  I  find  it  more  reasonable  to  admit  that  there  may  be  an 
infection  of  the  peritoneum  by  Eberth's  bacillus  independent  of  the  intestinal 
infection,  the  peritoneum  being  invaded  on  its  own  account,  like  the  pleura 
and  the  bones,  without  the  necessity  for  invoking  a  process  of  intestinal 
propagation  which  absolutely  lacks  demonstration.  I  hold,  therefore,  to 
my  opinion  that  peritonitis  by  propagation  such  as  Thirial  described  does 
not  exist. 

The  BaciUiis  typhosus,  like  the  Bacillus  coli,  can  pass  through  the  walls 
of  the  bow^el,  which  is  not  perforated,  only  under  special  conditions.  Thus,  as 
I  have  tried  to  show  under  Appendicitis,  in  order  that  migration  of  certain 
pathogenic  agents  may  take  place  through  the  non-perforated  wall  of  the 
bowel,  it  is  necessary  that  these  pathogenic  agents  be  endowed  with  the 
exalted  virulence  which  they  acquire  in  a  closed  cavity,  but  which  they  do 
not  possess  so  long  as  they  find  a  free  road  through  the  intestinal  track. 
We  can  find  peritonitis  by  propagation,  which  I  would  rather  call  peritonitis 
by  migration,  or  by  emigration,  whenever  a  portion  of  the  intestine  is 
transformed  into  a  closed  cavity.  Appendicular  peritonitis  is  the  typical 
form,  and  is  comparable  to  the  peritonitis  following  strangulated  hernia, 
internal  strangulation,  and  intussusception.  As  this  question  is  discussed 
in  detail  imder  Appendicular  Peritonitis,  I  shall  merely  state  the  following 
conclusion :  From  the  pathogenic  and  anatomo-pathological  point  of  view 
peritonitis  by  propagation,  such  as  has  been  understood  since  Thirial's  time, 
does  not  exist;  but  this  does  not,  of  course,  exclude  the  possibility  of 
adhesions  Avhich  localize  peritonitis  when  the  intestinal  fissure  is  in  process 
of  formation.  When  a  patient  with  enteric  fever  succumbs  with  s)inj)toms 
of  peritonitis  from  perforation,  and  when  no  intestinal  lesion  can  be  dis- 


1682  TEXT-BOOK  OF  MEDICINE 

covered,  careful  search  must  be  made  for  the  existence  of  an  intestinal 
fissure,  which  suffices,  even  though  small,  to  explain  the  pathogenesis  of 
this  peritonitis.  Careful  search  must  be  made  for  peritonitis  consecutive  to  a 
glandular  infection,  or  to  perforation  of  the  gall-bladder,  and  it  is  especially 
necessary  minutely  to  examine  the  appendix,  which  is  the  cause  of  peritoneal 
complications  more  often  than  has  been  previously  supposed. 

Paratyphoid  Appendicitis. — According  to  the  works  I  have  examined 
and  the  cases  I  have  seen,  the  appendix  may  be  affected  by  the  typhoid 
process  in  two  different  ways.  In  the  first  category  I  place  perforation  of  the 
appendix  following  typhoid  ulceration  of  its  walls,  the  process  being  in 
every  way  comparable  to  perforation  of  the  intestine  in  the  Peyer's  patches 
and  in  the  ulcerated  closed  foUicles.  Perforation  of  the  appendix  is  far 
from  being  rare,  since  it  figures  fifteen  times  in  Nacke's  statistics  of  133  cases 
of  intestinal  perforation  in  typhoid  patients,  verified  by  post-mortem 
examination.  Rolleston  has  twice  found  perforation  of  the  appendix  in 
sixty  autopsies  on  cases  of  typhoid  fever.  The  peritoneal  symptoms 
following  perforation  of  the  appendix  differ  in  no  way  from  those  following 
perforation  of  other  parts  of  the  intestine,  either  caecum  or  ileum.  Acute 
or  insidious  peritonitis,  possible  fall  of  temperature  and  hypothermia,  are 
the  same  in  all  these  cases. 

In  the  second  category  of  cases,  which  did  not  appear  to  me  to  have  been 
described  when  I  made  a  communication  to  the  Academic  de  Medecine  in 
1896,  it  is  a  question — and  I  repeat  it  intentionally — not  of  perforation  of  the 
appendix,  comparable  to  perforations  of  the  intestine,  but  it  is  a  question, 
at  least  in  my  opinion,  of  an  appendicitis,  in  the  true  sense  of  the  word, 
which  may  run  its  course  with  or  without  perforation,  and  with  the  various 
kinds  of  toxi-infection  and  all  its  consequences.  I  will  explain  what  I  mean. 
We  have  an  individual  suffering  from  typhoid  fever,  which  has  followed  a 
normal  course,  and  is  entering  on  convalescence.  Suddenly,  with  or  without 
warning,  sharp  pain  is  felt  in  the  right  iliac  fossa,  the  temperature  rises, 
vomiting  comes  on,  the  abdomen  is  distended,  and  as  the  patient  is  conva- 
lescent from  typhoid  fever,  a  diagnosis  of  late  intestinal  perforation  is  made  ; 
peritonitis  by  perforation  is  thought  to  be  present,  and  the  most  gloomy 
prognosis  is  given. 

Two  or  three  days  after  this  event,  which  has  given  rise  to  the  most  acute 
anxiety,  the  symptoms  improve,  and  the  patient  recovers.  In  other  less 
fortunate  cases,  in  spite  of  the  improvement  in  the  initial  symptoms,  the 
temperature  does  not  fall,  the  abdominal  pains  do  not  disappear,  the  beUy 
remains  sensitive  in  the  right  iliac  fossa  at  McBurney's  point,  palpation 
is  very  painful,  the  subjacent  muscles  become  rigid,  deep  matting  of  the 
tissue  becomes  perceptible,  and  in  a  few  days  a  collection  of  pus  forms  in 
the  Ueo-csecal  region.     Lastly,  in  other  cases,  which  are  much  more  f ormid- 


TYPHOri)  DISKARKS  Ui83 

able,  the  peritonitis  is  not  encysted,  but  is  diffuse,  and  remote  complications 
may  occur,  including  pleurisy,  he])atitis,  voniito-negro,  etc. 

Who  will  not  recognize  the  evolution  of  ordinary  appendicitis  in  its 
different  forms  in  the  picture  which  I  have  just  sketched  in  broad  outlines  1 
Will  he  not  find  in  it  the  different  forms  of  appendicular  toxi-infection,  such 
us  I  have  described  in  the  section  on  Appendicitis  ?  Sometimes,  in  typhoid 
appendicitis,  indeed,  the  whole  case  centres  in  an  acute  appendicular 
attack,  without  infection  of  the  peritoneum,  just  as  in  the  ordinary  form  ;  in 
other  cases  the  appendicular  attack  is  followed  by  limited  peritonitis,  or  by 
encysted  abscess ;  lastly,  the  appendicular  attack  is  the  prelude  of  more  or 
less  general  peritonitis,  of  remote  infections  and  of  fatal  toxaemia. 

How  can  we  explain  the  pathogenesis  of  this  appendicitis,  which  I  propose 
to  call  paratyphoid  ?  It  is  the  result  of  the  lesions  of  typhoid  fever,  which 
have  converted  a  portion  of  the  appendicular  canal  into  a  closed  cavity. 
It  may  not  end  in  perforation,  and  yet  all  the  complications  which  arise,  vnih 
or  without  perforation  of  the  appendix,  are  comparable  to  those  which  I 
have  described  in  detail  imder  Appendicitis,  and  therefore  I  shall  not  labour 
the  point  here.  I  think  that  many  cases,  published  under  the  title  of 
peritonitis,  supervening  during  convalescence  from  typhoid  fever,  and  under 
the  heading  of  Peritonitis  by  Propagation,  are  really  cases  of  paratyphoid 
appendicitis.  These  cases,  with  the  peritonitis  which  follows  them,  are  often 
less  formidable  than  those  due  to  perforation  of  the  intestine ;  they  result 
more  surely  in  adhesions  with  circumscribed  abscess  and  in  recovery. 

Do  these  cases  of  paratyphoid  appendicitis,  with  or  without  peritonitis, 
show  signs  distinguishing  them  from  perforative  peritonitis  in  typhoid 
fever  ?  Many  symptoms  are  indeed  common  to  both  these  diseases,  but 
I  shall  nevertheless  try  to  point  out  the  distiactions  between  paratyphoid 
appendicitis  and  perforation  of  the  bowel.  Appendicitis  usually  supervenes 
at  a  time  when  the  convalescent  is  more  able  to  describe  his  feelings,  so  that 
we  can  better  analyze  each  symptom  and  localize  more  clearly  the  seat  of 
the  pain  (McBurney's  point),  while  we  can  also  more  easily  estimate  the 
defensive  rigidity  of  the  subjacent  muscle  and  the  hyperaesthesia  in  this 
region.  Further,  appendicitis  does  not  set  in  with  an  abrupt  fall  of 
temperature,  as  is  the  case  in  most  perforations  ;  it  causes,  on  the  contrary, 
a  rise,  and  the  fever  reappears,  if  it  had  previously  disappeared.  Accord- 
ingly, the  following  symptoms  are  in  favour  of  appendicitis,  and  almost 
certainly  eliminate  the  idea  of  perforation  of  the  bowel,  if  a  patient,  during 
the  decline  or  the  convalescence  of  typhoid  fever,  is  seized  with  pain  limited 
to  the  appendicular  region,  and  at  the  same  time  with  nausea,  vomiting, 
fever,  and  high  temperature.     Examples  : 

In  June,  1896,  I  was  called  to  see  a  young  lady,  with  Bucquoy  and  Leval.  She  had 
fallen  ill  four  weeks  before  with  a  fairly  severe  attack  of  typhoid  fever.     In  the  early 


1684  TEXT-BOOK  OF  MEDICINE 

days  of  convalescence  she  experienced  sharp  pain  in  the  right  ihac  fossa,  and  symptoms 
simulating  perforation  of  the  bowel.  A  period  of  calm'  then  appeared,  but  the  improve- 
ment was  only  apparent ;  the  belly  remained  distended,  sharp  pains  reappeared,  with 
violent  crises  in  the  region  of  the  caecum  and  appendix,  and  the  pulse  was  much 
quickened-  We  found  on  examining  the  temperature  chart  that  these  symptoms  had 
coincided  with  an  attack  of  fever.  This  symptom -complex  allowed  us  to  state  that 
the  patient  had  had,  not  perforation  of  the  beUy,  but  paratyphoid  appendicitis.  More- 
over, Routier,  who  also  saw  the  patient,  was  of  the  same  opinion.  A  collection  of  pus  in 
the  neighbourhood  of  the  caecum  was  opened  by  Routier,  and  the  patient  recovered. 

My  colleague  Hue,  of  Rouen,  has  told  m.e  that  he  operated  upon  a  patient  who, 
during  the  decline  of  typhoid  fever,  was  seized  with  sharp  pain  in  the  right  ihac  fossa, 
and  peritoneal  symptoms  resembling  those  of  intestinal  perforation.  This  comphcation 
had  been  accompanied  with  fever,  and  had  finally  resulted  in  a  peritoneal  abscess  in  the 
caeco-appendicular  region,  which  was  operated  upon  and  followed  by  recovery.  The 
case  was  one  of  paratyphoid  appendicitis.  With  Thomas  I  saw  a  gentleman,  fifty 
years  of  age,  who  had  just  had  an  attack  of  acute  appendicitis  ;  he  had  not  consulted  his 
physician.  He  suspected  appendicitis  himself,  and  told  us  that  he  had  had  a  similar 
attack  some  years  before  during  the  decline  of  typhoid  fever.  These  cases  prove  therefore 
that  typhoid  appendicitis  may  later  be  the  origin  of  fresh  appendicular  attacks. 

The  case  which  ]VIillard,  in  1876,  brought  before  the  Societe  Medicale  des  H6pitaux 
was  only  one  of  paratyphoid  appendicitis. 

Zuber  saw  paratyphoid  appendicitis  in  a  child  suflFering  from  severe  typhoid  fever, 
which  had  run  a  normal  course.  After  some  days  oi  apyrexia,  appendicitis,  followed  by 
fatal  general  peritonitis,  appeared  four  weeks  after  the  onset  of  the  enteric  fever. 

Alexandroflf,  of  Moscow,  quotes  an  analogous  case  in  a  child  nine  and  a  half  years 
of  age,  in  whom  the  peritonitis  supervened  nearly  six  weeks  after  the  onset  of  the 
enteric  fever.  * 

I  have  said  that  paratyphoid  appendicitis  may  cause  a  rmmber  of  com- 
plications ;   it  may  also  be  the  origin  of  abscess  of  the  liver.     Examples  : 

A  young  man  suffering  from  typhoid  fever  was  taken  ill  during  convalescence, 
and  after  several  days  of  apyrexia,  with  a  severe  return  of  the  fever.  The  temperature 
rose  to  104°  F.,  the  abdomen  became  distended,  and  pain  was  present,  especially  in  the 
right  hypochondriac  region.  From  this  moment  general  infection,  with  peritonitis, 
set  in,  and  the  patient  died.  At  the  autopsy,  peritonitis,  especially  well  marked  in  the 
neighbourhood  of  the  caecum,  was  discovered,  and  about  a  dozen  abscesses,  varying  in 
size  from  an  egg  to  a  tangerine  orange.  Small  abscesses  of  the  areolar  type  were 
found  in  the  enlarged  hver.  In  order  to  explain  the  peritonitis  we  could  not  hold 
the  intestinal  lesions  guilty,  for  all  the  ulcers  were  cicatrized,  or  in  process  of  cicatriza- 
tion, and  it  was  one  of  those  cases  which  formerly  would  have  been  labelled  "  peritonitis 
by  propagation."  But  here  appendicitis  was  present ;  the  appendix  was  adherent  to  the 
caecum,  and  contained  a  longitudinal  ulcer.  These  appendicular  lesions  had  been  the 
origin,  and  were  stiU  evidence  of  the  pathological  process  which  had  ended  on  the  one 
hand  in  peritonitis,  and  on  the  other  in  suppurative  hepatitis. 

Osier  relates  the  case  of  a  man  who,  after  convalescence  from  typhoid  fever,  suc- 
cumbed to  acute  peritonitis  and  piunilent  infection  of  the  hver.  At  the  autopsy  scars, 
due  to  typhoid  ulcers,  were  found  in  the  ileum.  The  fatal  compHcations  were  due  to 
paratyphoid  appendicitis,  with  toxi-infection,  which  had  caused  peritonitis  and  phlebitis 
of  the  portal  vein,  with  multiple  abscesses  in  the  hver. 

Boialloche  has  reported  the  following  case  :  A  child  convalescent  from  typhoid 
fever,  and  prai3tically  cured,  was  taken  iU,  with  a  temperature  of  103°  F.  and  pain  in 
the  right  iliac  fossa  (this  marked  the  appearance  of  paratyphoid  appendicitis).  Ice- 
bags  were  apphed  to  the  painful  region,  and  the  pain  improved,  but  the  general  con- 


l'^  I'IKHl)  DISKASKS  1685 

ditioii  luxvimc  «i>rrt«< ;  the  intermittent  character  of  tim  fever,  1  he  pnifiiKo  sweating,  tho 
oartliy  tint,  and  the  r,i|)ifl  wasting  pointed  to  a  foyuH  of  Huppiiriitjon.  Tho  littlo  putiont 
diod  iti  a  state  of  eollupwe.  At  tho  autopsy  tho  hver  wan  found  to  ho  enormoiiHly 
enlarged,  and  cniinnied  with  alweessos  of  ovory  sizo.  rjIcorH  in  proeesH  of  cicatrization 
wore  visible  in  tlie  ileum.  Paratyphoid  a[)pcndicitis,  therefore,  had  been  tho  cause  of 
tho  trouble.  The  infection  from  the  appendi.x  had  spared  tho  peritoneum,  but  had 
been  carried  to  the  hver  by  tho  portal  vein  ;  it  was  a  typical  case  of  appendicular  Liver. 
Bacteriological  examination  of  tho  pus  revealed  the  existence  of  anaerobic  microbes. 

Perroiie  has  published  three  cases  of  paratyphoid  appendicitis  which 
were  operated  upon.  The  histological  and  bacteriological  examinations 
proved  that  the  term  "  paratyphoid  "  is  absolutely  applicable  to  this  form 
of  appendicitis  ;  it  supervenes  in  connection  with  typhoid  fever,  but  the 
appendicular  infection  is  not  due  to  Eberth's  bacillus. 

I  may  now  state  the  follomng  conclusions : 

1.  Peritonitis  by  perforation  usually  supervenes  during  the  stationary 
stage  or  during  relapses  in  typhoid  fever.  The  perforation  may  affect  the 
ileum,  c£ecum,  appendix,  or  colon.  These  cases  are  seen  not  only  in  severe 
typhoid  fever,  but  also  in  the  slight  forms.  The  symptoms  which  usher  in 
peritonitis  from  perforation  may  be  insidious  or  violent ;  whatever  the 
severity  may  be,  the  sudden  fall  of  temperature,  which  goes  as  far  as  hypo- 
thermia, is  often,  but  not  always,  a  valuable  sign.  This  form  of  peritonitis 
is  exceedingly  grave,  and  yet  it  may  be  checked  at  its  commencement  by 
adhesions  which  limit  the  perforation. 

2.  Paratyphoid  appendicitis  usually  supervenes  during  the  decline  or 
the  convalescence  of  typhoid  fever.  It  is  generally  accompanied  by  an 
elevation  of  temperature  ;  it  runs  its  course  like  a  commonplace  appendicitis  ; 
the  toxi-infectious  process  may  be  limited  in  its  action  to  the  simple  appen- 
dicular attack  without  peritonitis,  or  may  result  in  all  the  complications  of 
appendicitis — peritonitis,  abscess  of  the  liver,  etc. 

3.  The  so-called  peritonitis  by  propagation,  as  Thirial  understood  it, 
does  not  exist. 

Let  us  next  consider  the  treatment  to  be  employed  for  peritonitis  in 
typhoid  fever.  This  treatment  is  medical  and  surgical.  The  former  consists 
in  limiting,  as  far  as  possible,  the  movements  of  the  intestine  in  order  to 
lessen  or  to  prevent  the  passage  of  septic  material  into  the  peritonetmi,  and 
to  favour  the  formation  of  adhesions.  For  this  purpose  all  food  and  drink 
are  stopped.  The  patient  is  allowed  to  suck  small  pieces  of  ice,  and  every 
hour  a  pill  of  ^  grain  of  extract  of  opium  is  administered.  Injections  of 
morphia  may  be  given  if  necessary,  while  ice-bags,  suspended  from  a  hook 
to  avoid  the  weight  upon  the  abdomen,  are  applied,  or  the  belly  may  be 
covered  with  cold  compresses. 

Medical  measures  are,  however,  often  powerless,  and  the  important 
question  of  surgical  intervention  then  requires  consideration.  Is  it  necessary 
n.  107 


1686  TEXT-BOOK  OF  MEDICINE 

to  operate,,  and  at  what  time  should  intervention  be  made  ?  This  inter- 
vention takes  place  nnder  such  unfavourable  conditions — the  operator  finds 
the  intestine  so  damaged,  the  patient  himself  is  in  a  very  bad  condition  to 
stand  an  operation  and  its  results — that  at  first  sight  the  proposed  operation 
seems  rash,  to  say  the  least.  In  my  opinion,  the  question  must  be  con- 
sidered in  a  slightly  different  manner  to  that  in  which  it  has  been  previously 
looked  upon.  In  future  we  must  not  include  aU  cases  of  tvphoid  peritonitis 
in  the  same  category,  but  distinguish  as  far  as  possible  paratyphoid  appendi- 
citis from  peritonitis  by  perforation.  In  the  case  of  paratyphoid  infection, 
the  operation  is  indicated  for  the  reasons  set  forth  under  Appendicitis.  It 
is  not  enough  to  operate  ;  the  operation  must  be  performed  before  the  toxi- 
infection  has  had  time  to  complete  its  work.  The  examples  which  I  have 
quoted  show  once  more  that  in  appendicitis  speedy  operation  may  be  the 
only  means  of  saving  the  patient  from  fatal  complications.  The  patient 
whom  I  saw  with  Bucquoy,  and  upon  whom  Eoutier  operated,  recovered, 
as  did  Hue's  patient.  Letulle's  patient,  with  general  peritonitis,  would 
probably  have  recovered  if  he  had  been  operated  upon ;  and  the  patients 
quoted  by  Lannois,  Osier,  and  Boulloche  would  not  have  succumbed  to 
hepatic  compHcations  i£  the  indications  had  suggested  in  time  an  operation 
for  paratyphoid  appendicitis.  The  operation  for  appendicular  peritonitis 
ia  enteric  fever  is  much  simplified  by  the  fact  that  the  operator  has  not  to 
suture  an  ulcerated  and  perforated  bowel,  and  that  the  whole  lesion  is 
confined  to  the  appendix. 

If  the  problem  appears  to  me  easy  of  solution  in  the  case  of  paratyphoid 
appendicitis,  it  is  very  different  in  that  of  typhoid  peritonitis  from  intestinal 
perforation.  First,  is  it  quite  clear  that  there  is  a  perforation  ?  The 
svmptoms  of  peritonitis  are  sometimes  so  slight  and  so  vague  that  the 
diagnosis  would  remain,  doubtful  were  it  not  for  the  sudden  drop  in  the 
temperature.  On  the  other  hand,  if  we  wait  a  day  or  two  before  coming 
to  a  decision,  we  deprive  the  patient  of  the  few  chances  of  safety  remaining 
to  him. 

"We  can  only  form  an  opinion  as  to  the  value  of  surgical  intervention 
by  examining  the  cases  published  on  this  subject.  Unfortunately,  these 
observations  are  often  incomplete.  They  include  dissimilar  cases,  and  the 
diagnosis  is  not  always  irreproachable.  The  first  table  of  statistics  has 
been  published  by  Louis,  a  second  one  by  Lejars,  who  has  collected  twenty- 
five  cases  of  laparotomy,  with  six  recoveries,  of  which  three  at  least  did  not 
appear  to  afford  material  for  discussion.  These  results,  says  he,  are  not 
brilliant,  but  yet  they  are  not  of  such  a  nature  as  to  discourage  surgical 
intervention.  I  have  reread  these  cases  one  by  one,  and,  I  repeat,  most  of 
them  are  too  incomplete  to  permit  of  a  definite  opinion  being  formed.  We 
shall  see  later  the  results  obtained  in  other  statistics. 


TYPimil)  DISKASKS 


16«7 


The  following  case  was  imdcr  my  care  : 

A  man  sufforing  from  typhoid  fever  of  a  somowhat  adynamic  chjiractor  cumo  uiidiji- 
my  care  at  tho  Nockor  Hospital  about  the  twelfth  day  of  the  diaoaso.  On  the  fifteenth 
tlay  he  complained  of  general  abdominal  pain,  without  other  symptoms,  and  tho 
temperature  fell  eudili'nly.  It  rose  again  momentarily,  and  next  day  became  subnormal, 
as  may  be  seen  from  the  accompanying  chart.  Although  tho  abdominal  pain  hafl 
almost  disapiK>ared  luid  the  abdomen  was  but  little  distended,  and  in  spite  of  the 
absence  of  vomiting,  tho  hypothermia  and  hiccough  which  wore  also  present  appeared 
to  me  sufficient  for  a  diagnosis  of  intestinal  perforation,  and  I  decided  upon  an  operation, 
which  was  performed  the  same  morning  by  Routier. 


10  i>' 


105' 


I    

100'  t 

99' 

98" 

97° 

96° 

95° 

Fig.  80. — Tjemperature  Chakt  of  a  Case  of  Intestinal  Perforation 
followed  by  laparotomy. 

o,  Intestmal  perforation  and  subnormal  fall  of  temperature :  the  perforation  had, 
perhaps,  commenced  on  the  previous  evening,  and  appeared  to  take  place  about 
the  fifteenth  day  ;  b,  laparotomy. 

We  found  peritonitis,  with  a  few  spoonfuls  of  faecal  fluid  in  the  peritoneum.  The 
perforation,  of  the  size  of  a  small  lentil,  was  situated  at  the  end  of  the  ileum,  2  inches 
above  the  caecum.  The  intestine  was  sutured  in  two  layers,  so  as  to  form  a  prominent 
longitudinal  fold  projecting  into  the  lumen.  The  peritoneum  was  dusted  with  iodoform. 
A  large  wick  of  iodoform  gauze  was  left  for  drainage. 

In  the  evening  the  condition  had  improved :  the  pulse  was  of  better  quahty,  tho 
hiccough  had  not  reappeared,  and  the  temperature  rose  to  nearly  normal ;  but  during 
the  next  three  days  the  pulse  became  quick  and  small,  and  the  patient  was  very  restless 
and  deUrious.  These  phenomena,  in  the  absence  of  any  peritoneal  symptoms  (pain, 
vomiting,  and  hiccough),  were  considered  as  due  to  iodoform- poisoning  rather  than  to  a 
return  of  peritonitis.  The  dressing  was  soiled  with  pus,  which  flowed  out  in  fairly- 
large  amount.     The  restlessness  soon  became  less,  the  patient  looked  better,  the  pulse 

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1688  TEXT-BOOK  OF  MEDICINE 

improved,  and  the  situation  was  markedly  satisfactory,  in  spite  of  the  elevation  of 
temperature,  and  I  thought  for  a  time  that  the  patient  was  saved.  The  general  con- 
dition, however,  became  worse,  and,  although  the  abdominal  wound  improved  daily 
and  the  peritoneal  sjTnptoms  did  not  reappear,  the  patient  fell  into  a  condition  of 
collapse,  and,  in  spite  of  all  our  efforts,  died  ten  days  after  the  operation. 

At  the  autopsy  we  found  recent  peritonitis,  with  pus  and  faecal  fluid  in  the  right 
iliac  fossa,  and  we  thought  at  first  that  a  tear  had  taken  place  in  the  sutured  bowel. 
This  was  not  the  case,  and  an  examination  of  the  intestine  showed  that  the  sutured 
perforation  had  quite  healed ;  but,  unfortunately,  two  fresh  perforations  had  taken  place 
near  the  first,  the  one  as  large  as  a  pin's  head  and  the  other  considerably  larger.  The 
remainder  of  the  intestine  showed  the  characteristic  lesions  of  typhoid  fever.  I  am 
convinced  that  the  operation  would  have  cured  this  patient  if  two  new  perforations  had 
not  occurred.  We  know,  moreover,  that  it  is  not  rare  to  find  post  mortem  two,  three, 
or  even  a  much  larger  number  of  perforations,  which  take  place  simultaneously  or 
successively. 

What  are  we  to  conclude  from  this  discussion  on  peritonitis  by  perfora- 
tion and  paratyphoid  appendicitis  ?  It  establishes  the  fact  that  an  opera- 
tion is  clearly  indicated  in  the  case  of  paratyphoid  appendicitis,  and  that  it 
gives  some  chance  of  recovery  in  peritonitis  by  perforation.  In  spite  of  the 
intestinal  ulcerations,  suture  of  the  intestine,  when  properly  done,  ends  in 
cicatrization  of  the  perforation,  and  surgical  intervention  is  then  justified. 

I  give  here  the  latest  statistics  published  on  this  important  question. 
John  Finney's  figures  :  13  recoveries  in  47  cases  of  intestinal  perforations 
which  were  operated  upon  ;  Mauger's  figures  :  25  cures  in  107  cases.  Harvey 
Gushing  has  very  kindly  brought  to  my  notice  the  results  at  the  Johns 
Hopkins  Hospital,  where  5  recoveries  resulted  in  11  cases  of  perforation. 

Biliary  Apparatus — Liver. — The  intestinal  lesions  of  typhoid  fever  may 
allow  the  microbes  in  the  bowel  (coli  bacillus,  streptococci,  and  Eberth's 
bacillus)  to  pass  into  the  bile-ducts,  and  to  produce  angiocholitis,  chole- 
cystitis, and  hepatitis. 

Cholecystitis. — The  inflammation  of  the  gall-bladder  may  be  slight  or 
severe,  catarrhal,  muco-purulent,  purulent,  ulcerative,  or  perforating. 
Ulcerative  cholecystitis  is  often  associated  with  angiocholitis  of  the  cystic 
duct,  which  may  cause  obliteration  of  the  canal.  Typhoid  cholecystitis  is 
often  latent  in  its  evolution,  and  is  found  unexpectedly  at  the  autopsy.  In 
fourteen  cases  after  post-mortem  examination  reported  by  Hagenmiiller  the 
cholecystitis  had  on  eleven  occasions  caused  no  symptoms.  Pain,  swelling, 
and  jaundice  are  sometimes  noticed. 

The  acute  process  often  seems  to  become  extinct,  and  suppurative  or 
non- suppurative  cholecystitis  only  appears  several  months  after  the  typhoid 
fever.     I  wiU  quote  some  examples  : 

In  Gilbert  and  Girode's  case  a  patient  suffered  from  typhoid  fever  and  s5Tnptom3 
of  cholecystitis,  but  the  pain  and  swelling  soon  improved,  as  though  the  cholecystitis 
were  cured ;  they  appeared,  however,  five  months  later.  The  operation,  performed  by 
Terrier,  who  thought  the  cholecystitis  was  due  to  a  calculus,  showed  that  the  inflam- 


TYPIinli)  I ) [SEAS I' S  1G89 

tnation  of  tlic  ;^.ill  I>ln,(l(lcr'  was  diiu  l(j  Eboith'H  iKicilliiH.  In  ("ullii  r's  fano  a  yoiinK 
wiitiiiiii  aiilT(>n'(l  fioin  I yplioid  I'ovnr  and  from  Byiuploiiirt  of  cliulocystitiH,  from  wliicli 
slu*  :ocovor((d.  .Si>nm  dayH  lalnr  t  lio  syiiqitoiiiH  of  uciito  cliolfH^yHtitis  retipiXiarod  ;  an 
ojmration  was  [HMfoiinod,  and  calciilouH  nori-Hiip|)iiiati vo  cliolocy.stitia  was  ffjund.  TIki 
Itaotoriological  (examination  lovialcd  tlm  presc^nco  of  tlio  liacillnH  lyplinsus  and  of  IIk! 
li.  cult.  DupriVs  cast)  is  that  of  a  woman  siilTdririg  from  hovoio  ty[)lioid  fever,  with 
recovery.  She  sulTerod  four  montlis  hiter  from  attacks  of  hopatic  coH(;,  which  recurred 
on  several  occasions,  Avith  persistent  decoloration  of  the  fnecal  matter,  fever,  symptoms 
of  obstruction  and  of  biliary  infection.  An  opt^ration  was  decided  on  by  Letulle,  and 
jK'rformod  by  Monod.  TIk;  gall-bladder  contained  a  calculus,  but  no  pus  was  present. 
The  bacteriological  examination  gave  pure  cultures  of  Eborth's  bacillus. 

Typhoid  cholecystitis  is  fairly  often  accompamed  by  perforation,  which 
causes  circumscribed  or  general  peritonitis.  I  have  seen  a  case  of  this  kind 
which  ended  fatally,  and  several  analogous  cases  have  been  reported. 

Liver. — The  hepatic  complications  are  rarely  well  marked,  except  in  the 
case  of  jaundice  or  of  pyaemia  (suppurative  angiocholiti.s). 

In  some  cases  the  microbes  and  their  toxines  cause  more  or  less  complete 
degeneration  of  the  liver  cells.  The  functional  affection  of  the  liver  diminishes 
the  formation  of  glycogen,  disturbs  the  formation  of  bile,  and  gives  rise  to 
the  presence  of  urobilin  in  the  urine,  a  jaundice  colour  of  the  skin,  and  a 
series  of  symptoms  which  resemble  those  of  icterus  gravis. 

Abscess  of  the  liver  is  a  very  rare  complication  in  typhoid  fever.  Lannois 
gives  Romberg's  statistics  :  hepatic  abscess  once  in  667  autopsies  in  typhoid 
fever.  Dopfer,  in  927  autopsies,  found  abscess  of  the  liver  present  on  ten  occa- 
sions. Lannois  has  seen  only  one  case  in  seventy-one  autopsies,  and  expresses 
surprise  at  its  rarity.  "  It  is  well  calculated,"  says  he,  "  to  astonish  us,  if 
we  think  of  the  direct  venous  connections  between  the  intestine  and  the 
liver,  and  of  the  deep  lesions  of  the  intestinal  wall,  resulting  from  the  ulcera- 
tive process  of  typhoid  fever."  For  my  part,  I  am  less  surprised,  for  I  am 
convinced  that  in  typhoid  fever  in  our  climates  the  abscesses  of  the  liver 
do  not  result  from  the  intestinal  ulcerations,  but  from  typhoid  appendicitis, 
which  is  a  somewhat  rare  complication.  Such  was  the  case  m  the  patients 
of  Lannois,  Osier,  and  Boulloche.  The  infective  process  which  ends  in 
abscess  of  the  liver  (appendicular  liver),  with  or  without  pylephlebitis,  is 
elaborated  in  a  closed  cavity,  just  as  in  ordinary  appendicitis. 

In  addition  to  abscesses  of  the  liver,  which  are  nearly  always  the  result 
of  paratyphoid  appendicitis,  we  may  also  find  hepatic  abscesses  from  other 
sources.  Some  form  part  of  a  purulent  infection,  with  parotiditis,  peri- 
chondritis, and  cutaneous  abscesses,  while  others  are  the  result  of  pyle- 
phlebitis of  ill-known  origin,  as  the  autopsies  on  this  subject  are  incomplete 
or  silent  as  regards  appendicitis.  Let  us  further  take  note  of  hepatic 
abscesses  in  typhoid  fever  in  tropical  climates.  We  may  ask  whether 
dysentery  is  not  associated  with  typhoid  fever  in  this  last  variety. 

Different  bacilli,  including  that  of  Eberth,  may  remain  for  a  long  tinifl 


1690  TEXT-BOOK  OF  MEDICINE 

alive  in  the  gaU-bladder,  but  ia  a  latent  state.  Perhaps  they  give  rise  to 
biliary  calculi — a  question  discussed  under  Biliary  Lithiasis. 

Respiratory  System — Laryngeal  Complications.— Diphtheria  of  the 
larynx  is  excessively  rare  in  typhoid  fever,  but  laryngeal  erosions  and  ulcera- 
tions are,  on  the  other  hand,  so  common  that  Louis  considered  them  as 
almost  constant,  and  Griesinger  has  found  them  in  20  per  cent,  of  fatal 
cases.  This  development  of  ulcers  in.  the  larynx  need  not  surprise  us,  since 
Coyne  has  shown  that  the  mucosa  of  the  larynx  is  formed  of  reticular  tissue 
and  adenoid  follicles,  comparable  in  structure  to  that  of  the  intestinal 
mucous  membrane.  Ulceration  of  the  larynx  appears  in  the  course  of  the 
second  or  third  week.  It  affects  the  epiglottis,  the  aryteno-epiglottic  liga- 
ments, the  neighbourhood  of  the  arytenoid  cartUages,  and  the  posterior 
waU  of  the  larynx — in  short,  everywhere,  except  on  the  vocal  cords — at 
least,  in  its  initial  stage — which  explains  why  it  is  usually  latent  in  its 
progress,  without  vocal  troubles,  and  why  the  patient  recovers  from  ulcera- 
tion of  the  larynx,  as  from  that  of  the  gut.  Sometimes,  however,  the  vocal 
cords  are  invaded,  and  aphonia  results.  At  times  oedema  of  the  larynx 
appears,  and  asphyxia  becomes  imminent. 

The  ulceration  of  the  larynx  may  sometimes  be  subacute.  It  extends 
deeply,  invading  the  perichondrium  and  the  cartilage,  which  it  destroys, 
and  gives  rise  to  suppuration,  abscess,  perforation  of  the  larynx,  oedema 
of  the  glottis,  and  laryngeal  stenosis.  In  some  cases  perichondritis  and 
necrosis  at  once  attack  the  cartUages  of  the  larynx. " 

Perichondritis  nearly  always  ends  in  suppuration  and  detachment  of  the 
subjacent  cartilage,  which,  being  deprived  of  its  nutrient  membrane,  finally 
necroses.  Necrosis  frequently  attacks  the  cricoid  cartilage,  more  rarely  the 
arytenoid,  and  the  thyroid  cartilage  only  in  exceptional  cases.  The  necrosed 
cartUages  form  sequestra,  which  tend  to  be  eliminated.  As  a  result  of  this 
necrotic  process,  abscesses  infiltrate  the  submucosa  and  the  articulations, 
and,  with  their  sequestra,  open  into  the  larynx,  pharynx,  or  on  the  skin. 
This  laryngo-typhus  is  a  very  formidable  complication,  and  although  patients 
escape  oedema  of  the  larynx,  they  are  exposed  either  to  emphysema  fol- 
lowing the  perforation  of  the  larynx,  or  to  the  dire  results  of  stenosis  of  the 
cavities  of  the  larynx. 

Ulceration  of  the  cartUages  of  the  larynx  may  be  compared  to  the  ulcera- 
tion and  perforation  of  the  nasal  septum.  In  Roger's  case  the  perfora- 
tion of  the  septum  was  as  large  as  a  sixpenny-piece.  The  lesion  persisted, 
and  the  patient  had  a  somewhat  nasal  twang.  I  saw  an  analogous  case  in 
a  young  woman  in  whom  the  perforation  of  the  septum  was  as  large  as  a 
smaU  lentU. 

Broncho-Pulmonary  Inflammations. — Bronchial  catarrh  in  typhoid 
fever  is  a  common  and  generally  benign  phenomenon,  but  it  may  be  very 


TYPHOID  DISEASES  1691 

foriniilul)lt\  We  may  also  tind  pulmuiuiry  congestion,  atelectasis,  and 
splt'uiziition,  wliicli  are  very  grave  and  fairly  frequent  lesions,  since  atelec- 
tasis has  been  noticed  thirty-two  times  in  118  autopsies  (Griesinger). 
Lobular  and  pseudo-lobar  pneumonia  chiefly  appear  in  the  last  stage  of  th»' 
disease,  the  rise  of  temperature  and  the  severe  dyspnoea  indicating  the 
imminence  of  the  danger.  In  these  cases  dry-cupping  has  rendered  material 
service. 

Lobar  pneumonia  appears  at  different  stages.  I  have  already  spoken 
of  the  pneimionia  which  may  mark  the  onset  of  typhoid  fever,  and  in  which 
the  prognosis  is  usually  good.  Pneumonia  supervening  during  the  course 
of  the  disease  is  more  frequent.  It  is  insidious,  bastard  in  its  course  and 
symptoms,  and  usually  very  serious. 

These  pulmonary  complications  are  started,  and  in  some  cases  (conges- 
tion, splenization)  consummated,  by  the  Bacillus  typhosus.  Pneumonia  is 
the  result  of  a  parallel  or  associated  infection  due  to  the  pneumococcus.  The 
streptococcus  and  staphylococcus  favour  the  appearance  of  broncho- 
pneumonia. 

Pleurisy  is  much  less  common  than  pneumonia.  It  is  accompanied  by 
fever  and  prostration,  which  are  in  relation  to  its  origin.  Typhoid  pleurisy 
may  remain  sero-fibrinous  throughout,  but  it  is  sometimes  purulent,  and 
often  hsemorrhagic.  The  effusion  may  be  loculated,  being  purulent  in  one 
pocket  and  sero-fibrinous  in  another.  Cultivations  taken  at  different 
intervals  may  be  sterile  or  may  swarm  with  Eberth's  bacilli.  This  inter- 
mittence  in  the  presence  of  the  Bacillus  typhosus  proves  that  apparent 
sterility  of  an  exudate  in  typhoid  fever  does  not  make  it  certain  that  it  is 
not  of  a  typhoid  nature. 

The  frequency  of  pleuro-broncho-pulmonary  inflammations  varies  in 
different  epidemics.  Gangrene  of  the  lung  has  been  seen  in  seven  out  of 
118  autopsies  (Griesinger). 

Tuberculosis. — Tjrphoid  fever  and  tuberculosis  are  not  at  all  antagonistic, 
as  was  formerly  said.  It  is  by  no  means  rare  for  a  tubercular  patient  to  be 
stricken  with  enteric  fever,  and  the  course  of  the  latter  disease  is  in  no  way 
influenced,  but  the  phthisis  imdergoes  a  recrudescence  (Vulpian).  In  some 
cases  tuberculosis  appears  during  convalescence  in  a  patient  who  was  not 
tubercular,  or  who  at  least  showed  no  signs  of  it.  The  patient  appears 
cured  of  typhoid  fever,  but  the  fever  reappears,  and  a  relapse  is  promptly 
suspected,  when  it  is  really  a  question  of  more  or  less  rapidly  progressive 
tuberculosis. 

We  may  in  such  a  case  accuse  contagiousness,  but  most  frequently  we 
find,  on  making  careful  inquiry  as  to  the  cause,  that  the  patient  comes  of 
suspicious  stock.  Tuberculosis  is  sometimes  clearly  marked  in  the  parents, 
or  at  other  times  the  disease  orf  the  father  or  of  the  mother  is  hidden  under 


1692  TEXT-BOOK  OF  MEDICINE 

the  guise  of  haemoptysis,  of  pleurisy,  and  of  chronic  bronchitis,  which  have 
recovered  without  further  complications.  The  disease— or,  at  least,  the 
morbid  predisposition — has,  however,  been  transmitted  to  the  child,  in 
whom  it  has  been  present  in  a  latent  state,  only  waiting  for  a  favourable 
opportunity,  such  as  whooping-cough,  measles,  or  typhoid  fever,  to  offer  to 
the  microbes  a  suitable  culture  medium. 

Cardio-Vascular  System. — Endocarditis  is  exceptional,  but  myocarditis 
is  fairly  common  in  typhoid  fever.  The  change  in  the  heart  muscle  is  often 
shown  by  no  appreciable  symptom,  and  yet,  when  the  lesion  is  sufficiently 
marked,  the  precordial  shock  is  less  forcible.  A  murmur  is  sometimes  dis- 
covered, but  as  this  murmur  is  frequently  modified  by  the  respiratory  move- 
ments and  by  the  position  of  the  patient,  it  is  probable  that  it  is  more  often 
an  extracardiac  bruit,  which  can  give  no  information  as  to  the  state  of  the 
myocardium  (Potain).  The  change  in  the  heart  in  part  explains  the  soft- 
ness and  the  irregularity  of  the  pulse,  and  favours  the  pulmonary  congestion, 
the  coldness  of  the  extremities,  as  weU  as  the  state  of  collapse  which  appears 
at  an  advanced  stage,  and  is  generally  of  evU  omen. 

The  degeneration  of  the  heart  muscle  is  due  to  the  Bacillus  typhosus,  to 
its  products  of  secretion,  to  the  phagocytic  reaction,  and  to  the  secondary 
infections.  It  may  produce  the  symptom-complex  known  as  the  cardiac 
form  of  typhoid  fever.  These  cardiac  troubles,  which  contribute  to  the  fatal 
ending  by  their  progressive  severity,  are  not  the  true  cause  of  sudden  death. 

Experimental  Typhoid  Myocarditis. — Various  opinions  had  been  enun- 
ciated as  to  the  nature  and  pathogenesis  of  fibrosis  of  the  myocardium 
before  the  question  was  experimentally  treated.  We  know  to-day  that  it 
is  the  result  of  an  intoxication  which  is,  as  a  rule,  slow  and  progressive  in 
its  course. 

If  small  and  repeated  doses  of  typhoid  toxine  are  injected  under  the 
skin  of  animals  (guinea-pigs,  rabbits,  and  dogs)  (Chantemesse),  various 
lesions  are  produced,  and  in  particular  the  appearance  in  the  myocardium 
of  spots,  patches,  or  zones  of  fibrosis,  comparable  to  those  of  the  hyper- 
trophied  heart  in  the  cardiac  forms  of  arterio -sclerosis. 

The  survival  of  the  animals  depends  on  the  doses  of  toxine  administered. 
They  may  succumb  in  twenty-four  hours,  or  may  live  for  several  years  with 
cardiac  fibrosis  (Chantemesse).  In  those  which  succumb  rapidly  we  find 
in  the  heart  an  inflammatory  reaction,  characterized  by  slight  leucocytic 
infiltration,  congestion  of  the  vessels,  and  perivascular  oedema  ;  but  the 
chief  lesion  consists  in  acute  degeneration  of  the  muscular  fibre,  which  has 
lost  its  regular  striation,  the  discs  being  blended  together  and  the  fibre 
having  a  "  watered  "  appearance.  The  protoplasmic  zone  around  the  nuclei 
has  undergone  more  or  less  marked  vacuolar  degeneration.  At  certain 
points  the  striation  is  no  longer  recognizable. 


TV  PI K  tin  DISEASES  1093 

Wiieii  tlio  intoxication  has  been  of  lonj^  diinifinfi,  jrn'^nilur  jcitches  of 
librosis  are  seen  in  the  niyocardiuni.  In  the;  human  heart  these  patches  are 
attributed  by  classical  writers  to  the  pn^sence  (jf  adult  connective  tissue. 
Regaud  and  Mollard,  in  their  experiments  with  the  diphtheritic  toxine,  also 
regard  the  zones  of  fibrosis  as  a  neo-formation  of  connective  tissue,  and 
consider  the  lesions  to  be  purely  inHainmatory.  Chantcmesse,  who  has 
experimented  with  typhoid  toxine,  holds  a  different  opinion.  He  considers 
that  the  fibrosis  is  not  formed  of  connective  tissue,  but  results  from  a 
peculiar  hyaline  change  in  the  muscular  tissue,  so  that  the  lesion  is  not 
iuHaiumatory,  but  degenerative.  He  has  been  able  to  follow  step  by  step 
the  process  of  this  change  in  the  hearts  of  animals  who  were  submitted  to 
typhoid  intoxication,  and  survived  from  one  day  to  two  years. 

When  the  intoxication  is  slow  in  its  progress,  we  find  in  the  heart  hyaline 
degeneration  of  the  muscular  fibres  (staining  by  Van  Giessen's  method). 
This  degeneration  first  sho\vs  itself  by  a  modification  in  the  staining  pro- 
perties of  the  fibre,  which  assumes  a  reddish  colour  instead  of  the  yellowish 
tint  of  normal  muscle.  The  nucleus  is  still  recognizable,  although  increased 
in  size.  Later,  the  fibrOlae  which  constitute  the  fibre  swell  up,  and  become 
homogeneous.  They  are  often  separated  from  one  another,  and  are  increased 
in  thickness  and  length.  They  become  tortuous,  and  very  closely  simulate 
small  bundles  of  connective  tissue.  The  contractUe  substance  has  under- 
gone hyaline  degeneration,  while  the  nuclei  preserve  their  vitality  for  quite 
a  long  while. 

According  to  Chantemesse,  this  is  the  chief  cause  of  the  formation  of 
patches  of  fibrosis,  but  he  admits  that  connective  tissue,  newly  formed  by 
organization  of  immigrant  leucocytes,  is  found  in  these  hearts.  The  lesion 
of  experimental  fibrosis  would,  therefore,  consist  in  a  mixture  of  connective 
tissue  of  inflammatory  origin  and  of  hyaline  degeneration  of  the  contractile 
fibre. 

The  change  in  this  variety  of  fibrosis  is  not  localized  to  the  ventricles  ; 
the  degeneration  affects  the  wall  of  the  auricles  with  as  much  severity.  The 
vessels  chiefly  show  the  attack  in  their  tunica  media,  which  becomes  thick 
and  hyaline.  The  change  sometimes  extends  to  the  aorta.  It  is  then 
thickened,  and  shows  zones  of  aortitis,  projecting  into  the  limien  of  the 
vessel.  The  culminating-point  of  these  patches  in  contact  with  the  blood 
is  also  affected  by  hyaline  degeneration. 

The  intracardiac  nerve  fibres  are  most  probably  ajffected,  although  no 
direct  observation  of  this  has  been  obtained.  In  return,  Chantemesse  has 
found  in  the  hearts  of  guinea-pigs  submitted  to  typhoid  intoxication  two 
years  previously  changes  in  the  nerve  cells  of  the  ganglion  in  the  articular 
wall  behind  the  septum.  These  cells  were  less  numerous,  their  volimie  had 
diminished,  and  some  of  them  showed  immigration  of  leucocytes  similar  to 


1694  TEXT-BOOK  OF  MEDICINE 

that  seen  in  the  ganglion  ceUs  of  the  nervous  system  as  the  result  of  microbio 
poisoning  (rabies,  typhoid  fever,  etc.). 

This  last  discovery — namely,  the  change  in  the  intracardiac  nervous 
system — explains  the  pathogenesis  of  the  sudden  crises  of  asystole  in  indi- 
viduals sufiering  from  fibrosis  of  the  myocardium.  In  spite  of  grave  lesions 
of  the  cardiac  muscle,  the  functional  power  of  the  organ  may  be  sufficient 
for  a  long  while,  but  the  resistance  of  the  nervous  system  of  the  heart, 
already  materially  affected,  may  suddenly  yield  under  the  influence  of  a 
poison  upon  the  nerve  cells  (various  intoxications,  fatigue,  moral  shock, 
etc.). 

Arteritis. — In  the  course  or  in  the  convalescence  of  typhoid  fever,  which 
may  have  been  severe  or  benign,  more  or  less  acute  pain  appears  in  the 
foot,  calf,  bend  of  the  knee,  Scarpa's  triangle,  hand,  arm,  or  axilla.  This 
pain  is  not  accompanied  by  oedema,  as  in  phlebitis,  and  sometimes  follows 
the  course  of  the  inflamed  artery.  When  the  artery  is  accessible  to  the  touch 
(dorsalis  pedis,  popliteal,  femoral,  radial,  or  temporal),  we  can  feel  an 
indurated  cord.  The  pulse  disappears,  the  whole  limb  undergoes  a  hard 
swelhng  which  is  not  oedema,  and  the  skin  supplied  by  the  obliterated 
artery  becomes  cold  and  mottled  with  violet  patches.  The  paia  contiaues 
to  be  extremely  acute,  and  if  the  permeability  of  the  vessel  is  not  re-estab- 
lished, dry  gangrene,  of  which  I  quote  examples,  may  result. 

Case  1  (Botirgeois) :  Following  a  slight  attack  of  typhoid  fever,  gangrene  of  the 
right  limb  below  the  knee ;  loss  of  the  leg,  and  recovery.  Case  2  (Patry) :  Dry  gangrene 
of  the  leg  and  moist  gangrene  of  the  thigh ;  crural  artery  found  obhterated  at  the 
autopsy.  Case  3  (Gigon) :  (Edema  and  gangrene  of  the  right  arm ;  at  the  autopsy  a 
clot  was  found  plugging  the  subclavian  artery.  Case  4  (Hayem) :  Dry  gangrene  of  the 
feet  and  of  the  left  leg ;  at  the  autopsy,  clots  in  both  femoral  arteries,  extending  into 
the  aorta ;  endocarditis  and  laminated  clots  in  the  heart. 

These  cases  of  iifective  arteritis  are  due  to  endarteritis  obliterans ; 
fortunately,  typhoid  arteritis  does  not  always  end  in  obliteration  of  the 
vessel,  but  may  occur  as  a  parietal  non- obliterating  arteritis.  Barie,  in  his 
monograph,  reports  ten  cases,  in  which  the  signs  of  arteritis  comprised  pain, 
diminution  in  the  pulse,  more  or  less  marked  swelling  of  the  limb,  and 
coldness  of  the  skin ;  but  the  absence  of  a  hard  cord  and  the  persistence  of 
the  pulse  indicated  that  the  vessel  was  not  completely  obliterated.  Under 
these  conditions  recovery  took  place  without  further  complications. 

Phlebitis. — Phlebitis  in  typhoid  fever  is,  like  arteritis,  a  common 
complication  in  convalescence  from  typhoid  fever.  Phlegmasia  alba  dolens 
affected  the  left  leg  forty-five  times  in  seventy  cases  collected  by  Veillard. 

In  ten  cases  under  my  care  the  phlebitis  affected  the  left  leg.  The 
phlebitis  is  sometimes  bilateral ;  it  may  affect  the  iliac  veins,  the  innominate 
vein,  the  axillary  vein,  the  veins  of  the  arm,  the  cerebral  sinuses,  and  the 


TYPHOTT)  DISEASES  1695 

sacral  veius.  It  is  usually  ushered  in  by  a  rise  of  temperature ;  pain  and 
cedema  occur,  as  iu  phlegmasia  alba  dolens,  but  the  oedematous  skin 
is  sometimes  rosy. 

The  chief  danger  lies  in  the  possibility  of  pulmonary  embolism.  The  large 
emboli  produce  sudden  death  by  syncope  and  by  asphyxia  ;  the  small  emboli 
provoke  infection  of  the  lung,  a  curable  though  grave  condition.  The 
phlebitis  mav  be  followed  by  general  infection  and  septicaemia.  It  appears 
that  phlebitis  obliterans  may  cause  gangrene  of  the  limbs  without  any 
concomitant  arteritis.  Nevertheless,  gangrene  of  the  limbs  in  typhoid  fever 
is  usuallv  the  result  of  arteritis  obliterans  alone,  or  combined  with  phlebitis 
obliterans  ;  the  infection  perhaps  spreads  from  the  artery  to  the  vein. 
These  combinations  (gangrene,  phlebitis,  and  arteritis)  are  nowhere  more 
common  than  in  t^-phoid  fever,  and  I  do  not  know  of  any  disease  showing  a 
greater  predilection  for  the  vascular  system.  The  pathogenesis  of  phlebitis 
in  t\-phoid  is  still  obscure  ;  account  must  be  taken  of  the  dyscrasias  and  of 
secondary  or  specific  infections. 

The  phlebitis  is  followed  by  cedema  and  trophic  troubles,  consisting  of 
permanent  hypertrophy  of  the  muscles  of  the  calf.  In  Burlurcaux's  case 
the  whole  of  the  right  leg  was  hypertrophied ;  oedema  was  absent,  and  the 
hvpertrophy  appeared  to  afiect  the  muscles  and  the  bones.  In  Lesage's  case 
the  hypertrophy  afiected  the  left  leg,  and  the  softness  of  the  muscles  appeared 
to  indicate  an  excess  of  fat  in  the  muscle.  In  Ceme  s  case  the  left  leg  was 
involved ;  the  muscular  power  was  increased,  and  the  examination  of  the 
muscles  appeared  to  indicate  genuine  hypertrophy  of  the  muscle.  Babinski 
has  told  me  of  two  cases  of  persistent  hypertrophy  of  the  left  calf  in  patients 
who  had  previously  sufiered  from  phlebitis  in  the  course  of  typhoid  fever. 
These  trophic  disorders  should  be  looked  for  in  every  case  of  phlebitis.  I 
have  seen  them  in  a  woman  who  had  had  puerperal  phlebitis  four  years 
previously.  Chantemesse  has  employed  a  diet  free  from  salt  in  the  treatment 
of  typhoid  phlebitis. 

Dropsy. — Dropsy  in  typhoid  fever  is  of  mechanical  or  of  dyscrasic 
origin.  The  former  is  the  result  of  phlebitis.  Dropsy  of  dyscrasic  origin  is 
more  frequent  in  certain  countries  and  epidemics.  Although  it  is  very  rare 
in  Paris,  it  has  frequently  been  noted  at  Rouen  (Leudet),  and  in  an  epidemic 
in  Germany  (Griesinger)  25  per  cent,  of  the  patients  were  attacked.  Its 
cause  is  not  known,  but  possibly  some  cases  are  associated  with  the  nephritis 
which  at  times  accompanies  typhoid  fever. 

Genito-Urinary  Organs. — Albuminuria  is  often  the  only  svmptom  of 
typhoid  nephritis,  which,  as  a  rule,  is  not  serious.  The  nephritis  is  some- 
times associated  with  haematuria  ;  the  urine  is  of  a  rosy  or  brownish  colour, 
and  may  contain  clots.  At  the  autopsy  ulcerations  are  found  in  aU  parts 
of  the  urinary  system,  including  the  bladder.     In  some  cases  the  nephritis  is 


1696  TEXT-BOOK  OF  MEDICINE 

so  marked,  and  the  albuminuria  is  so  severe,  and  the  symptoms  are  so 
prominent,  that  the  course  of  the  typhoid  fever  is  altered,  ursemic  symptoms 
being  added  to  those  of  the  original  disease,  and  the  renal  condition  becoming 
a  very  formidable  complication.  In  some  cases  of  typhoid  nephritis  miliary 
abscesses  may  be  present. 

The  nephritis  is  due  either  to  the  Bacillus  typhosus  or  to  toxic  substances. 

Rendu  has  published  the  case  of  a  young  woman  suffering  from  typhoid  fever,  with 
albuminuria,  hyperpyrexia,  and  a  raspberry-like  erythema.  Death  from  uraemia 
supervened  on  the  fifteenth  day  of  the  disease.  The  ordinary  lesions  of  typhoid  fever 
were  found  post  mortem.  In  addition,  the  kidneys  were  congested  with  numerous 
subcortical  ecchymoses.  The  histological  examination  revealed  the  typical  lesions  of 
epithehal  nephritis.  The  interest  of  this  case  hes  in  the  fact  that  Eberth's  baciUi  were 
collected  en  masse  in  the  interior  of  the  tubules. 

The  morbid  process  in  the  kidney  does  not  always  become  completely 
extinct ;  it  may  be  the  starting-point  of  Bright's  disease. 

Orchitis. — Orchitis  may  occur  during  convalescence  in  typhoid  fever. 
I  have  seen  eight  cases,  of  which  one  ended  in  suppuration.  The  orchitis 
shows  itself  by  very  acute  pain  in  the  testis,  or  in  the  groin  along  the  sper- 
matic cord ;  the  testis  becomes  heavy  and  large ;  the  epididymis  is  also 
affected,  and  resolution  does  not  occur  for  two  or  three  weeks.  If  we  study 
these  symptoms  in  the  testis,  which  sometimes  show  an  ephemeral  con- 
gestive character,  and  at  other  times  an  inflammatory  character,  sometimes 
ending  in  suppuration,  we  see  that  the  process  is  analogous  to  that  seen  in 
the  parotid  glands  during  the  decline  of  typhoid  fever. 

Several  characteristics  differentiate  this  orchitis  from  that  of  mumps. 
Thus,  typhoid  orchitis  is  unilateral ;  it  may  suppurate  and  leave  limited 
induration  of  the  organ,  but  it  never  ends  in  atrophy  and  impotence. 
Orchitis  in  mumps  is  more  often  double  ;  it  does  not  suppurate,  and  fairly 
frequently  results  in  atrophy  of  the  testis.  Typhoid  orchitis  is  due  to 
Eberth's  bacillus,  which  has  been  found  in  the  testis,  and  the  suppuration  is 
caused  either  by  this  bacillus  or  by  secondary  infection. 

Oophoritis  and  salpingitis,  mastitis  and  inflammation  of  the  labia  majora, 
have  been  seen  on  several  occasions. 

Pregnancy  is  not  incompatible  with  typhoid  fever.  The  frequency  of 
miscarriages  varies  with  the  duration  of  the  pregnancy  and  the  severity  of 
the  fever.  The  child  succumbs  in  most  cases  of  premature  birth,  but  the 
prognosis  is  less  serious  for  the  mother. 

Infection  of  the  foetus  results  from  the  fact  that  the  Bacillus  typhosus  is 
transmitted  from  the  mother  to  the  foetus  through  the  placenta.  Eberth's 
bacillus  has  been  found  in  the  placenta  (Chantemesse),  and  also  in  the  spleen 
of  the  foetus  (Ernst). 

Nervous  Complications. — We  sometimes  see  during  the  course  of  the 
disease,   or  during  convalescence,   especially  in  patients  predisposed  by 


TVIMInll)  DISIOASKS  1697 

personal  or  hereditary  antecedents,  mental  troubles,  attai^ks  of  acute  mania, 
dolirium  with  ideas  of  persecution,  hallucinations,  and  t<'ndency  to  suicide, 
to  such  an  extent  that  some  patients  have  been  considt-rcd  insjinr*.  These 
attacks  of  mania  last  only  a  few  days  or  weeks. 

vSomctimos  the  delirium  assumes  an  ami)itious  chariictcr,  and  simulates 
general  paralysis.  In  other  patients  stupor  is  the  chief  symptom  ;  the 
expression  is  vacant,  the  eyes  are  half-closed,  and  the  patient  is  in  a  condition 
of  torpor,  which  simulates  idiocy  or  imbecility.  This  condition  may  last 
months  and  years.  In  other  cases  delirium  is  associated  with  symptoms 
of  meningitis,  which  proves  fatal. 

The  s}Tnptoms  of  delirium  in  typhoid  fever  are  sometimes  associated 
with  the  cerebral  lesions,  characterized  by  a  hydrangea  tint  of  the  grey 
matter,  with  capillary  congestion,  with  punctate  haemorrhages,  and  with 
cfidema  of  the  brain  and  ventricles.  Phagocytic  reaction  is  seen  around  the 
nerve  cells  which  are  more  or  less  degenerated,  and  the  BaciUus  typhosus  is 
frequently  found  in  the  brain.  In  some  autopsies  suppurative  meningo- 
encephalitis, with  Eberth's  bacillus,  has  been  found  (Fernet). 

T\'phoid  fever  is  sometimes  followed  by  loss  of  memory,  dullness, 
imbecility,  and  dementia,  which  may  last  for  several  months,  or  even  for 
the  remainder  of  the  patient's  life. 

Aphasia  in  t^'phoid  fever  deserves  close  attention.  It  is  more  common 
in  children  than  in  adults,  both  in  the  severe  and  the  slight  forms  of  typhoid 
fever,  and  in  the  stationary  stage,  or  during  the  onset  of  convalescence. 

WTien  we  read  the  cases  published  on  this  subject,  we  see  that  they  may 
be  di\'ided  into  two  classes.  Aphasia  of  the  first  class  occurs  in  children, 
and  is  nearly  always  a  pure  aphasia,  without  hemiplegia.  The  loss  of  speech 
is  absolute,  but  the  aphasia  is  transitory,  rarely  lasting  more  than  a  week 
or  a  fortnight,  and  disappearing  without  lea\Tng  any  traces.  In  a  chUd 
of  ten  years  of  age  with  typhoid  aphasia,  the  aphasia  partially  disappeared 
after  the  first  cold  bath,  and  definite  recovery  soon  followed.  Whatever  be 
the  explanation  of  this  infantUe  aphasia,  we  can  exclude,  considering  the 
benign  nature  and  the  rapid  disappearance  of  this  complication,  arteritis 
obliterans,  and  any  lesion  of  Broca's  convolution.  The  symptoms  are 
different  in  the  aphasia  of  adults,  and  most  of  the  cases  show  that  it  is 
associated  with  right  hemiplegia,  with  or  without  hemianeesthesia.  The 
aphasia  disappears  very  slowly,  and  the  hemiplegia  is  even  more  persistent. 
In  these  cases  endarteritis  obliterans  of  the  Sylvian  artery  is  present. 

The  spinal  cord  may  be  affected  by  the  t\^hoid  infection,  and  in  some 
cases  rachialgia,  hvperaesthesia  of  the  dorsal  and  nuchal  muscles,  contrac- 
tures, convulsions,  and  oculo-pupillary  troubles  indicate  invasion  of  the 
spinal  meninges.  These  symptoms,  which  constitute  the  spinal  form  of 
some  writers,  are  early  or  late.     When  they  are  associated  with  rachialgia 


1698  TEXT-BOOK  OF  MEDICINE 

and  vomiting,  we  can  hardly  eliminate  the  idea  of  cerebro-spinal  meningitis, 
and  the  diagnosis  is  the  more  difficult  in  that  in  some  cases  observers  have 
found  post  mortem  myelitis  or  cerebro-spinal  meningitis,  which  has  super- 
vened during  the  course  of  the  typhoid  fever.  I  refer  the  reader  for  the 
study  of  this  question  to  the  section  on  Cerebro- Spinal  Meningitis.  Myelitis 
in  typhoid  fever  may  assume  different  types,  including  the  focal,  ascending, 
and  disseminated  forms. 

In  some  cases  contractures  of  the  extremities  have  been  noted.  Tetanus 
has  also  been  seen. 

Paralysis. — Paralytic  troubles  are  rare  during  the  onset  of  typhoid  fever, 
being  especially  seen  in  convalescence.  They  are  sometimes  general,  and 
affect  to  an  equal  degree  the  special  senses,  the  power  of  movement,  and 
sensation  ;  at  other  times  they  occur  in  the  form  of  paraplegia  and  of  hemi- 
plegia (endarteritis  or  embolism  of  the  Sylvian  artery).  They  may  be 
limited  to  a  single  organ  (bladder),  to  the  territory  of  a  single  nerve  branch, 
or  to  a  single  group  of  muscles.  These  different  localizations  show  that  the 
paralyses  result  from  different  causes.  Thus,  those  which  affect  the  para- 
plegic form  are  due  to  changes  in  the  spinal  cord,  while  the  more  limited 
paralyses  of  a  cranial  nerve  or  one  arm  are  due,  on  the  one  hand,  to  peripheral 
neuritis,  and  on  the  other  hand  to  muscular  changes,  which  are  sometimes 
marked  in  typhoid  fever.  Most  of  these  paralyses  are  transitory,  and  end 
in  recovery. 

Eschars — Suppuration. — The  tendency  to  sloughing  is  especially  marked 
in  the  adynamic  forms  of  typhoid  fever.  Bedsores  appear  on  the  sacrum, 
on  the  trochanters,  on  the  occiput  (Chomel),  as  well  as  on  the  surface  of 
blisters  or  in  the  neighbourhood  of  leech-bites.  Gangrene  of  the  mouth, 
vulva,  penis,  face,  ear,  cheek,  and  pupils,  has  been  seen. 

The  sacral  bedsore  may  extend  deeply,  and  affect  the  coverings  of  the 
spinal  cord.  The  gangrenous  ulcerations  of  the  skin  are  at  times  the 
starting-point  of  erysipelas. 

During  convalescence  a  tendency  to  suppuration  shows  itseK  by  a 
succession  of  boils,  and  by  abscesses.  Chauffard  thinks  that  in  some  cases 
the  boils  and  abscesses  are  due  to  the  entrance  of  the  staphylococcus,  which 
is  facilitated  by  the  baths.  The  fact  is  possible,  but  boils  and  abscesses  of 
convalescence  were  seen  before  typhoid  fever  was  treated  by  cold  baths. 

Suppuration  sometimes  appears  in  the  form  of  purulent  effusion  into  the 
joints,  or  into  the  serous  cavities;  of  abscesses  in  the  muscles  (rectus 
abdominis,  psoas) ;  and  of  suppuration  in  the  thyroid  and  parotid  glands. 

Parotiditis. — Parotiditis  may  supervene  in  typhoid  fever,  as  in  the  course 
of  serious  infections.  It  is  somewhat  rare,  but  indicates  a  grave  prognosis. 
Louis  quotes  only  two  examples  in  fifty-nine  cases  of  typhoid  fever,  and 
Bouillaud  has  seen  it  only  five  or  six  times  in  many  hundreds  of  patients. 


TYPHOID  D1SEASI<:S  1699 

On  the  other  hand,  it  appears  that  parotiditis  was  more  frequent  in 
fornuT  epideniios  (Hildenbrand,  Pinel),  while  in  a  recent  epidemic  in  Paris 
(1899-1900),  remarkable  for  the  variotv  of  rfnuplications,  I  saw  one  case  at 
the  Hotel-Dieu. 

Parotiditis  may  appear  in  the  course  of  the  fever,  or  during  convalescence. 
Hippocrates  divided  these  cases  into  critical  and  acritical,  attributing  a 
favourable  influence  to  the  former.  This  division  has  long  dominated  the 
history  of  parotiditis,  but  Trousseau  was  one  of  the  first  to  show  the  error. 
"  What  the  ancients,"  says  he,  "  called  a  crisis  or  a  metastasis  I  call  a  verv 
gloomy  complication.  I  regard  parotiditis  as  a  most  serious  complication." 
Bacteriology  has  classed  parotiditis  among  the  secondary  infections  of 
typhoid  fever.     It  is  only  a  complication. 

The  onset  is  more  or  less  clearly  marked,  and  is  generally  ushered  in  by 
dryness  of  the  mouth.     Such  was  the  mode  of  onset  in  my  patient. 

She  came  under  my  care  for  severe  typhoid  fever,  with  persistent  hiccough,  which 
yielded  to  cold  baths.  The  temperature  had  been  normal  for  four  days,  when  one 
evening  the  thermometer  registered  104°  F.,  but  the  patient  made  no  complaint,  except 
of  dryness  of  the  mouth.  Two  days  later  she  experienced  acute  pain  at  the  angle  of 
the  jaw,  in  front  of  the  tragus,  and  in  the  anterior  process  of  the  parotid  gland.  The 
right  side  of  the  face  was  sUghtly  swollen,  but  there  was  neither  tension  nor  redness  of 
the  skin.  Palpation  was  painful,  and  I  foimd  slight  brawny  swelling  of  the  parotid 
gland,  while  the  lymphatic  gland  in  front  of  the  tragus  was  sUghtly  enlarged.  The 
cheek  was  dry  on  the  right  side,  and  the  gum  red  and  swollen,  especially  opposite  the 
second  upper  molar.  The  orifice  of  Stenson's  duct  projected,  and  seemed  to  open  in  a 
papilla  which  was  larger  than  that  of  the  opposite  side.  Pressure  on  the  gland  caused 
one  or  two  drops  of  sero- purulent  fluid  to  issue  from  the  duct.  Bacteriological  examina- 
tion revealed  the  presence  of  the  Staphylococcus  aureus,  to  the  exclusion  of  Eberth's 
bacillus.  During  the  next  few  days  the  temperature  fell,  the  sweUing  diminished,  the 
pain  disappeared,  and  in  a  week  there  was  no  trace  of  parotiditis. 

Such  is  the  slight  form  of  parotiditis  in  t\^hoid  fever,  and  it  would 
rather  deserve  the  name  of  stensonitis.  In  the  severe  cases  the  symp- 
toms, instead  of  diminishing,  become  worse.  The  pain  in  the  temporo- 
masdllary  articulation  increases.  A  hard  and  painful  nodule,  which  rapidly 
enlarges,  appears  at  some  point  of  the  parotid  region,  most  frequently  near 
the  angle  of  the  jaw.  The  sweUing  may  invade  the  whole  of  one  side  of  the 
face  and  neck,  corresponding  to  the  inflamed  gland.  The  face  becomes 
unrecognizable,  and  the  movements  of  the  jaw  are  almost  impossible.  The 
parotid  tumour  soon  becomes  tense,  painful,  and  tender  on  pressure.  The 
skin  over  it  is  shiny,  red,  or  sometimes  of  a  \aolet  colour,  and  presents  a 
certain  softness,  which  soon  gives  place  to  well-marked  fluctuation.  The 
patient  complains  of  pain  in  the  neck  and  shoulders.  The  opposite  side  is 
sometimes  affected.  The  pulse  is  smaU  and  quick,  the  dyspnoea  is  acute, 
the  mouth  is  dry,  and  the  general  condition  is  very  grave.  Deafness  super- 
venes, and  the  patient  dies  in  an  adynamic  condition. 


1700  TEXT-BOOK  OF  MEDICINE 

At  the  autopsy  Stenson's  duct  and  all  the  excretory  channels  of  the 
gland  are  distended  with  pus.  Their  waU  is  destroyed  in  many  places,  and 
the  bands  of  connective  tissue  separating  the  acini  oppose  but  a  feeble 
obstacle  to  the  ever-increasing  invasion  of  the  suppuration.  The  lesion 
commences  in  the  excretory  duct  of  the  acinus,  and  is  always  due  to  ascend- 
ing infection,  caused  by  the  micro-organisms  of  the  mouth,  and  especially 
by  the  Staphylococcus  aureus  or  by  the  streptococcus.  Eberth's  bacillus  is 
said  to  have  been  found  in  two  cases. 

The  microbes  do  not  normally  enter  Stenson's  duct,  and  the  saliva  is 
sterile.  This  asepsis  is  explained  by  the  direction  of  the  duct,  and  by  the 
fact  that  the  saliva  forms  a  bad  culture  medium  (Sanarelli).  In  typhoid 
fever  the  sordes  on  the  teeth  and  on  the  mucous  membrane  of  the  mouth 
afford  the  organisms  the  favourable  medium.  In  addition,  the  salivary 
secretion  is  notably  diminished,  as  in  all  forms  of  pyrexia.  The  physiological 
equilibrium  is  broken,  and  the  microbes,  no  longer  finding  obstacles,  are 
able  to  pass  along  Stenson's  duct.  My  patient  suffered  from  well-marked 
gingivitis  on  the  right  side  three  days  before  the  first  signs  of  parotiditis. 
It  seems  probable  that  this  gingivitis  may  have  marked  the  first  stage  of 
the  ascending  salivary  infection ;  it  may  have  been  the  immediate  cause 
of  it. 

It  is,  therefore,  necessary  in  infection  of  the  mouth  to  take  prophylactic 
measures  and  to  institute  rigid  antisepsis.  These  antiseptic  measures  are 
sufficient  in  slight  cases,  but  in  the  severe  ones  early  surgical  intervention 
must  be  resorted  to. 

Hsematoma  and  Muscular  Abscesses. — Lesions  of  the  muscles  in  typhoid 
fever  are  various. 

I  had  in  the  Hotel-Dieu  a  patient  suffering  from  suppurating  hsematoma  of 
the  rectus  abdominis.  The  man  was  convalescent  when  fever  reappeared,  and  I  fotmd 
a  somewhat  painful  swelling  in  the  suprapubic  region.  The  skin  was  of  an  ecchymotic 
colour,  and  pressure  gave  blood  crepitus,  due  to  haemorrhage  in  the  rectus  muscle.  On 
the  next  day  the  swelling  and  the  ecchymosis  had  increased,  and  exploratory  puncture 
gave  exit  to  hsemorrhagic  and  purulent  fluid,  in  which  the  Bacillus  typhosus  alone  was 
found.  The  tumour  was  incised,  and  6  ounces  of  purulent  blood-stained  fluid,  enclosed 
in  the  sheath  of  the  muscle,  were  let  out.     The  patient  recovered  some  days  later. 

As  a  general  rule,  the  infection  due  to  Eberth's  bacillus  and  its  toxine 
causes  fatty,  waxy,  and  vacuolar  degeneration  of  the  muscles.  The  degenera- 
tion attacks  the  fibre  itself,  and  limits  its  action  to  the  contractile  substance. 
"  This  change  consists  in  a  modification  of  the  contractile  fibre,  probably 
due  to  coagulation  of  the  myosin.  Complete  loss  of  muscular  elasticity 
results,  and  is  followed  by  very  marked  friability  of  the  muscle  "  (Chante- 
messe).  These  changes  show  themselves  by  ruptures,  hsematomata,  or 
abscesses,  chiefly  found  in  the  rectus  abdominis  and  in  the  adductor  muscles 
of  the  thigh. 


TYPHOID  DISKASKS  1701 

Ruptures  muy  be  painful  or  painless.  Rupturr-  of  the  rectus  abdorninia 
ha-!  Urrii  mistakt'ii  in  some  cases  for  the  onset  of  peritonitis. 

Haeniatonia  of  the  muscle  is  generally  consecutive  to  rupture.  The 
haeinatoma  oiten  remains  in  a  pure  state,  without  purulent  change,  so  that 
the  blood  found  on  incision  is  fluid  or  clotted,  without  any  trace  of  pus. 

Ijctulle  has  given  mo  notes  of  a  case  of  tliis  kind  in  which,  on  the  sixteenth  day  of 
typhoid  fever,  sharp  pain  appeared  in  the  region  of  the  rectus  abdominis  on  the  left  sidr'. 
The  painful  region  was  prominent,  ecchymosis  appeared,  and  haematoma  of  the  muscle 
was  diagnosed.  The  patient  died  of  intestinal  perforation,  and  rupture  and  hematoma 
of  the  muscle  were  found  at  the  autops}'.  The  histological  examination  by  Letulle 
may  be  thus  summed  up  :  Dififuse  haemorrhage  in  the  rectus  abdominis,  separation  of 
the  muscle  fibres  by  masses  of  red  corpuscles  with  interstitial  cedema,  and  infiltration, 
with  innumerable  lymphatic  cells,  for  the  most  part  mononuclear. 

Remy  told  me  of  the  following  case  : 

In  a  young  man  suffering  from  a  relapse  in  typhoid  fever  a  haematoma  appeared, 
occupying  the  whole  of  the  thigh,  from  the  knee  to  Scarpa's  triangle  ;  the  skin  was  of  a 
violet  colour.  The  swelhng  appeared  a  few  minutes  after  a  strain,  and  cure  was 
obtained  by  pressure,  without  incision.  Boisson  and  Simonin  published  a  case  of 
haematoma,  mthout  suppuration,  in  the  course  of  typhoid  fever. 

The  haematoma  often  suppurates,  as  in  my  case,  to  which  I  may  add 
other  examples.     Tollemer  communicated  the  following  case  to  me  : 

A  patient  with  typhoid  fever,  under  Brissaud's  care,  raised  himself  and  separated 
his  legs  in  order  to  sit  down  on  the  stool,  when  he  experienced  a  sharp  pain  on  the  inside 
of  the  left  thigh.  On  the  next  day  swelling  appeared,with  great  pain  and  ecchymosis  of 
the  skin.  The  brawny  induration  became  fluctuating,  and  incision  gave  exit  to  hemor- 
rhagic and  pumlent  fluid,  and  brought  about  recovery  of  the  lesion. 

In  some  cases  the  suppuration  invades  the  muscle  from  the  first,  without 
previous  haematoma.  On  closer  inspection,  however,  we  see  that  a  small 
quantity  of  blood  is  present  in  addition  to  the  pus. 

Lastly,  the  muscle  may  become  gangrenous  (Millard). 

These  muscular  lesions — rupture,  pure  haematoma,  suppurating  haematoma , 
or  suppuration  without  haematoma — are  sometimes  more  or  less  painful  at 
first,  and  are  then  followed  by  brawny  induration,  ecchymoses,  and  fluctua- 
tion. These  various  forms  may  be  due  to  Eberth's  bacillus,  without  other 
microbes,  or  to  streptococci  and  staphylococci.  Surgical  intervention  is 
almost  always  indicated. 

Osseous  Lesions. — Many  osseous  and  articular  lesions  may  be  seen  during 
convalescence  from  typhoid  fever — rapid  growth  of  the  bones,  rheumatic 
pains,  fixed  pain  in  the  tibia  or  the  femur,  swelling  of  the  bones  and  joints, 
deformity  of  the  long  bones,  hypertrophy  of  the  epiphyses,  exostoses,  acute 
osteomyelitis  and  suppurative  periostitis,  chronic  osteomyelitis  and  peri- 
ostitis. 

In  the  first  place,  it  is  certain  that  in  mankind,  as  in  experimental 
animals,  the  bone-marrow  is,  next  to  the  spleen,  the  seat  of  election  of  the 

11.  108 


1702  TEXT-BOOK  OF  MEDICINE 

Bacillits  typhosus  (Wyssokowitch,  Chantemesse,  and  Widal),  which  causes 
more  often  than  any  other  microbe  disease  of  the  marrow  in  typhoid  fever. 
If  pure  cultures  of  Eberth's  bacUlus  are  injected  into  the  blood  of  rabbits, 
the  microbe  is  found  most  often  ia  the  bone-marrow  and  the  spleen,  although 
observation  has  long  since  proved  that  children  and  adolescents,  when  con- 
valescent from  typhoid  fever,  show  exaggerated  growth  of  the  limbs,  proving 
rapid  increase  in  the  length  of  the  bones.  It  is  certain,  therefore,  that  the 
typhoid  infection  causes  hyperactivity  of  growth  in  the  bones,  and  especially 
in  those  which  are  in  process  of  growth.  This  hyperactivity  is  shown 
anatomically  by  increased  proliferation  of  the  bone-marrow  and  of  the  sub- 
periosteal layers.  The  bone-marrow  and  the  periosteum  are  equally 
infected  by  the  Bacillus  typhosus,  but  the  lesion  (osteomyelitis)  appears 
to  commence  in  the  marrow,  and  spreads  thence  to  the  periosteum.  Ac- 
cordingly, we  see  osteomyelitis  and  osteoperiostitis,  but  the  former  is 
sometimes  the  more  important  lesion. 

The  bone  infections  generally  take  place  during  convalescence,  or  some 
time  after  recovery  from  typhoid  fever.  They  are  especially  frequent  in 
children  and  youths^  in  whom  the  skeleton  has  not  reached  its  full  develop- 
ment.    They  assume  the  following  forms  : 

A  rheumatoid  form  has  been  described  by  Dehu.  In  this  form  the 
infective  process  is  not  localized,  but  causes  pain  in  the  limbs  and  joints 
which  are  like  the  so-called  "  growing  pains."  Pressure  on  the  bones  and 
joints  is  painful.  Walking  and  standing  rapidly  induce  fatigue.  The  con- 
dition lasts  some  weeks,  and  is  accompanied  by  rapid  increase  in  stature. 

In  other  cases  the  infective  process  may  be  localized  to  the  tibia,  to  the 
femur,  to  the  bones  of  the  arm,  to  the  sternum,  or  to  the  ribs,  in  the  form  of 
acute  osteomyelitis  or  osteoperiostitis.  The  first  symptoms  are  pain  and 
fever,  and  the  patient  complains  of  a  painful  spot,  which  is  at  first  very 
limited.  The  least  pressure  on  the  diseased  bone  sometimes  causes  most 
acute  pain,  which  is  increased  by  movement.  The  pain  is  continuous  or 
paroxysmal,  and  more  marked  at  night.  This  acute  febrile  period,  however, 
with  or  without  rigors,  does  not  always  end  in  suppuration.  The  skin  in  the 
painful  region  is  somewhat  oedematous,  but  shows  no  change  in  colour. 
Palpation  reveals  a  swelling  of  the  bone,  over  which  the  skin  sHdes  freely. 
The  pain  and  swelling  disappear,  and  recovery  results  after  a  period  which 
is  sometimes  very  long.     Relapses  may  occur. 

I  had  under  my  care  a  case  of  osteomyelitis  of  the  ribs.  The  patient  was  a  young 
man,  eighteen  years  of  age,  who  was  convalescent  from  severe  typhoid  fever.  Acuto 
pain  ia  the  right  side  came  on  a  fortnight  after  defervescence ;  it  was  exactly  localized 
to  the  seventh  rib,  2  iaches  from  the  chondro-vertebral  joint.  No  swelling  was  present 
at  this  spot.  I  made  a  diagnosis  of  commencing  osteomyelitis,  and,  in  fact,  sweUing 
and  paia  made  their  appearance  in  a  few  days  ;  there  was  no  rise  of  temperature.  Slight 
fluctuation  was  thought  to  be  felt  on  the  sixteenth  day,  but  the  process  remained 


TYPHOID  DISEASES  1703 

Blalionary,  resolution  luok  place,  aiicl  at  the  oiid  of  a  rnoiil  h  the  patient  was  diHchurged 
with  a  small  painloHs  oxoHtoHis.  Tho  oostal  localization  of  this  ostoomyolitis  waa 
intorostiug,  for  it  corresponded  with  tho  centre  of  ossification  for  the  tuberosity  which 
appears  at  tho  eighteenth  year. 

When  osteoperiostitis  ends  in  suppuration,  the  pain  is  very  severe,  the 
oedema  of  the  afEected  region  increases  in  amount,  the  skin  becomes  red  and 
shiny,  and  the  pus  forces  its  way  outwards  if  surgical  interference  is  not 
forthcoming.  The  pus  is  thick,  brownish,  and  odourless.  The  fever  and 
pain  cease,  or  improve  with  the  free  exit  of  the  pus,  and  a  probe  introduced 
into  the  fistula  shows  the  condition  of  the  bone.  In  the  case  of  necrosis, 
however,  very  troublesome  fistuloe  occuj,  and  do  not  close  until  the  seques- 
trima  is  removed. 

In  some  cases  the  osseous  infection  passes  into  a  chronic  condition,  or 
assumes  from  the  first  a  slow  course.  It  lasts  for  months  and  years  under 
the  mask  of  s}'^hilitic  osteopathy  or  tubercular  cold  abscess  (Chantemesse 
and  Widal).  Even  when  the  lesion  is  chronic  from  the  outset  it  is  always 
painful  at  some  period.  The  pain  at  times  coincides  with  the  onset  of  the 
lesion,  but  in  other  cases  it  supervenes  months  or  years  later.  The  bony 
tumour  increases  very  slowly  in  size,  and  ends  in  resolution,  in  exostosis,  or 
in  suppuration.  The  exostosis  may  become  as  large  as  a  nut  or  an  orange, 
causing  deformity  of  the  limbs,  or  hampering  their  function. 

In  atcase  reported  by  Achard  and  Broca  the  fluctuating  swelling  of  the  bone  lasted 
for  eleven  months ;  the  pus  which  was  drawn  off  contained  Eberth's  bacillus.  Pean 
has  pubUshed  a  very  interesting  case  of  a  patient  who  was  attacked,  during  the  decline 
of  typhoid  fever,  with  osteoperiostitis  of  the  right  femur,  which  was  operated  upon  and 
drained.  Pain  had  at  this  time  also  appeared  in  the  left  femur ;  it  gradually  disap- 
peared, and  did  not  reappear  until  some  years  later.  This  fresh  lesion  ended  in  osteo- 
myeUtis,  which  was  operated  upon  ;  the  Bacillus  typhosus  was  found  in  the  pus. 

The  diagnosis  presents  no  difiiculty  when  the  osteomyelitis  or  the  osteo- 
periostitis supervenes  in  a  classical  manner  during  or  after  convalescence. 
When  they  do  not  appear  until  long  afterwards,  the  lesion  having  remained 
for  a  longer  or  shorter  period  in  the  latent  state,  we  must  not  confuse  the 
lesion,  when  accompanied  by  induration  or  by  softening  of  the  bone,  with 
Bjrphilitic  or  tubercular  osteitis.  The  osteomyelitis  of  adolescents  must 
also  be  difierentiated  from  them. 

The  prognosis  is  very  rarely  serious.  In  most  cases,  says  Schwartz,  the 
superficial  nature  and  the  small  extent  of  the  damage  is  very  striking. 

Medical  treatment  consists  in  relieving  the  pain  and  limiting  the  lesion 
as  far  as  possible.  For  this  purpose  leeches,  inunction  of  mercury,  rest,  and 
fixation  are  employed.  Surgical  treatment  is  often  indicated,  and  good 
results  may  be  looked  for.  Bacteriological  examination  at  the  time  of 
operation  gives  valuable  information  as  to  the  nature  of  the  pathogenic 
agents.     Eberth's  bacillus  is  sometimes  associated  with  staphylococci  or 

108—2 


170i  TEXT-BOOK  OF  MEDICINE 

streptococci.  In  other  cases  it  may  no  longer  be  present  at  the  time  of 
operation. 

Organs  of  the  Senses. — Ulcers  of  the  cornea,  panophthalmitis,  and 
inflammation  of  the  orbit  have  been  seen.  In  one  of  Panas's  cases  the 
Bacillus  typhosus  was  present  in  a  pure  state. 

Deafness  is  a  frequent  symptom  in  the  stationary  stage  of  typhoid  fever. 
It  may  depend  on  nerve  trouble,  or  on  catarrh  of  the  Eustachian  tube  and 
of  the  middle  ear,  coincident  with  the  laryngeal  catarrh.  These  auditory 
troubles  are  not  serious.  In  some  cases  they  are  due  to  purulent  otitis, 
which  may  cause  perforation  of  the  membrana  tympani,  spread  to  the 
mastoid  cells,  and  induce  caries  of  the  petrous  bone,  with  all  its  consequences. 

The  skin  may  be  affected  by  multiple  eruptions  resembling  those  of 
measles  or  of  scarlatina.  In  some  cases  it  is  not  a  question  of  simple  erup- 
tions, but  of  infective  erythemata,  which  may  carry  off  the  patients  in 
thirty-six  or  in  forty-eight  hours. 

Course — Relapse. — I  have  mentioned  in  the  description  of  the  disease 
the  possible  irregularities  of  the  onset  and  the  slowness  of  convalescence, 
which  is  sometimes  excessive,  but  there  are  other  peculiarities  deserving  of 
notice.  Typhoid  fever  may  at  its  onset  simulate  an  intermittent  fever, 
with  tertian  or  quotidian  attacks.  The  fever  then,  from  being  intermittent, 
becomes  remittent,  and  assumes  the  type  of  typhoid  fever.  Typhoid  fever 
chiefly  assumes  an  intermittent  character  in  countries  where  malaria  is 
endemic,  or  in  persons  who  have  recently  left  these  countries.  Old  writers 
knew  these  facts,  but,  in  their  opinion,  the  intermittent  marsh  fever  became 
transformed  into  ataxic  or  malignant  fever.  In  this  they  were  wrong,  for 
the  disease  does  not  change  its  nature,  although  it  presents  a  change  of 
type  (Trousseau). 

I  have  said  that  convalescence  in  typhoid  fever  may  be  interrupted  by 
innumerable  complications,  and  I  have  reserved  the  question  of  relapses  in 
order  to  speak  of  them  here.  The  relapse  m\ist  not  be  confounded  with  the 
second  attack.  The  latter — very  rare,  because  typhoid  fever  confers 
immunioy — only  concerns  cases  which  supervene  several  months  or  several 
years  after  the  first  attack.  The  relapse,  on  the  contrary,  is  a  fairly  frequent 
complication,  and  affects  the  patient  during  convalescence,  after  some  days 
of  complete  apyrexia,  just  as  though  the  disease  ran  its  course  in  several 
distinct  attacks,  relapses  occurring  in  from  6  to  10  per  cent.  They  are  more 
common  in  children. 

The  relapse  may  give  no  warning  of  its  onset.  It  often  begins  with 
vomiting,  and  the  temperature  rises  and  the  rose  spots  reappear,  although 
in  very  small  numbers.  The  relapse  usually  lasts  eight  to  twelve  days,  and 
generally  ends  in  recovery.  Complications,  however,  may  occur.  As  many 
as  four  and  even  five  relapses  have  been  seen  (Jaccoud). 


TV?TTOTr>  DTRF.ASES  170." 

It  is  not  rare,  especially  in  chiKlreirs  liospitals,  to  see  a  patient  suflering 
from  typhoid  fever  contract  scarlatina,  moaslos,  or  variola  ;  but  the  reciprocal 
condition  is  extremely  rare,  because  the  typhoid  fever  is  far  from  being  as 
contagious  as  the  eruptive  fevers. 

Prognosis-  Sudden  Death. — The  foregoing  descriptions  give  an  account 
of  the  various  modes  of  termination  in  typhoid  fever.  Its  gravity  and  its 
mortality  vary  in  different  epidemics,  countries,  and  surroundings  (hospital, 
town,  country).  The  mean  mortality  varies  from  18  to  20  per  cent.  (Murchi- 
son,  Griesinger,  Jaccoud).  We  shall  see  later  that  the  mortality  has  been 
much  lowered. 

The  prognosis  in  this  disease  must  always  be  reserved,  as  the  most 
terrible  accidents  (peritonitis,  sudden  death)  may  supervene  in  apparently 
slight  cases,  and  also  because  the  most  serious  complications  may  appear 
during  convalescence,  when  the  patient  is  looked  upon  as  cured. 

Sudden  Death. — This  pathological  fact  had  been  almost  ignored  until 
my  first  publications  on  Sudden  Death  in  Typhoid  Fever,  and  the  few 
scattered  cases  in  various  writings  had  passed  unnoticed.  In  less  than  a 
year  I  was  able  to  collect  fourteen  cases,  which  served  as  the  theme  of  my 
inaugural  thesis.*  Some  years  later,  in  a  fresh  work  on  the  same  subject,f 
I  collected  sixty-three  cases,  and  I  am  now  in  possession  of  nearly  eighty. 
These  figures  are,  in  my  opinion,  more  than  sufficient  to  establish  the  fact 
that  sudden  death  is  far  from  being  exceptional  in  typhoid  fever,  and  is 
almost  as  common  as  intestinal  perforation  or  peritonitis.  I  place  its  frequency 
at  2  per  cent.,  which  gives  it  an  important  place  in  the  history  of  this  disease. 

Two  questions  belong  to  the  study  of  sudden  death,  the  one  purely 
clinical,  and  the  other  theoretical,  which  seeks  for  the  cause  and  mechanism 
of  this  accident. 

Sudden  death  usually  occurs  without  warning  in  mild  or  moderate  cases, 
when  aU  danger  appears  at  an  end.  When  we  compare  cases  with  one 
another,  we  find  that  the  circumstances  accompanying  sudden  death  usually 
occur  imder  the  same  conditions.  We  see  that  the  two  first  weeks  are 
passed  without  mishap,  the  temperature  begins  to  fall,  the  patient  feels 
better  and  begs  for  food,  and  convalescence  commences,!  when  suddenly, 

*  Dieulafoy,  "  De  la  Mort  Subite  dans  la  Fi^vre  Typhoide"  {These  de  Paris,  1807). 

t  Gaz.  Hebdom.,  1877,  Xos.  20  and  21. 

t  In  twenty -three  cases  sudden  death  occurred  as  follows ; 

2  cases  on  the  17th  day. 


2 

18th 

4   „ 

19th 

c  „ 

20th 

6   „ 

21st 

2   „ 

23rd 

2   „ 

24th 

1706  TEXT-BOOK  OF  MEDICINE 

without  pain  or  warning,  the  patient  becomes  exceedingly  pale,  suffers  from 
a  few  convulsive  movements,  and  dies.  Death  is  evidently  due  to  syncope, 
but  what  is  the  explanation  of  this  syncope  ?  It  has  not  been  difficult  for 
me  to  coUect  a  fair  number  of  cases  in  which  sudden  death,  apart  from 
typhoid  fever,  is  due  to  trifling  circumstances,  such  as  drinking  a  glass  of 
iced  water,  cauterization  of  the  pharynx,  etc.  We  know,  on  the  other  hand, 
that  foreign  bodies  in  the  intestine,  such  as  worms,  fruit-stones,  etc.,  may 
cause  epileptiform  troubles,*  which  are  sometimes  followed  by  syncope  and 
death.  I  have,  therefore,  fixed  my  base,  on  the  one  hand,  upon  clinical 
facts,  and,  on  the  other  hand,  upon  the  experiments  of  Brown-Sequard  and 
Goltz,  which  show  the  special  excitability  of  the  intestine,  and  the  mechanism 
of  syncope  following  such  excitation,  and  I  have  put  forward  the  following 
theory  :  Syncope  in  typhoid  fever  is  partly  due  to  a  reflex  action  starting  in 
the  diseased  intestine.  The  stimulus  is  transmitted  by  the  centripetal  fibres 
of  the  great  sympathetic  to  the  cells  of  the  spinal  cord  and  bulb,  and  pro- 
duces a  fulminant  action  upon  the  nuclei  of  the  vagus. 

Hayem  has  defended  a  theory  which  attributes  sudden  death  to  the 
changes  in  the  cardiac  muscle  seen  in  typhoid  fever,  as  well  as  in  most 
severe  fevers.  This  theory  is  seductive,  for  it  appears  based  upon  patho- 
logical anatomy ;  but  if  we  admit  that  sudden  death  is  due  to  cardiac 
degeneration,  we  ought  to  find  this  degeneration  in  all  cases  of  sudden  death. 
It  is,  however,  often  absent.  In  the  seven  cases  so  far  published  histological 
examination  has  shown  no  change  in  the  heart.  Accordingly,  if  sudden 
death  has  occurred  seven  times  without  any  change  in  the  heart,  we  must 
look  elsewhere  for  the  cause.  Sudden  death  from  syncope  is  not,  then,  the 
end  of  the  so-called  cardiac  form.  As  I  have  already  said,  it  is  quite  a 
diflerent  thing.  The  study  of  the  typhoid  toxine  on  the  nerve  ganglia  of 
the  heart  may  perhaps  elucidate  the  pathogenesis  (Chantemesse). 

Diagnosis. — Any  typhoid  condition  may  simulate  typhoid  fever — as, 
for  instance,  the  condition  caused  by  lumbricosis,  to  which  Chauffard  has 
just  drawn  attention  afresh  in  the  case  of  a  little  boy  who  had  all  the  symp- 
toms of  typhoid  fever.  In  this  case  recovery  occurred  after  the  passage 
of  thirty-nine  worms. 

The  diagnosis  of  typhoid  fever  by  clinical  methods  alone  is  often  very 
diffi-cult,  and  the  exceptional  cases  which  commence  with  angina,  gastric 
catarrh,  lobar  pneumonia,  or  intermittent  fever  are  well  calculated  to 
puzzle  the  clinician.  The  same  remark  applies  to  the  slight  forms  and  to 
the  ataxic  form,  with  early  delirium,  which  simulates  meningitis  or  acute 
mania.    According  to  Wunderlich,  any  disease  in  which  the  temperature 

*  I  saw,  with  Krishaber,  a  child,  eleven  years  old,  who  had  swallowed  plum -stones. 
He  was  seized  with  convulsions,  and  died.  At  the  autopsy  we  found  the  plum-stones 
accxunulated  in  the  latter  part  of  the  ileum. 


TYPHOID  DISEASES  1707 

has  not  reached  10i°  F.  by  the  evening  of  the  fourth  clay  is  not  typhoid 
fever,  and  every  disease  in  which  the  temperature  reaches  104°  F.  on  the 
first  day  ia  not  typhoid  fever.  The  latter  proposition  cannot  be  accepted, 
and  the  former  is  subject  to  many  exceptions. 

Cerebro-spinal  meningitis  has  many  symptoms  in  common  with  typhoid 
fever,  more  especially  as  the  typlioid  infc^ction  may  at  the  same  time  cause 
cerebro-spinal  infection.  I  will  ask  the  reader  to  turn  to  the  section  on 
Cerebro-spinal  Meningitis,  where  he  will  find  this  difficult  question  discussed 
in  detail. 

Malignant  hypertoxic  syphilis  may  simulate  typhoid  fever.  Fournier 
has  described  this  condition  under  the  name  of  syphilitic  typhosis.  I  have 
seen  a  case  at  the  Hotel-Dieu  which  ended  in  death.  LetuUe  has  given  me 
the  following  notes  : 

A  young  woman  came  into  hospital  suffering  from  secondary  syphilis,  the  temperature 
varying  between  102°  and  104°  P.  ;  the  spleen  was  enlarged  and  the  abdomen  distended, 
just  as  in  typhoid  fever.  Three  days  later  the  temperature  fell,  the  general  condition 
improved,  and  the  syphiUs  ran  its  course. 

In  syphilitic  typhosis  (hypertoxic  form)  the  secondary  rash  appears 
with  symptoms  which  sometimes  recall  the  invasion  of  an  eruptive  fever, 
and  at  other  times  of  typhoid  fever.  The  temperature  reaches  103°  or 
104°  F.  Prostration,  adynamia,  headache,  vertigo,  epistaxis,  vomiting,  and 
dyspnoea  are  the  sjonptoms  usually  seen  in  syphilitic  typhosis.  In  my 
patient,  to  whom  I  alluded  above,  the  symptoms  of  hypertoxia  reached  a 
maximum,  and  the  haemoglobin  was  diminished  to  50  per  cent.  The  tachy- 
cardia, dyspnoea,  and  adynamia  ended  in  fatal  collapse,  although  at  the 
autopsy  we  were  unable  to  discover  the  slightest  lesion. 

Influenza,  cerebral  meningitis,  infective  endocarditis,  and  acute  tuber- 
culosis may  closely  simulate  typhoid  fever.  Everyone  in  his  hospital  career 
or  in  his  private  practice  has  often  found  himself  in  the  awkward  situation 
where  it  was  impossible  to  say  whether  a  patient  had  or  had  not  typhoid 
fever.     For  example : 

A  yomig  man,  twenty  years  old,  has  been  taken  ill  a  few  days  before  with  fever, 
severe  headache,  and  vomiting.  He  is  troubled  with  cough,  and  auscultation  of  the 
chest  shows  some  scattered,  whistling  rales.  The  evening  temperature  is  104°  P., 
there  is  no  diarrhcea,  the  insomnia  is  persistent,  and  we  wonder  whether  the  case  is  one 
of  typhoid  fever,  likely  to  end  in  recovery,  or  whether  it  is  commencing  mihary  tubercu- 
losis, which  is  nearly  always  fatal.  On  what  can  we  base  the  diagnosis  ?  On  the 
temperature  curve  ?  Unfortimately,  it  rarely,  in  any  special  case,  follows  the  well- 
known  classical  form.  Can  we  rely  upon  the  appearance  of  spots  ?  Unfortunately,  they 
have  not  yet  appeared,  and  perhaps  they  will  not  do  so.  The  rales,  however,  become 
general,  dyspnoea  appears,  and  our  fears  of  acute  tuberculosis  increase,  while  time  runs  on 
and  the  diagnosis  still  remains  indefinite. 

We  shall  see  later  that  it  is  necessary  to  think  of  paratyphoid  fever. 
Bacteriology  has  been  employed  as  an  aid  to  diagnosis.     The  method 


1708  TEXT-BOOK  OF  MEDICINE 

consists  in  examination  of  blood  withdrawn  by  puncture  from  the  spleen, 
but  this  is  a  very  complicated  and  often  impracticable  method.  Eisner 
proposed  search  for  the  bacillus  in  the  stools,  which  is  an  unpractical  and, 
furthermore,  an  insufficient  method.  Widal  made  a  most  irdportant  com- 
munication at  the  Societe  Medicale  des  Hopitaux.*  He  showed  how  to 
make  in  a  few  minutes  an  accurate  diagnosis  of  typhoid  fever. 

I  was  anxious  to  confirm  these  results,  and  I  at  once  made  a  communica- 
tion to  the  Academic  de  Medecine.f  This  method  of  sero-diagnosis  is  based 
on  the  fact  that  the  serum  of  persons  suffering  from  typhoid  fever,  or  even 
of  convalescents,  possesses  the  power  of  immobilizing  and  agglutinating  in 
vitro  Bberth's  bacilli  suspended  in  broth. 

Accordingly,  if  we  place  a  young  broth  culture  of  Eberth's  bacillus  under 
the  microscope,  we  see  that  the  bacilli  are  isolated,  and  endowed  witn 
extreme  mobility.l 

*  F.  Widal,  "  Sero -diagnostic  de  la  Fievre  Typhoide  "  {Soc.  Med.  des  Hopit.,  26  Juin, 
1896  ;  Congr.  de  Nancy,  1896  ;  Pr.  Med.,  8  Avril,  1896). 

f  Dieulafoy.      Communication  faite  a  I'Acad.,  le  7  Juillet,  1896. 

J  Widal  adopts  the  following  method :  "  I  begin  with  the  extemporaneous  micro- 
scopical examination,  after  mixing  serum  with  an  active  culture  in  the  proportion  of  1 
to  IQ,  or  even  1  to  6.  When  the  preparation  is  disturbed  by  Brownian  movements,  we 
must  let  it  remain  for  a  quarter  or  for  half  an  hour  in  order  to  see  the  agglutination.  We 
should  always  examine,  for  the  sake  of  comparison,  a  preparation  of  the  culture  made 
before  the  addition  of  serum.  The  employment  of  a  young  culture  which  is  only  one 
or  two  days  old  is  preferable.  I  may  even  say  that  if  the  development  of  a  culture  is 
sufficiently  rich,  the  younger  it  is  the  better.  A  broth  culture  which  is  quite  neutral 
and  several  days  old  may  give  the  reaction,  provided  that  we  carefully  follow  the 
indications  stated  later.  Practically,  in  a  hospital  laboratory  we  can  always  have 
cultures  some  days  old  which  are  sufficient  for  immediate  examination. 

"  If  the  extemporaneous  examination  shows  numerous  confluent  masses,  made  up 
of  bacteria,  and  scattered  all  over  the  preparation  hke  the  islands  of  an  archipelago,  the 
diagnosis  is  certain.  If  the  masses,  though  characteristic,  be  not  especially  confluent, 
or  if  I  find  only  mobile  or  isolated  baciUi,  I  examine  the  mixture  again  several  hours 
afterwards,  both  with  the  naked  eye  and  with  the  microscope.  After  this  time  the 
reaction  is  often  apparent.  In  case  of  a  negative  result  I  repeat  the  examination 
several  days  following,  as  long  as  suspicious  symptoms  last. 

"  If  we  only  possess  a  very  old  culture,  or,  indeed,  one  some  days  old,  which  under 
the  microscope  shows  precipitation  of  false  masses  before  the  addition  of  serum,  we 
must  not  hesitate  to  make  a  fresh  culture,  and  to  delay  the  answer  to  the  next  day. 
The  seruJB  may  be  mixed  with  broth,  sown,  and  put  in  the  oven.  In  fifteen  hours, 
or  even  less,  the  microbes  are  found  in  masses  at  the  bottom  of  the  tube,  forming  small 
whitish  flakes,  and  leaving  the  broth  almost  clear.  On  shaking,  these  flakes  do  not 
dissolve  completely  ;  they  always  leave  a  precipitate  floating  in  the  Kquid  as  a  very  fine 
dust.  I  constantly  employ  this  procedure  concurrently  with  the  extemporaneous  one 
when  I  am  dealing  with  a  serum  taken  under  conditions  of  absolute  purity.  If  I  am 
not  sure  of  the  asepsis  of  my  serum,  I  make  a  new  culture  by  sowing  it  on  simple  broth. 
In  less  than  twenty-four  hours  I  have  a  fresh  culture  sufficiently  turbid  to  give  the 
phenomenon  under  the  microscope  immediately  after  the  addition  of  the  typhoid 
serum.  I  may  add  that,  some  hours  after  mixing,  the  clots  may  be  visible  to  the 
naked  eye." 


TVPIIolJ)  DISF.ASKS  1709 

On  tlie  otlior  hand,  if  we  mix  in  a  test-iuhe  ten  drops  of  a  culture  of 
Ebertli's  bacillus  and  one  drop  of  serum  from  the  patient,  and  then  examine 
this  mixture  under  the  microscope,  we  notice  very  striking  changes.  The 
bacilli  no  longer  remain  isolated  and  mobile,  as  in  the  preceding  prepara- 
tion. They  tend  to  lose  their  mobility,  and  agglutinate  in  masses,  separated 
by  vacant  spaces.  These  empty  spaces  are  still  traversed  by  some  bacilli, 
wliich  are  less  mobile,  and,  as  it  were,  siderated,  and  are  finally  attracted 
to  one  of  these  masses,  in  which  they  in  turn  are  engulfed. 

If  a  patient  jdelds  serum  capable  of  causing  agglutination  in  a  broth 
culture  of  typhoid  bacilli,  he  is  suffering  from  typhoid  fever. 

The  reaction  has  been  found  by  Widal  in  patients  who  had  been  suffering 
from  typhoid  fever  for  seven,  twelve,  fifteen,  sixteen,  nineteen,  and  twenty- 
one  days.  On  the  other  hand,  the  serum  of  patients  suffering  from  other 
diseases,  such  as  nephritis,  tuberculosis,  pneumonia,  jaundice,  rheumatism, 
etc.,  when  mixed  with  a  broth  culture  of  Eberth's  bacillus,  leaves  the  micro- 
organisms mobile  and  isolated, 

Sero-diagnosis  has  been  adopted  both  in  France  and  abroad.  We 
have  "  a  simple  and  rapid  method,  which  requires  no  elaborate  material, 
not  even  stains.  All  that  is  required  is  a  pure  broth  culture  of  Eberth's 
bacilli,  which  can  be  kept  for  weeks,  a  microscope  with  an  immersion  lens, 
and  a  drop  of  blood  or  of  serum  from  the  patient "  (Widal). 

The  experiment  may  also  be  made  in  another  manner.  If  typhoid 
serum  is  added  to  a  broth  culture  of  active  bacilli,  or  if  \argin  broth  is 
impregnated  immediately  after  the  serum  has  been  added,  and  kept  for 
some  hours  in  the  oven,  we  see  that  the  broth  becomes  clear,  and  little 
whitish  flakes  collect  at  the  bottom  of  the  tube. 

The  agglutinating  property  appears  to  belong  to  the  albuminoid  matter 
of  the  blood,  or  of  the  fluids  which  form  a  kind  of  chemical  precipitate 
around  the  microbes  (Widal  and  Sicard).  Further,  the  agglutinative 
reaction  is  obtained  not  only  with  typhoid  serum,  but  also  with  other 
secretions  from  typhoid  patients  —  serous  fluid  of  blisters  or  of  cedema, 
tears,  bUe,  and  exceptionally  urine  (Widal  and  Sicard). 

The  agglutinative  reaction  has  been  seen  in  the  milk  of  wet-nurses 
suffering  from  typhoid  fever  (Achard  and  Bensaude). 

In  a  case  published  by  Etienne  the  reaction  did  not  take  place  with  the  blood  of  a 
foetus,  although  the  mother  was  suffering  from  typhoid  fever,  and  gave  the  agglutinative 
reaction.  This  observation  should  not  be  set  up  as  a  precedent,  for  the  passage  of  the 
agglutinating  property  from  the  mother  to  the  foetus  occurs  in  rabbits  (Widal  and 
Sicard). 

In  short,  as  I  said  in  1896  at  the  Academic  de  Medecine,  we  can  foresee 
the  services  which  sero-diagnosis  will  render.  We  shall  now  know  how  to 
regard  these  fevers,  called  in  turn  sjmochal,  gastric,  autumnal,  mucous,  or 


1710  TEXT-BOOK  OF  MEDICINE 

typhoidal,  febrile,  and  infectious  diseases,  wMch,  according  to  the  current 
teaching,  helped  to  increase  or  diminish  the  balance-sheet  of  typhoid  fever. 

We  can  now  diagnose  cases  of  influenza  resembling  typhoid  fever  and 
presenting  insuperable  obstacles  to  correct  diagnosis.  We  can  understand 
the  cases  in  which  typhoid  fever  appears  to  localize  itself  in  a  typhoid  lung, 
and  those  in  which  pneumonia  assumes  a  typhoid  course,  although  it  has 
nothing  in  common  with  infection  due  to  Eberth's  bacillus.  We  can  tell 
whether  patients  who  come  to  us  with  obscure  symptoms  of  typhoid  fever 
and  a  cardiac  murmur  are  suffering  from  typhoid  fever  or  from  endocarditis 
of  the  typhoid  type. 

We  can  promptly  decide  the  diagnosis  of  typhoid  fever  and  acute  tuber- 
culosis. We  can  form  a  correct  opinion  of  typhus  ambulatorius,  typhus 
levissimus,  and  abortive  tjrphoid  fever,  which  will  take  a  properly  defined 
place  in  the  list  of  diseases. 

In  future  we  shall  not  hesitate  in  deciding  whether  the  disease  is  menin- 
gitis, cerebro-spinal  typhus,  or  tjrphoid  fever  of  a  meningeal  type. 

The  specific  nature  of  typhoid  fever  has,  therefore,  been  clearly  demon- 
strated, the  work  being  that  of  the  French  school,  an  inheritance  from  our 
great  clinicians,  Bretonneau  and  Trousseau. 

Eeaction  of  fixation  or  deviation  of  the  complement. — We  have,  in 
addition  to  Widal's  sero-diagnosis,  a  more  complicated  laboratory  method, 
which  permits  an  exact  diagnosis,  not  only  of  typhoid  fever,  but  also  of 
other  infections  in  which  the  agglutination  reaction  may  not  be  found,  as, 
for  example,  in  syphilis  (Wassermann's  reaction),  or  in  hydatid  cysts 
(Weinberg's  reaction).  This  method  was  discovered  by  Bordet  and 
Gengou.     Widal  and  Le  Sourd  have  applied  it  to  typhoid  fever. 

The  principle  is  as  follows  : — 

I.  If  the  red  corpuscles  of  a  sheep  are  repeatedly  injected  into  the 
peritoneal  cavity  of  a  rabbit,  we  find  that  the  rabbit  serum,  obtained  after 
bleeding  and  retraction  of  the  clot,  has  become  hsemolytic  to  the  red 
corpuscles  of  the  sheep.  Sheep-serum  prepared  in  this  way  dissolves 
in  vitro  the  red  corpuscles  of  the  rabbit.  This  heemolytic  property  of 
rabbit-serum  disappears  on  heating  to  55°  0.  for  half  an  hour ;  serum 
that  has  lost  its  hsemolytic  power  is  said  to  be  inactivated. 

We  can,  however,  restore  the  hsemolytic  power  to  this  inactivated 
serum  by  adding  to  it  serum  from  an  indifferent  animal  (man,  guinea-pig, 
etc.).  In  this  way  we  can  isolate  from  the  prepared  rabbit-serum  two 
substances  :  the  one  sensibilatrice  (Bordet),  amboceptor  (Ehrlich),  cytase 
(Metchnikoff).  This  specific  substance  has  been  formed  in  the  rabbit  by  a 
defensive  reaction  against  the  foreign  corpuscles  ;  it  is  not  destroyed  by  a 
temperature  of  55°  0. ;  it  is  thermostabile.  The  other  substance,  alexine 
(Bordet),  or  complement  (Ehrlich),  is  not  specific  ;  it  is  found  in  the  serum 


TYPHOID  DISEASES  1711 

of  all  atilin.ils.  FiiiLlitM-,  it  is  destroyed  by  heating  to  Hf)"  C.  ;  it  is 
thermolabile. 

If  we  mix  inactivated  anti-sheep  serum  from  a  rabbit  with  normal  serum 
from  a  guiuoa-ing,  in  the  presenco  of  sheep's  red  corpusoleR,  we  produce  a 
lia^molytic  serum,  containing  an  amboceptor  and  a  complement,  which 
will  unite  to  cause  haemolysis  of  the  red  corpuscles.  If  this  mixture  be 
placed  in  the  oven  at  37°  C.  for  half  an  hour,  the  red  corpuscles  are 
dissolved,  and  the  complement  is  no  longer  found ;  it  has  all  been  used  up 
in  order  to  produce  haemolysis  with  the  amboceptor. 

This  reaction  may  be  used  to  show  whether  a  given  serum  does  or 
does  not  contain  complement.  For  this  purpose  we  have  merely  to  mix 
sheep's  corpuscles  and  inactivated  rabbit-serum,  next  adding  the  serum  to 
be  tested,  and  placing  the  mixture  in  the  oven  at  37°  C.  for  half  an  hour. 
If  the  serum  contains  complement,  haemolysis  will  occur ;  if  it  does  not, 
the  red  corpuscles  are  not  dissolved. 

II.  A  similar  reaction  occurs  with  micro-organisms.  A  person  who 
has  contracted  typhoid  fever,  possesses  in  his  serum  an  amboceptor 
which,  united  with  serum  still  containing  its  own  complement,  has  the 
power  of  destroying,  in  vitro,  Eberth's  bacilli.  Eberth's  bacillus  takes  the 
generic  name  of  antigen,  and  the  bacteriolgical  substance  in  the  patient's 
serum  is  called  antibody. 

If,  in  the  obverse  reaction,  we  replace  the  red  cells  by  Eberth's  bacilli 
and  the  hsemolytic  serum  by  typhoid  serum  containing  antibodies,  we 
shall  have,  in  the  presence  of  Eberth's  bacilli,  inactivated  typhoid-serum 
and  normal  guinea-pig's  serum.  In  this  case  bacteriolysis  occurs,  and 
the  complement  (guinea-pig's  serum)  is  absorbed ;  it  disappears  after  the 
bacteriolysis.  On  the  other  hand,  if,  instead  of  serum  from  a  typhoid 
patient,  we  use  serum  from  an  individual  suffering  from  some  other 
disease,  the  amboceptor  will  not  be  present,  bacteriolysis  will  not  occur, 
and  the  complement  will  not  disappear. 

Accordingly,  in  order  to  diagnose  typhoid  fever,  it  is  sufficient  to  know 
whether  the  complement  is  or  is  not  present  after  some  hours  in  the  oven 
at  37°  C.     For  this  purpose  we  take  : 

(a)  Eberth's  bacilli  (0*1  c.c.  of  an  emulsion  in  0'8  per  cent,  saline 
fluid  from  a  large  colony,  forty-eight  hours  old). 

{h)  Patient's  serum  rendered  inactive  by  heating  to  55°  C.  for  half  an 
hom\ 

(c)  Serum  from  a  freshly  killed  guinea-pig  (complement). 

{d)  Sterile  physiological  salt  solution  (0  6  c.c). 

The  mixing  is  done  in  a  small  sterile  glass  tube  by  means  of  a  Levaditi 
pipette  graduated  to  tenths  of  a  cubic  centimeter.  The  mixture  is  kept 
at  37"^  C.  for  three  to  five  houi's. 


1712  TEXT-BOOK  OF  MEDICINE 

By  this  time,  if  the  patient  is  suffering  from  typhoid  fever,  the  com- 
plement will  have  been  absorbed.  We  now  add  a  mixture  composed  of 
sheep's  corpuscles  (1  c.c.  of  a  five  per  cent,  solution  of  corpuscles)  and 
inactivated  anti-sheep  rabbit-serum  (dose  varying  according  to  its  hsemo- 
lytic  power).  The  whole  is  placed  in  the  oven  at  37°  C.  for  thirty 
minutes. 

If  the  patient  has  typhoid  fever,  haemolysis  will  not  occur,  because  the 
complement  necessary  to  produce  haemolysis  has  been  absorbed  during  the 
first  or  bacteriolytic  reaction. 

The  absence  of  haemolysis  indicates,  therefore,  a  positive  reaction. 
If,  on  the  contrary,  the  patient  has  not  typhoid  fever,  the  complement 
will  remain  free  because  it  is  not  used  in  the  bacteriolytic  reaction,  and  in 
the  second  or  hsemolytic  reaction,  hasmolysis  will  occur.  Haemolysis, 
therefore,  indicates  a  negative  reaction. 

It  is  well  to  use  control  tests,  taking  serum  from  a  healthy  individual 
and  also  from  a  person  undoubtedly  suffering  from  typhoid  fever. 
Widal's  reaction,  and  Bordet  and  Gengou's  reaction  usually  lead  to  the 
same  result.  The  simplicity  of  the  former  gives  it  a  marked  advantage 
over  the  latter. 

Hsemo-Diagnosis. — In  the  severe  form  of  typhoid  fever  Courmont  and 
Lesieur  have  always  found  Eberth's  bacillus  in  the  blood  up  to  the  end  of 
the  third  week.  To  carry  out  this  examination,  it  is  sufficient  to  sow  2  to 
4  c.c.  of  blood  immediately  after  withdrawal  on  300  to  500  c.c.  of  broth. 
As  a  rule,  the  culture  is  positive  in  the  first  few  days.  The  following  table 
mdicates  the  dates  : 

Posi 


tive  cultui'e 

on  the 

1st  day 

. .     11  cases. 

»             >> 

,, 

2ad  „         .. 

. .     17      „ 

,             „ 

,j 

3rd    „ 

..       4      „ 

3                                  ,, 

J' 

4th    „ 

..       8      „ 

J       .  r   i  1 

i  1 

5th    „ 
1  i 

..       4      „ 

...               .           ^ 

In  60  per  cent,  of  the  cases  the  culture  is  positive  in  from  twenty-four 
to  forty-eight  hours.  The  delay  seen  in  the  development  of  cultures  is 
most  probably  due  to  the  hindering  action  of  the  typhoid  serum,  rather 
than  to  the  small  number  of  microbes  present  in  the  blood.  The  discovery 
of  the  bacillus  in  the  blood  may  be  useful  in  cases  where  the  serum  reaction 
is  delayed.  Thus,  the  bacillus  existed  in  the  blood  four  times  in  thirty- 
three  positive  cases,  although  agglutination  was  not  appreciable.  Never- 
theless, "  sero-diagnosis  is  more  easily  carried  out,  and  remains  the  favourite 
method  whenever  it  gives  positive  information."  There  is  no  relation 
between  the  agglutinative  power  of  the  blood  and  the  rapidity  of  growth 
of  the  cultures.  In  any  case,  we  do  not  fuid  other  microbes  in  the  blood. 
Eberth's  bacillus  is  present  in  a  pure  condition. 


TVruoll)   DISFIASFS  171:^ 

Gelo-Diagnosis.-  Tliis  iuuLIkhI,  [)ii)[)ust'cl  by  ('haiitcinossci,  is  based  on 
the  discovery  ol"  the  /!<tcillus  /i/i^/tosua  iu  the  dejecta.  It  dupends  on  the 
properties  of  Eberth's  bacillus. 

(1)  This  bacillus  can  stand  a  fairly  largo  dose,  of  (larbojic  arid  (Chaiite- 
inossc  and  Widal)  ;  (li)  it  does  not  cause  fermentation  of  milk-sugar,  while 
the  BacUlns  coli  gives  rise  to  lactic  acid  (Chantemesse  and  Widal,  1892) ; 
(.'J)  on  plates  of  agar,  to  which  milk-sugar  and  litmus  have  been  added,  the 
B.  typhosus  gives  blue  colonies  with  lactic  acid,  and  the  B.  coli  gives  red 
ones  (VViirtz,  1893) ;  (4)  this  microbe  is  agglutinated  by  a  specific  serum 
(Pfeiffer,  1891:) ;  (5)  before  looking  for  it  in  the  dejecta,  it  is  an  advantage 
previously  to  cause  its  multiplication,  and  to  make  the  search  easier,  the 
material  should  be  sown  on  an  extremely  thin  layer  of  agar  (Chantemesse, 
1901) ;  (6)  in  order  to  find  these  bacilli  in  the  suspected  fluid,  it  is  useful 
before  analysis  to  collect  them  in  masses  by  means  of  a  specific  agglutinative 
serum  (Chantemesse,  1902). 

Chantemesse  and  Decobert*  have  found  by  the  aid  of  gelo-diagnosis 
typhoid  bacilli  in  the  stools  of  all  those  suffering  from  well-marked  typhoid 
fever,  and  have  controlled  their  observations  by  sero-diagnosis.  They  have 
also  found  them  in  some  patients  who  have  been  well  for  a  month.  Finally, 
they  have  been  able  to  prove  the  presence  of  the  B.  typhosus  in  the  dejecta 
at  the  onset  of  the  typhoid  fever  before  the  agglutination  reaction  could  be 
obtained. 

Ophthalmo-Diagnosis. — This  method,  employed  by  Chantemesse,  con- 
sists in  dropping  into  the  eye  a  solution  of  the  toxines  of  the  B.  typhosus. 

Diagnosis  from  Paratyphoid  Infection. — Some  patients  appear  to  have 
typhoid  fever,  when  they  are  really  suffering  from  a  paratyphoid  infection. 
Sero-diagnosis  is  negative  in  these  cases.  When  a  patient  is  in  the  typhoid 
state,  we  may  suspect  paratyphoid  infection  if  sero-diagnosis  and 
ophthalmo-diagnosis  are  negative.  Paratyphoid  infection,  however,  is  not 
certain,  unless  the  patient's  serum  agglutinates  a  culture  of  paratyphoid 
bacilli.  These  are  the  Bacillus  paratyphosus  A  of  Brion  and  Kayser,  the 
Bacillus  paratyphosus  B  of  Schottmiiller,  the  Bacillus  enteriditis  of  Gartner, 
and  the  Bacillus  paratyphosus  F  of  Faroy.  The  proper  method  of  ex- 
amination for  paratyphoid  bacilli  is  haemoculture,  similar  to  that  used  in 
the  case  of  Eberth's  bacillus.  The  B.  typhosus  and  the  paratyphoid 
bacilli  are  sometimes  associated,  the  infection  being  mixed.  Aside  from 
typhoid  conditions,  the  paratyphoid  bacilli  give  rise  to  gastro-intestinal, 
pyaemic,  and  remittent  infection,  to  infective  jaundice,  and  to  cholecystitis. 

etiology. — Eberth's  bacillus  is  the  specific  agent  in  typhoid  fever.  The 
pathogenic  conditions  of  the  disease  are  those  which  govern  the  hatching 

♦  Decobert.  "  Du  Gelo-diajriiostic  des  Selles  et  de  son  Emj)loi  au  Diagnostic 
Precoee  de  la  Fie\i*e  Typhoide  "  {These  de  Paris,  1933). 


1714  TEXT-BOOK  OF  MEDICINE 

of  all  infectious  diseases  due  to  micro-organisms  :  (1)  It  is  necessary  that 
the  microbe  introduced  iuto  the  economy  be  present  in  such  numbers  or  be 
endowed  with  such  virulence  that  it  can  overcome  the  resistance  of  the 
body ;  (2)  this  more  or  less  feeble  resistance  in  the  economy  constitutes  the 
occasio  morbi. 

Typhoid  fever  has  been  seen  in  practically  every  country,  but  still  it 
shows  a  marked  predilection  for  the  Temperate  Zones.  It  is  endemic  in 
large  towns. 

It  reaches  its  maximum  in  the  autumn  (Besnier).  It  is  epidemic,  but 
only  to  a  sHght  degree  contagious,  and  the  first  attack,  as  a  rule,  confers 
immunity.  In  this  disease,  as  iu  all  epidemic  diseases,  each  epidemic  may 
present  special  forms  and  characters,  distinguishing  it  from  other  epidemics. 
Typhoid  fever  by  choice  attacks  young  people,  and  especially  those  who 
have  come  to  a  city  from  the  country,  and  who  are  in  a  special  state  of 
receptivity,  favoured  by  bad  hygienic  conditions,  home-sickness,  worry, 
and  excess  of  fatigue  or  of  work. 

The  spread  of  typhoid  fever  by  "  typhoid  carriers  "  has  recently  been 
the  subject  of  much  research.  The  bacillus  may  long  remain  in  certain 
organs  of  persons  who  have  had  typhoid  fever ;  for  instance,  it  has  been 
found  in  the  dejecta  years  after  the  patient  has  recovered.  In  such  a  case 
it  is  probable  that  the  bacillus  has  come  from  its  favourite  haunt,  the 
gall-bladder,  merely  passing  through  the  bowel.  The  percentage  of  chronic 
excretors  of  the  bacillus  is  said  to  vary  from  three  to  six.  These  persons, 
though  in  good  health,  may,  therefore,  play  some  part  in  the  spread  of 
typhoid  fever. 

Eberth's  bacillus  may  live  in  the  bladder  for  months,  perhaps  for 
years,  after  recovery  from  typhoid  fever  (six  months,  Bussing  ;  five  years, 
Gwinn).  The  bacillus  shows  a  partiality  for  the  gall-bladder,  where  it 
has  been  found  as  long  as  eight  years  after  recovery.  The  bacilli  enter 
the  intestine  and  pass  out  in  the  stools.  Although  the  chronic  typhoid 
carrier  appears  to  be  healthy,  he,  nevertheless,  has  some  share  in  the 
spread  of  typhoid  fever. 

In  this  way  we  can  explain  many  endemics  and  epidemics,  of  which  the 
cause  was  unknown ;  most  suggestive  cases  of  the  spread  of  typhoid  fever 
by  chronic  carriers  of  bacilli  can  be  quoted  by  the  dozen. 

Some  persons  carry  Eberth's  bacilli,  although  they  have  never  had 

typhoid   fever;    the  gall-bladder,   the   bladder,   and   the  gut  may  have 

become  infected  without  the  appearance  of  the  characteristic  symptoms 

of  typhoid  fever. 

Bliunentlial  lias  reported  the  case  of  a  ■woman  wlio  was  operated  upon  for  empyema 
of  tlie  gaU-bladder ;  Eberth's  bacillus  was  found  in  the  pus,  and  yet  the  woman  bad 
no  recollection  of  having  suffered  from  typhoid  fever  or  any  similar  malady.  Pratt 
reports  a  similar  case  of  suppui-ative  cholecystitis,  in  which  Eberth's  bacillus  was 


TYPHOID  DlSIiASES  1715 

present,  alUiouffli  tlie  paiiout  hml  never  suffered  from  any  fliseaw  rew^mblinjr  typlioid 
fever.  Houston  haa  rt'portt'd  the  case  of  a  woman  who  hud  novor  hiul  tyjihoid  fover, 
and  yet  slie  l>ad  cystitis,  duo  to  Elwrth's  bacillus.  Park  rpioU'S  the  case  of  a  cook 
who  could  not  riMuember  ever  haviiiv"  had  typhoid  fever,  and  yet  twenty-nine  persons 
from  contact  with  her  contracted  typhoid  fever  in  the  courso  of  eight  years,  these 
persons  belonging  to  families  in  whose  sernce  the  cook  was.  An  examination  showed 
that  she  excreted  tlie  bacilli  in  her  stools. 

These  facts  prove  the  direct  infection  of  the  gall-bhidder,  intestine  or 
Madder,  without  a  previous  invasion  of  the  economy  by  the  bacillus  of 
Eberth. 

And  yet,  though  the  bacillus  of  Eberth  may  live,  without  causing 
harm,  in  the  carrier  (just  as  the  streptococcus  or  the  pneumococcus  may 
do),  there  is  no  reason  why,  as  a  result  of  certain  conditions  (fatigue, 
overwork),  it  may  not  become  pathogenic,  and  produce  an  auto-infection. 
This  fact  affords  a  partial  explanation  of  the  old  dogma  of  morbid  spon- 
taneity, and  the  motto  " Multa  renascentur  gucejam  ceddere"  applies. 

As  we  shall  see  in  a  moment,  water,  is  one  of  the  chief  agents  of  con- 
tagion ;  milk,  oysters,  and  vegetables  must  also  be  held  guilty.  I  would 
especially  insist  upon  the  spread  of  contagion  by  oysters ;  Chantemesse 
has  published  several  convincing  cases. 

The  bacillus  of  Eberth,  as  is  well  known,  possesses  extraordinary 
vitality  and  powers  of  resistance.  As  Chantemesse  remarked  ten  years 
ago,  "  the  dominant  feature  in  the  aetiology  of  typhoid  fever  is  the  biological 
properties  of  Eberth's  bacillus,  its  resistance  to  desiccation,  to  cold  and  to 
heat,  the  modest  nature  of  its  needs,  its  faculty  of  supporting  itself  in  the 
presence  or  absence  of  oxygen.  On  leaving  the  human  body,  the  virus 
mixes  with  foodstuffs,  air,  dust,  soil,  river-mud,  water,  etc.,  and  maintains 
its  vitality ;  perhaps  it  even  shows  an  increase  of  strength  for  some  time." 

Bacteriology. — The  pathogenic  agent  in  typhoid  fever  was  discovered  by 
Eberth  in  1880.  Since  this  time  numerous  observers,  including  Friedlander 
and  Meyer  (1881),  Letzerich  (1885),  Gaffky  (1884),  Artaud,  Brieger  (1885), 
etc.,  have  verified  Eberth's  discovery,  and  have  added  many  interesting  facts. 

Eberth's  bacillus  can  be  cultivated  on  broth,  gelatine,  agar-agar,  and 
potato.  Colonies  of  Eberth's  bacillus,  obtained  by  culture  on  gelatine- 
plates,  and  examined  with,  a  low  power,  present  the  form  of  islets  with  cut 
edges.  "  They  appear  traversed  by  wrinkles,  wldch  are  more  or  less  marked 
throughout  their  whole  extent.  Their  surface  is  often  irregular,  and  the 
whole  colony  resembles  the  twisted  coUs  of  the  small  intestine.  The  com- 
bination of  these  two  aspects,  joined  to  the  shining  colour,  sometimes  causes 
the  colony  to  look  like  a  mountain  of  ice  "  (Chantemesse  and  Widal). 

In  cultures  the  B.  typhosus  is  polymorphous.  It  is  exceedingly  mobile, 
and  shows  no  tendency  to  agglutination.  As  a  rule,  it  has  the  shape  of  a 
small  rod,  with  rounded  ends,  while  its  length  is  three  times  its  breadth. 


1716  TEXT-BOOK  OF  MEDICINE 

In  addition  to  the  usual  forms,  the  B.  typhosus  is  sometimes  very  short,  or 
at  other  times  elongated  in  the  form  of  threads,  which  are  two  or  three  times 
as  long  as  the  bacillus.  The  stained  bacillus  often  presents  at  its  centre  or 
at  its  extremities  clear  spaces,  wrongly  taken  for  spores. 

After  staining,  we  may  see  cilia,  which  may  be  very  numerous  and  tuft- 
like, and  which  proceed  from  the  ends  of  the  rod  or  from  its  body.  Eberth's 
bacillus  is  found  in  the  fasces,  the  walls  of  the  intestine,  Peyer's  patches,  the 
mesenteric  glands,  the  liver,  the  kidneys,  the  lungs,  and  the  spleen,  from 
which  organ  it  may  be  obtained  during  life  by  puncture  with  a  capillary 
trocar  after  the  tenth  day  of  the  disease.  It  is  not  found  in  the  blood, 
except  in  that  from  the  rose  spots.  It  is  sometimes  found  in  the  urine,  as 
was  shown  by  Bouchard  before  its  morphological  characters  were  known. 

Cultures  of  Eberth's  bacillus  yield  a  specific  tj^ho-toxine,  which,  on 
injection  into  a  guinea-pig,  produces  marked  secretion  from  the  intestinal 
and  salivary  glands,  and  deprives  the  animal  of  the  power  of  voluntary 
motion.  The  microbe  of  typhoid 'fever  secretes  a  vaccine,  which  is  still 
under  study. 

Water  offers  an  excellent  natural  culture  medium,  and  most  epidemics 
of  typhoid  fever  at  the  present  day  may  be  explained  by  this  property. 

The  infiltration  of  cesspools  and  manure-heaps,  upon  which  the  dejecta 
of  typhoid  patients  are  sometimes  thrown,  are  quite  enough  to  pollute  the 
water  of  wells,  cisterns,  streams,  etc.,  with  the  result  that  a  local  epidemic 
is  seen,  or,  on  the  other  hand,  an  epidemic  appears  in  a  town  far  from  the 
primary  focus  of  contagion,  but  situated  on  the  same  river. 

This  fact  is  proved  by  the  recent  epidemics  at  Zurich,  Auxerre,  Ply- 
mouth, Pierrefonds,  Clermont-Ferrand,  and  Havre.  It  also  explains  how 
inhabitants  in  a  town  who  drink  the  water  from  one  source  may  be  attacked, 
while  those  whose  reservoirs  are  supplied  by  a  different  water  may  escape 
contagion.  This  fact  has  several  tunes  been  seen  in  Paris  (Chantemesse 
and  Widal),  where  the  water  of  the  Seine  above  and  below  the  city  (Thoinet) 
constantly  contains  typhoid  bacilli,  while  the  water  of  the  Vanne  and  of 
the  Ourcq,  as  a  rule,  does  not  contain  them. 

At  certain  seasons  of  the  year,  when  the  water  in  these  two  rivers  is 
low,  some  quarters  then  receive  their  supply  from  the  Seine,  with  the 
result  that  typhoid  fever  appears  there  almost  at  once  in  an  epidemic  form, 
and  it  has  been  proved  that  the  water  supplied  for  consumption  contains 
pathogenic  bacilli.  Oysters  may  harbour  the  B.  typhosus,  and  cause  typhoid 
fever,  just  as  they  may  transmit  cholera.  Flies  have  been  held  guilty  as 
propagating  agents. 

The  air  may  also  carry  the  contagion.  The  faeces  of  patients  with 
typhoid  fever,  mixed  with  the  soil,  are  finally  transformed  into  dust.  The 
bacilli,  by  reason  of  their  great  vitality,  preserve  in  a  latent  state  their 


TVIMlOin   nrSKASKS  1717 

patliogoui(^  properties  for  a  more  or  less  lengthy  period,  and  then,  niitigling 
with  the  air,  they  finally  enter  the  bronchi,  and  contagion  takes  place, 
although  much  less  fre([uently  than  by  ingestion  of  polluted  water.  In  a 
similar  way  linen  impregnated  with  the  fajcal  matter  from  typhoid  patients 
has  formed  an  important  element  of  contagion  in  some  families. 

The  B.  ti/pJiostis  can  be  inoculated  in  some  animals,  such  as  mice,  guinea- 
pigs,  and  rabbits.  The  soluble  products  of  various  microbes,  when  injected 
into  animals,  favour  infection  by  Eberth's  bacillus,  even  though  it  is  of 
slight  virulence  (Chantemesse  and  Widal,  Sanarelli).  The  disease  produced 
in  this  manner  is  not  a  copy  of  the  disease  in  man,  but  is  a  kind  of  experi- 
mental septicsemia,  which  allows  us  to  manipulate  the  virulence  of  the 
microbe,  and  to  make  attempts  at  vaccination  and  serotherapy  in 
animals. 

The  experiments  of  Chantemesse  and  Widal  have  shown  that  the  serum 
from  animals  vaccinated  with  the  soluble  products  of  cultures  of  Eberth's 
bacillus  possesses  immimizing  properties  against  the  action  of  the  virus, 
and  that  the  same  serum  also  possesses  curative  properties  in  experimental 
typhoid  infection  which  is  in  process  of  evolution.  The  serum  from  an 
individual  who  has  recovered  from  typhoid  fever  weeks,  months,  and  even 
years  previously  possesses  preventative  and  therapeutic  properties  against 
experimental  infection,  while  the  serum  of  an  individual  who  has  not  had 
typhoid  fever  is  not,  as  a  rule,  endowed  with  the  same  power. 

An  attempt  has  been  made  to  identify  the  B.  typhosus  with  the  B.  coH, 
a  micro-organism  always  present  in  the  bowel  (Rodet  and  Roux).  Chante- 
messe and  Widal  have  answered  the  various  arguments  brought  forward, 
and,  while  confining  themselves  to  clinical  study  and  pathological  anatomy, 
have  shoA\Ti  that  the  B.  coli,  in  passing  through  the  human  organism,  does 
not  assume  the  characters  of  Eberth's  bacillus,  as  had  been  supposed,  but 
that  it  preserves  its  own  proper  characters.  It  causes  in  man  common- 
place lesions,  and  never  those  which  are  special  to  typhoid  fever.  We 
know  that  the  B.  coli,  which  is  an  ordinary  inhabitant  of  our  digestive  tube, 
may,  like  the  pneimaococcus,  become  pathogenic,  and  cause  acute  pleurisy, 
suppurative  peritonitis,  cholera-like  complications,  and  even  suppurative 
infection  of  the  urinary  tract,  according  to  Krogius,  Renaut,  and  Achard. 

From  the  technical  point  of  view,  Chantemesse  and  Widal  have  always 
maintained  that  the  B.  typhosits  and  the  B.  coli,  though  apparently  similar, 
present  only  differences.  In  order  to  distinguish  these  two  microbes,  they 
give  a  simple  and  easy  method  of  procedure,  which  consists  in  sowing  the 
one  or  the  other  upon  broth  to  which  lactose  has  been  added.  Under  these 
conditions,  the  B.  coli  causes  bubbles  of  gas,  which  are  always  absent  when 
the  broth  is  inoculated  with  Eberth's  bacillus. 

The  coagulating  property  (Widal),  discussed  under  Sero-Diagnosis, 
11.  109 


1718  TEXT-BOOK  OF  MEDICIIS^E 

closes  the  epoch  of  these  discussions,  and  proves  the  specific  nature  of  the 
B.  typhosus. 

Pathological  Anatomy. — "  Considering  only  the  first  steps  in  the  patho- 
logical anatomy,  we  notice  the  invasion  and  the  multiplication  of  the  bacilli, 
and  the  struggle  on  the  part  of  the  phagocytes.  Further,  the  fixed  cells  of 
the  tissues,  being  incapable  of  destroying  the  microbe,  submit  to  its  attacks, 
and  show  granular,  fatty,  waxy,  pigmentary,  and  other  degenerations  of 
varying  nature  and  gravity.  In  addition  to  these  lesions,  we  find  changes 
depending  on  the  physiology  and  structure  of  the  vessels. 

"  The  course  of  this  process,  when  studied  in  any  organ,  may  be  summed 
up  as  follows  :  infiltration  with  bacilli,  phagocytic  reaction,  circulatory 
changes,  degeneration  of  the  parenchyma,  normal  or  abnormal  repair 
(Chantemesse). 

It  is  impossible  to  give  a  better  sketch  of  the  process.  The  characteristic 
changes  in  typhoid  fever  afiect  the  small  intestine,  and  are  most  marked  in 
the  isolated  follicles  and  in  Peyer's  patches. 

The  mucous  membrane  of  the  small  intestine  is  composed  of  reticular  connective 
tissue,  containing  in  its  meshes  a  large  number  of  lymphatic  cells  (His).  The  isolated 
or  agminated  closed  follicles  belong  to  this  mucous  membrane  ;  the  former  are  rounded, 
and  measure  |^  to  1  millimetre  in  diameter,  while  the  latter  are  flattened  one  against  the 
other,  and  arranged  in  groups  of  twenty,  thirty,  fifty,  or  sixty,  to  form  the  Peyer's 
patches,  which  commence  in  the  ileum,  and  become  more  numerous  towards  the 
termination  of  the  small  intestine.  They  are  situated  on  the  free  border  of  the  intestine, 
opposite  to  the  insertion  of  t?he  mesentery ;  their  prominence  and  their  opaque  nature 
render  them  conspicuous  with  transmitted  Kght.  They  are  elongated  in  form,  and 
parallel  to  the  long  axis  of  the  bowel ;  their  long  diameter  varies  from  a  few  millimetres 
to  several  centimetres,  and  their  number  from  thirteen  to  fifty.  Both  the  isolated 
foUicles  and  the  Peyer's  patches  are  composed  of  reticular  lymphatic  tissue,  which  is 
very  vascular  and  continuous  with  the  adjacent  tissue,  without  any  limiting  membrane. 

Post  mortem  the  intestinal  lesions  vary,  according  to  the  stage  of  the 
disease.     They  present  the  following  peculiarities  : 

1.  During  the  first,  or  so-called  catarrhal,  period,  which  lasts  from  four 
to  five  days,  the  mucous  membrane  is  congested,  and  secretes  diarrhoeal 
fluid ;  the  isolated  follicles  stand  out,  as  in  cholera  (psorenteria) ;  and  the 
Peyer's  patches  are  swollen.  During  this  period  the  bacilli,  which  abound 
in  the  mucus,  enter  the  glands  of  Lieberkiihn,  and  reach  the  deep  layers  of 
the  mucous  membrane  either  individually  or  in  colonies.  Some  days  later 
the  follicles  assume  the  appearance  of  hard  and  prominent  buttons,  and 
the  Peyer's  patches  present  two  difEerent  forms — namely,  hard  and  soft 
(Louis).  The  hard  patches  are  resistant  to  the  touch  and  very  prominent, 
thus  bearing  witness  to  the  severity  of  the  process,  which  involves  most  of 
the  follicles  in  the  patch.  The  soft  patches  are  less  prominent  and  more 
supple  to  the  touch,  because  the  foUicles  in  the  patch  are  only  in  part 
affected.     It  is  possible  that  they  may  represent  a  more  advanced  period 


TYi'liUll)   DLSEASKS  1719 

of  tho  process.  IMu!  patches  called  crinn^ed,  or  ntidiliir,  owe  their  appear- 
ance to  the  imecjual  (listrihutioii  of  the  innaiiimatioti  in  tin;  follicles  which 
make  up  the  patch. 

On  secticm,  the  follicles  and  patches  present  an  a])f)<^araiice  reseinbliiij? 
the  tissue  of  the  lymphatic  glands.  There  is  abundant  proliferation  of  the 
adenoid  tissue,  and  the  lymphatic  infiltration  extends  to  the  connective 
tissue  around  the  <.;lands,  and  to  the  deep  layer  of  the  mucous  membrane. 
The  tubular  glands  are  elongated,  doubtless  because  of  the  development 
which  the  septa  undergo ;  the  vessels  and  the  capillaries  are  engorged  with 
blood,  and  thrombosis  is  frequent.  During  this  period  the  bacilli  have 
penetrated  the  follicles  and  Peyer's  patches,  and  the  phagocytes  are  present 
in  abundance,  but  the  most  virulent  bacilli  are  difficult  to  ingest  and  digest. 
The  lymphatic  vessels  are  blocked  with  leucocytes  and  bacilli.  The  bacilli  enter 
the  vessels,  and  are  found  in  the  submucous  and  even  in  the  muscular  coats, 

2.  Ulceration  begins  about  the  tenth  day  of  the  disease.  The  bacilli 
and  their  toxines,  and  the  dystrophy  consecutive  to  obliteration  of  the 
vessels,  affect  the  fixed  cells  of  the  tissue  and  the  leucocytes,  which  have 
accumulated  there  in  numbers,  causing  granulo-fatty  and  vitreous  degenera- 
tion, followed  by  necrosis  and  ulceration. 

The  ulceration  takes  place  in  successive  stages,  and  often  commences  in 
the  patches  nearest  to  the  ileo-csecal  valve.  The  mortification  of  the  soft 
patches  is  slow  and  molecular,  so  that  the  resulting  ulceration  is  not  very 
deep.  In  the  hard  patches,  on  the  other  hand,  the  mortification  seizes  on 
the  most  prominent  parts  of  the  patch,  and  forms  cores,  markedly  stained 
with  bile,  which  is  secreted  in  abundance  at  this  period  of  the  disease. 
Next,  the  dead  portions  become  detached,  and  leave  deep  ulcerations, 
which  sometimes  reach  the  number  of  six  or  seven  in  a  single  patch,  and 
which  usually  rest  on  the  muscular  coat  of  the  intestine.  The  small  ulcers 
are  cupuliform,  or  oval ;  the  large  ulcers  are  aligned  in  the  long  axis  of  the 
intestine,  and  may  measure  some  inches. 

The  ulcerated  surfaces  are  covered  with  fleshy  buds.  They  are  poor  in 
typhoid  bacilli,  whose  part  is  played,  and  rich  in  other  organisms,  which 
sometimes  cause  secondary  infections. 

The  inflammation  also  attacks  the  connective  tissue  between  the  two 
muscular  layers  and  the  subserous  tissue,  and  the  intestinal  peritoneum 
over  the  ulcerated  hard  patches  is  sometimes  red,  congested,  and  thickened. 
"  It  is  certain  that  the  infiltration  of  all  the  coats  of  the  intestine  by  cells, 
as  well  as  the  softening  and  friability  of  the  fibrous  bundles,  favour  ulcera- 
tion, which  extends  in  depth  towards  the  serous  coat,  and  subsequent 
perforation  (Cornil  and  Ranvier).  The  elimination  of  the  sloughs  and  the 
embryonic  structure  of  the  vascular  walls  favour  haemorrhage. 

In  sixty  out  of  200  autopsies  (Leudet)  the  large    intestine    presents 

109—2 


1720  TEXT-BOOK  OF  MEDICINE 

t}'p]ioid  ulcers,  because  it  also  possesses  lymphoid  tissue,  and  there  are  cases 
in  which  the  lesion  is  exclusively  situated  in  the  colon  (coleo-typhus). 

3.  Cicatrization  of  the  intestinal  ulcers  takes  place  slowly,  but  complete 
repair  occurs.  It  is  sometimes  followed  by  fibrous  change,  but  stenosis  of 
the  bowel  is  never  found.  The  surface  of  the  cicatrized  patches  may  remain 
pigmented  for  several  years. 

In'some  exceptional  cases  the  intestinal  lesions  may  be  absent,  or  scarcely 
appreciable.     In  the  foetus  they  are  wanting. 

The  mesenteric  glands,  which  normally  are  no  larger  than  a  lentil,  and 
are  separated  from  one  another,  may  be  as  large  as  a  walnut  in  the  first 
week  of  the  disease.  They  form  a  tumour,  composed  of  a  chain  of  glands, 
in  front  of  the  vertebral  column.  During  this  period  the  glands  are  usually 
hard  and  globular.  The  microscope  shows  that  the  lesion  consists  in  dilata- 
tion of  the  vessels,  with  considerable  proliferation  of  lymphatic  cells.  At 
a  later  period,  during  the  second  week,  the  glands  become  soft  and  decrease 
in  size.  Those  which  correspond  to  the  most  diseased  portions  of  the  bowel 
are  themselves  the  most  affected.  The  change  in  the  glands,  however, 
appears  to  be  independent  up  to  a  certain  point,  for  very  large  mesenteric 
glands  are  met  with,  although  the  intestinal  lesion  is  trifling.  The  retro- 
peritoneal glands,  and  in  some  cases  the  bronchial  and  peripheral  glands, 
are  afiected  by  the  typhoid  poison.  The  bacilli  and  the  phagocytic  reaction 
are  seen  in  the  glands,  just  as  in  the  Peyer's  patches. 

The  spleen  is  large,  soft,  friable,  congested,  and  engorged  with  lymphatic 
cells.  It  is  sometimes  the  seat  of  small  haemorrhages.  Its  normal  weight 
is  5  ounces,  but  it  may  exceed  12  ounces  in  this  disease.  The  lesions  include 
infiltration  by  phagocytes,  changes  in  the  arteries,  marked  congestion,  and 
swelling.  They  are  caused  by  the  bacilli,  which  swarm  in  the  parenchyma 
from  the  very  first.  A  drop  of  blood  drawn  from  the  spleen  during  the 
first  ten  days  of  typhoid  fever  always  yields  colonies  of  the  B.  typhosus. 

The  liver  is  slightly  enlarged.  Its  colour  resembles  that  due  to  advanced 
fatty  degeneration.  The  cells  show  cloudy  swelling  or  fatty  degeneration. 
Numerous  Ijmaphoid  nodules  are  found.  The  bacilli  are  present  in  large 
numbers  in  the  portal  vein  and  its  capillaries.  The  bUe-ducts  and  the  gall- 
bladder show  catarrhal  changes,  suppuration,  or  ulceration  (B.  typhosus 
and  B.  coli). 

The  changes  in  the  muscular  system,  though  frequent,  but  not  constant, 
are  vitreous  (Zenker,  Weber)  or  granulo-vitreous  degeneration  (Hayem), 
changes  also  found  in  other  diseases,  but  rarely  as  marked  as  in  typhoid 
fever.  This  muscular  dystrophy,  which  has  a  predilection  for  certain 
muscles,  does  not  always  spare  the  heart,  and  two  concomitant  lesions  are 
found  on  histological  examination,  the  one  afiecting  the  muscular  fibre  and 
the  other  the  small  vessels.     The  muscular  fibre  loses  its  transparency  and 


TVrilUlI)   DISEASES  ITi'l 

its  striation.  It  hocomos  granular,  and  is  irililt rated  with  fatty  ol«Tn<'nt.s. 
The  surrounding  (•(•nnectivo  tissue  and  the  pcriniysiuni  are  the  seat  of  active 
proliferation,  which  fills  the  surface  of  the  primary  bundles.  The  tunica 
externa  of  the  small  vessels  participates  in  this  proliferation,  and  the  tunica 
interna  shows  endarteritis  (Hayem,  Laveran).  These  changes  are  doubtless 
of  importance  in  the  production  of  the  intramuscular  haemorrhages  some- 
times seen  in  typhoid  fever.  The  B.  typhosus  is  often  found  in  the  cardiac 
muscle  (Chanteinesse  and  Widal). 

Pathological  Physiology. — The  discordance  existing  at  the  onset  of  the 
disease  between  the  pulse-rate  and  the  rise  of  temperature  is  an  interesting 
peculiarity.  The  pulse  beats  less  frequently  than  we  should  expect,  con- 
sidering the  height  of  the  fever.  In  some  cases  the  rate  may  be  diminished. 
Murchison  saw  a  patient  whose  pulse  was  only  sixty  during  the  early  stages 
of  the  fever.  In  the  later  stages  of  the  disease,  when  the  pulse  becomes 
quickened  on  the  verge  of  severe  complications,  this  sign  is  so  valuable  that 
examination  of  the  pulse  has  been  considered  as  the  keynote  in  the  prognosis 
of  typhoid  fever  (Liebermeister).  To  what  are  these  two  successive  condi- 
tions in  the  working  of  the  heart  due  ? 

According  to  Chantemesse  and  Courtade,  the  action  of  the  typhoid 
toxine  is  more  clear  in  cold-blooded  animals,  because  it  is  not  disturbed 
by  the  severe  phenomena  of  reaction  that  occur  in  warm-blooded  creatures. 
A  dose  of  typhoid  toxine  (fatal  in  a  few  hours)  injected  under  the  sldn  of  a 
frog  causes  after  a  quarter  of  an  hour  general  sluggishness,  which  hampers 
the  animal's  movements.  They  become  more  and  more  difficult,  and  the 
animal  does  not  respond  to  any  sensory  stimulus.  If  the  thorax  is  opened, 
the  heart  is  seen  to  beat  very  slowly,  and  then  to  stop  in  diastole.  While 
the  paralysis  lasts,  we  can  show  that  the  muscles  react  well  to  the  faradic 
current.  The  poison  attacks  neither  the  terminal  end-plates  of  the  motor 
nerves  (as  can  be  proved  by  the  classical  experiment  of  Bernard)  nor 
the  nerve  filaments,  the  excitation  of  which  brings  about  the  usual  muscular 
contraction.  The  toxine  first  acts  upon  the  spinal  cord,  and  we  know  that 
section  of  the  frog's  head  increases  the  reflex  irritability  of  the  cord.  If 
this  section  is  made  on  a  frog  poisoned  with  t}Tphoid  toxine,  we  see  that 
the  reflex  irritability  has  disappeared,  and  yet  the  electrical  excitation  of 
the  cord  through  the  white  tracts  still  causes  strong  contractions  in  the 
limbs.  In  the  living  animal,  therefore,  the  typhoid  poison  at  first  acts  upon 
the  grey  matter  of  the  cord.  We  shall  see  that  it  affects  later  the  nerve  cells 
of  the  cerebral  centres  and  of  the  cardiac  ganglia. 

Chantemesse  and  Lamy,  employing  defibrinated  blood  from  a  normal 
rabbit,  in  order  to  produce  an  artificial  circulation  through  the  heart  of  a  • 
tortoise,  have  found  that  the  cardiac  contractions  remain  perfectly  regidar 
for  more  than  twenty-four  hours.     If  the  blood  is  taken  from  a  rabbit  which 


1722  TEXT-BOOK  OF  MEDICINE 

haK  an  hour  previously  has  received  a  fatal  dose  of  typhoid  toxiae,  it  behaves, 
as  regards  the  heart  of  the  tortoise,  in  practically  the  same  way  as  normal 
blood.  Further,  the  same  dose  of  toxine  added  {in  vitro)  to  normal  defibri- 
nated  blood  no  longer  produces  any  effect.  If  the  dose  of  toxine  added  {in 
vitro)  is  two  or  three  times  stronger,  we  witness  after  several  hours  the  slow 
appearance  in  the  heart  of  the  tortoise  of  disturbances,  characterized  by 
slowness  and  feebleness  of  the  beats,  and,  finally,  arrest  of  the  heart  in  dias- 
tole. These  phenomena  result  from  slow  poisoning  of  the  heart.  When 
the  heart  is  arrested  in  diastole,  electric  stimuli,  massage,  and  the  passage 
of  fresh  blood  are  unable  to  cause  it  to  beat  again.  When  the  results  have 
been  less  marked,  the  substitution  of  normal  blood  for  the  toxic  blood 
allows  the  heart  gradually  to  resume  its  work.  The  addition  to  the  blood, 
in  vivo  or  in  vitro,  of  typhoid  toxine  then  produces  cardiac  symptoms, 
characterized  by  slowing,  enfeeblement,  and  arrest  of  the  heart  in  diastole. 

These  effects  of  pure  typhoid  poison  upon  the  heart  explain  the  cardiac 
symptoms  at  the  onset  of  typhoid  fever.  As  regards  the  cardiac  phenomena 
in  the  later  stages  of  the  disease,  the  experiments  of  Chantemesse  and  Lamy 
also  furnish  some  information  on  this  point.  Indeed,  if  we  take  blood 
from  an  animal  sufficiently  long  after  the  injection  of  typhoid  toxine,  while 
the  animal  is  in  the  reaction  stage — for  instance,  in  the  sheep  when  the 
fever  reaches  its  maximum  point,  or  in  the  rabbit  when  the  temperature 
finally  begins  to  fall — the  effects  of  the  artificial  circulation  through  the 
heart  of  the  tortoise  are  diametrically  opposite  to  those  above  mentioned. 
This  blood  acts  rapidly.  It  causes  marked  tachycardia  and  short  systole, 
and  the  effects  gradually  disappear  as  if  the  blood,  possibly  through  the 
influence  of  oxygen,  lost  the  property  of  exciting  the  heart.  It  is  sufficient 
to  add  a  fresh  dose  of  blood,  taken  from  the  animal  suffering  from  fever, 
in  order  to  reproduce  the  same  effects  of  excitation  in  the  heart  of  the 
tortoise. 

Chantemesse  and  Lamy  draw  the  following  conclusions  from  their 
researches  :  (1)  As  the  result  of  reaction,  toxic  substances  are  produced  in 
the  organism,  but  their  properties  are  distinct  from  those  of  the  toxine. 
These  substances  manifest  themselves  physiologically  by  effects  which  are 
opposite  to  those  caused  by  the  primary  typhoid  poison.  (2)  These  new 
substances,  once  formed,  are  not  amenable  to  treatment  with  antitoxic 
serum,  which  neutralizes  only  the  primary  typhoid  poison. 

Treatment. — The  cold  bath  may  be  regarded  almost  as  a  specific  in 
typhoid  fever.  I  have  studied  carefully  the  action  and  the  results  of  the 
cold  bath  for  many  years,  both  in  hospital  and  in  private  practice,  and  I 
am  ready  to  do  the  fullest  justice  to  Brand's  method.  I  am  quite  convinced 
that  the  cold  bath  is  as  efficacious  in  typhoid  fever  as  is  quinine  in  malaria 
or  mercury  in  syphilis. 


TYPHOID   DISEASES  1723 

I  would  state,  as  the  first  jirinciple,  that  every  patient  suffering  from 
typhoid  fever  should  be  treated  with  cold  baths.  At  the  onset  of  typhoid 
fever,  even  tliough  the  rose  spots  have  not  yet  appeared,  every  indi\ndual 
who  is  taken  ill  with  fever,  accompanied  by  headache,  insomnia,  epistaxis, 
loss  of  appetite,  prostration,  and  a  rising  temperature,  which  reaches  about 
102°  F.  at  night,  is  probably  suffering  from  typhoid  fever,  and  should  be 
treated  with  cold  baths.  If  we  delay  giving  cold  baths  imtil  spots  have 
appeared  and  the  temperature  has  reached  104°  F.,  we  lose  valuable  time. 

Cold  baths  are  most  efficacious  when  they  are  given  at  the  very  com- 
mencement of  the  disease.  I  have  often  proved  the  truth  of  this  statement. 
When  we  receive  in  hospital  a  patient  who  has  had  typhoid  fever  for  twelve 
or  for  thirteen  days,  cold  baths  are  not  as  efficacious  as  in  a  sufferer  who 
has  been  treated  at  an  earlier  period.  Cold  baths  have  not  only  a  beneficial 
action  upon  the  symptoms  of  the  moment,  but  they  also  have  an  action 
upon  the  symptoms  of  the  future — that  is  to  say,  they  change  an  attack 
of  fever  which  would  have  been  very  severe  into  one  of  moderate  severity. 
Unfortunately,  we  are  often  too  slow  in  making  our  decision,  especially  in 
private  cases. 

The  bath  treatment  does  not  only  aim  at  removing  complications  which 
have  already  appeared  ;  it  is  employed  to  moderate  the  disease,  to  modify 
its  course,  and  to  lower  the  vindence  of  the  bacillus.  Accordingly,  it  is 
not  a  method  of  treatment  reserved  for  special  symptoms ;  it  practically 
comprises  the  whole  treatment. 

The  bath  is  placed  near  the  patient's  bed,  the  temperature  of  the  water 
being  75°  F.  The  patient  is  placed  naked  in  the  bath,  and  water  is  added 
until  the  temperature  gradually  falls  to  68°  F.  As  the  cold  water  is  added, 
an  equal  quantity  of  water  is  drawn  off  from  the  bath.  This  procedure 
has  the  advantage  of  avoiding  or  lessening  the  discomfort  and  chill  which 
accompany  the  bath  given  at  68°  F.  on  commencement.  The  patient  should 
remain  in  the  bath  twelve  to  fifteen  minutes.  Cold  compresses  are  applied 
to  the  head,  and  the  body  and  limbs  may  be  rubbed. 

On  leaving  the  bath  the  patient,  wbo  has  not  been  dried,  is  placed  in  a 
blanket,  and  well  covered  up.  He  is  given  warm  tea  with  a  teaspoon- 
ful  of  brandy,  and  then  left  quiet.  The  bath  is  nearly  always  followed 
by  a  feeling  of  comfort,  sleep,  perspiration,  and  marked  fall  of  temperature. 

Another  bath  is  given  three  or  four  hours  later,  according  to  the  case, 
the  patient  taking  six  or  eight  baths  in  the  twenty-four  hours.  The  number 
of  baths  is  regulated  by  the  condition  of  the  patient  and  by  the  height  of 
the  temperature.  If  the  general  condition  is  good,  if  nervous  symptoms  are 
absent,  and  if  the  temperature  does  not  exceed  104°  F.,  or  if  it  does  not  rise 
rapidly  after  the  temporary  fall  which  follows  the  bath,  it  will  be  sufficient 
to  bathe  the  patient  four  times  in  the  twenty-four  hours.     On  the  other 


1724  TEXT-BOOK  OF  MEDICINE 

hand,  if  the  temperature  is  very  high,  and  if  it  remains  so  in  spite  of  the 
baths,  or  if  the  patient  shows  a  tendency  to  ataxo-adynamia,  the  tempera- 
ture of  the  bath  must  be  lowered,  and  a  bath  given  every  three  hours  at 
68°  F,,  the  temperature  being  gradually  lowered  to  60°  F. 

Balneotherapy  must  be  continued  during  the  whole  period  of  the  disease, 
but  the  number  of  baths  is  diminished  and  their  temperature  gradually 
raised  in  proportion  as  the  fever  falls  and  convalescence  approaches. 

If  the  patient  has  soiled  the  bath-water  with  faeces  or  with  urine,  it 
must  be  changed  for  the  next  bath.  In  the  opposite  case,  it  is  unnecessary 
to  change  the  water  more  than  once  in  twenty-four  hours.  In  the  interval 
between  the  baths  it  is  useful  to  place  upon  the  abdomen  of  the  patient 
cold  compresses,  changed  frequently ;  but  the  patient  should  not  be  wakened 
if  he  is  sleeping  comfortably. 

Let  us  next  consider  the  contra-indications. 

Are  we  to  place  the  patient  who  is  perspiring  freely  in  the  cold  bath  ? 
In  such  a  case,  it  is  better  to  wait  till  the  perspiration  ceases. 

Are  we  to  put  a  patient  suffering  from  bronchitis  or  from  broncho- 
pulmonary congestion  in  the  bath  ?  Bronchitis  in  typhoid  fever  forms  part 
of  the  morbid  process,  with  or  without  secondary  infection,  and  is,  therefore, 
to  be  treated  in  the  same  way.  In  typhoid  fever,  as  in  measles  of  the  typhoid 
form,  I  have  remarked  that  the  broncho-pulmonary  symptoms  are  improved 
by  cold  baths. 

Are  we  to  place  a  patient  who  has  intestinal  haemorrhage  in  the  bath  ? 
I  do  not  hesitate  to  do  so.  I  have  lost  only  three  patients  suffering  from 
haemorrhage  and  treated  by  cold  baths.  According  to  my  experience, 
intestinal  haemorrhage  is  neither  brought  on  again  nor  increased  by  the 
baths.  Improvement  follows,  and  success  may  be  obtained  even  in  cases 
which  appear  desperate.  Accordingly,  except  for  special  reasons,  and 
unless  the  haemorrhage  by  its  extreme  abundance  threatens  to  carry  ofi 
the  patient  with  syncope,  I  am  of  opinion  that  intestinal  haemorrhage  is  not 
a  contra-indication  to  the  cold  bath. 

Are  feeble  heart  action,  intermittence,  and  signs  of  myocarditis  a  contra- 
indication to  the  use  of  cold  baths  ?  They  are  if  these  signs  be  very  marked, 
but  we  can  modify  them  by  treatment,  and  the  cold  baths  are  then  again 
indicated. 

Balneotherapy  does  not  comprise  the  whole  treatment  of  tj^^hoid 
fever,  and  another  indication  of  the  highest  importance  must  be  fulfilled 
— ^namely,  that  of  nourishing  the  patient.  For  this  purpose,  nothing  is 
better  than  milk  diet,  which  is  at  once  food  and  drink,  as  well  as  being 
diuretic.  In  hospital  my  patients  take  in  twenty-four  hours  3  pints  of 
milk,  to  which  lime-water  has  been  added.  In  addition  to  the  milk,  they 
are  given  2  or  3  pints  of  pure  fresh  water,  to  which  lactose,  with  citron, 


TVl'ilUlD    DISEASES  1725 

orange,  clarot,  or  c]iam])agne  may  or  may  not  be  addccl.  if  the  patient 
cannot  take  milk,  he  is  given  meat,  or  vegetable  broth  and  raw  eggs,  but 
nothing  is  so  good  as  milk  diet. 

As  the  result  of  this  treatin(>nt  with  (lold  })aths,  milk  diet,  and  abundant 
fluid,  the  urine  is  chjar,  and  the  patient,  who  was  passing  only  V2  or  I'.i 
ounces  of  thick  urine,  now  voids  3  or  4  pints  of  practically  normal  urine. 
This  abundant  diuresis  is  one  of  the  best  features  in  prognosis.  As  long 
as  the  kidneys  act  well,  even  though  the  symptoms  are  severe,  we  may 
be  quite  satisfied,  for  the  poison  is  almost  eliminated,  and  severe  complica- 
tions are  usually  absent. 

This  method  of  treatment  has  changed  the  classical  picture  of  typhoid 
fever.  We  rarely  see  the  dry  red  tongue,  sordes  on  the  teeth,  tympanitic 
abdomen,  and  general  condition  of  stupor.  The  disease  has  changed  its 
appearance,  and  its  two  great  factors,  intoxication  and  infection,  are 
practically  conquered.  I  may  even  say  that,  as  a  result  of  cold  baths 
given  in  good  time,  severe  complications  have  become  much  less  common, 
thus  lowering  the  death-rate.  Laryngo-typhus,  peritonitis,  perforation  of 
the  bowel,  and  ataxic  s}Tnptoms  are  seen  much  less  frequently  than  formerly, 
and  I  have  not  seen  a  case  of  sudden  death  for  several  years,  although  I  did 
so  fairly  often  prior  to  this  method  of  treatment. 

Are  these  fortunate  results  due  to  the  treatment  itself,  or  do  they  result 
from  a  natural  change  in  the  cyclical  evolution  of  the  disease  ?  Is  not 
typhoid  fever  less  fatal  than  it  was  twenty  years  ago  ?  Has  it  become  less 
virulent  in  nature  ?*  These  hypotheses  are  admissible,  for  the  history  of 
medicine  tells  us  that  epidemic  diseases  appear  to  undergo  not  only  changes 
in  different  years  and  seasons  (medical  constitution),  but  they  also  appear 
to  undergo  more  lasting  changes  (Stoll's  stationary  fever).  I  am  quite 
willing  to  admit  this  hypothesis,  and  I  have  respect  for  certain  traditions 
which  have  been  handed  down  to  us  by  our  forebears  ;  but  I  cannot  forget 
that  in  a  number  of  circumstances,  and  notably  in  the  treatment  of  typhoid 
fever,  the  greatest  progress  has  been  realized.  Systematic  balneotherapy, 
when  properly  applied,  has  reduced  to  5,  6,  or  7  per  cent,  the  mortality  in 
typhoid  fever,  which  was  formerly  18  to  20  per  cent.,  and  in  this  respect 
immense  progress  has  been  realized.f 

For  the  early  headache  we  may  give  antipyrin  or  aspirin,  cold  com- 
presses being  applied  to  the  head,  and  frequently  changed. 

Purgatives  are  indicated  at  the  onset  of  the  disease,  but  later,  when 
ulceration  is  present,  we  must  give  only  enemata  or  gentle  laxatives,  such 

*  I  find  that  the  epidemics  of  typhoid  fever  which  we  have  dealt  with  in  Paris  have 
been  more  severe  and  fatal. 

f  It  must,  however,  be  remembered  that  in  the  last  few  years  wo  have  had  in  the 
comilry,  as  well  as  in  Paris,  very  severe  epidemics,  Avith  high  mortality. 


1726  TEXT-BOOK  OF  MEDICINE 

as  manna,  in  doses  of  from  3  to  5  drachms  in  milk.  In  the  case  of  constipa- 
tion, I  usually  prescribe  tliis  mixture  of  milk  and  manna,  and  have  often 
seen  its  beneficial  action. 

Diarrhoea  is  checked  by  lime-water,  Sydenham's  decoctum  album,  in 
doses  of  5  ounces  daily,  or  salicylate  of  bismuth  in  a  daUy  dose  of  30  to 
90  grains.  Intestinal  antisepsis  (Bouchard),  if  rigorously  employed,  is 
very  difficult  to  carry  out,  and  is  sometimes  ill  borne  by  patients. 

In  case  of  pulmonary  congestion,  dry-cupping  of  the  thorax  and  of  the 
legs  may  be  employed.  The  cupping-glass  is  applied  thirty  or  forty  times 
morning  and  evening.  Wet-cupping  and  leeches  may  also  be  used.  Care 
must  be  taken  to  raise  the  bed,  so  that  the  patient  is  in  the  sitting  posture. 

The  following  draught,  in  spoonful  doses,  may  be  employed  for  intestinal 
hsemorrhage  s 

Water         . .  . .  . .  . .     nicxx. 

Syrup  of  rhatany    , .  . .  . .     mxxx. 

Rabel  water  . .  . .  . .     niii. 

If  the  heart  is  weak  and  the  pulse  is  feeble  and  irregular,  subcutaneous 
injections  of  caffeine  should  be  given. 

Musk  (10  grains),  ether,  chloral,  and  bromide  of  potassium  are  of  con- 
siderable service  in  the  nervous  forms  with  ataxia. 

In  adynamic  cases,  with  a  tendency  to  coUapse,  we  must  employ  tinc- 
tures of  kola,  coca,  or  cinchona,  acetate  of  ammonia,  brandy,  subcutaneous 
injections  of  ether,  and  rubbing  with  alcohol. 

I  would  recommend,  provided  the  kidneys  are  normal,  injections  of 
serum,  repeated  several  times  during  the  day.  I  usually  add  benzoate  of 
caffeine.     For  further  details,  see  the  Appendix  on  Therapeutics. 

Quinine  should  be  reserved  for  special  cases  in  which  the  fever  appears 
to  show  a  malarial  type.  As  I  have  explained  the  treatment  of  typhoid 
peritonitis  and  of  paratyphoid  appendicitis  in  detail,  I  shall  not  refer  to  it 
again. 

Eeisores  should  be  washed  with  a  weak  solution  of  hot  boric  acid,  or 
with  a  solution  of  sublimate  (4  in  1,000),  and  dusted  with  powdered  cin- 
chona. 

The  details  given  as  to  the  pathogenesis  of  typhoid  fever  show  clearly 
what  prophylactic  measures  must  be  employed.  As  soon  as  an  epidemic 
appears  in  a  house,  in  a  camp,  or  in  a  school,  the  patients  must  be  isolated, 
the  healthy  removed,  and  an  active  search  made  for  the  origin  of  the  disease, 
in  order  to  remove  it. 

Serotherapy. — Serotherapy  in  typhoid  fever  is  based  on  the  experi- 
mental fact  that  animals  may  gradually  become  accustomed  to  doses  of 
typhoid  poison  capable  of  killing  healthy  animals,  and  that  from  this  time 
their  blood  has  acquired  properties  antagonistic  to  those  of  the  typhoid  virus. 


TYnrorp  dtskases  1727 

The  problem  at  issue  is  to  know  whether  the  senim  of  immunized  animals 
may  profitably  be  injected  into  persons  suffering  from  typhoid  fever,  and 
what  is  the  measure  of  its  efficacy. 

Several  poisons  are  present  in  the  bacillus  of  typhoid  fever,  just  as  in 
all  pathogenic  microbes.  The  poison  upon  which  the  peculiar  symptoms 
of  typhoid  fever  in  man  depend  was  isolated  first  by  Chantemesse.  It  has 
the  characteristic  of  being  very  sensitive  to  oxygen.  It  multiplies  rapidly 
in  certain  culture  media,  and  is  destroyed  very  quickly  by  contact  with  air. 
The  effects  produced  by  injecting  it  into  animals  have  been  studied  by 
Chantemesse  and  Balthazard.  The  soluble  toxine,  when  injected  into  the 
blood,  has  little  effect  on  the  red  corpuscles,  but  shows  an  energetic  action 
on  the  white  blood-corpuscles,  and  especially  upon  the  polynuclear  cells. 
If  a  rapidly  fatal  dose  is  given,  it  produces  hypoleucocytosis,  which  increases 
till  death.  With  a  smaller  dose,  the  initial  destruction  of  polynuclear  cells 
is  followed  by  a  hyperleucocytic  reaction. 

In  the  spleen  the  toxine  produces  a  double  series  of  changes.  In  the 
first  place,  it  increases  the  number  and  the  size  of  the  macrophages  which 
are  present  in  the  pulp  and  in  the  lymphatic  follicles,  and  causes  them  to 
ingest  and  to  destroy  the  white  and  red  corpuscles  poisoned  by  the  toxine. 
In  the  second  place,  it  causes  a  new  formation  of  the  elements  of  the 
lymphogenous  series  in  the  follicles  and  in  Billroth's  cords,  thiis  constituting 
an  act  of  repair. 

In  the  lymphatic  glands  and  Payer's  patches  the  poison  produces  the 
same  hypertrophy  as  in  the  spleen  (Balthazard),  calling  into  activity  the 
macrophages,  which  are  soon  filled  with  red  cells,  and  causing  enlargement 
of  the  lymphocjrtes  and  rapid  multiplication  of  the  cells  of  the  follicles. 

The  bone-marrow  becomes  the  seat  of  great  activity.  Its  usual  yellow 
tint  gives  place  to  a  reddish- violet  colour  when  the  intoxication  is  fatal,  and 
blood  flows  out  on  section.  The  red  corpuscles  pass  through  the  broken 
cells  of  the  capillaries,  invade  the  intervesicular  bands,  and  check  the 
cellular  proliferation.  In  the  slighter  forms  of  poisoning,  however,  we  find 
that  the  marrow  rapidly  gives  birth  to  polynuclear  corpuscles  destined  to 
replace  those  destroyed  by  the  toxine. 

In  the  intestine,  besides  abundant  diarrhoea,  we  may  note  dilatation  of 
the  vessels,  oedema  of  the  connective  tissue  of  the  villi  and  of  the  sub- 
mucosa,  as  well  as  an  increase  in  the  epithelial  cells  of  the  mucous  mem- 
brane. 

In  the  liver  congestion  is  seen,  with  cloudy  swelling  and  fatty  degenera- 
tion of  the  cells.  The  amoimt  of  glycogen  is  diminished,  and  the  lecithin 
accumulates  (Balthazard). 

The  kidney  is  especially  affected  by  the  typhoid  toxine.  The  most 
frequent  changes  comprise  degeneration  of  the  cells  of  the  convoluted 


1728  TEXT-BOOK  OF  MEDICINE 

tubules,  abrasions,  blocking  of  the  tubules  witli  amorphous  debris  and 
cylindrical  casts,  glomerulitis,  and  in  chronic  cases  fibrous  changes. 

If  we  compare  the  preceding  lesions  vvlth  the  pathological  anatomy  of 
human  typhoid  fever,  we  cannot  mistake  the  close  resemblance. 

Immimization  of  horses  by  repeated  injection  of  a  similar  toxine  requires 
much  time  if  we  desire  to  avoid  all  danger,  and  if  we  are  anxious  to  make 
certain  that  the  blood  of  the  animal  furnishing  the  material  is  quite  free 
from  any  toxic  property. 

Serum  thus  obtained  possesses  great  agglutinative  power,  and  on  injec- 
tion into  animals  immunizes  them  against  doses  of  living  bacilli  or  of  soluble 
toxine  which  prove  fatal  to  the  control  animals. 

If  we  inject  the  same  dose  of  typhoid  baciUi  under  the  skin  of  the  ear 
in  several  rabbits,  of  which  some  have  been  given  2  or  3  c.c.  of  serum  nine 
hours  previously,  while  others  have  been  given  the  serum  several  hours 
previously,  we  notice  after  eight  to  ten  hours  that  the  microbes  swarm  in 
the  ear  of  the  control  rabbits  just  as  in  broth  culture.  In  the  rabbits  which 
have  been  given  serum  the  bacilli  are  for  the  most  part  engulfed  by  the 
leucocytes,  and  undergo  rapid  destruction.  The  preventive  injection  of 
serum,  which  renders  the  microbes  sensitive,  constitutes,  therefore,  an  anti- 
infectious  as  well  as  an  antitoxic  treatment.  Serum  injected  as  a  preven- 
tive from  two  to  twenty-four  hours  before  the  toxine  protects  the  rabbit 
against  three  or  four  times  a  fatal  dose.  The  animals  then  behave  as  regards 
leucocytic  changes  just  as  do  rabbits  immunized  by  small  and  repeated 
injections  of  toxine. 

When  the  serum  is  injected  at  the  same  time  as  the  toxine,  its  action  is 
less  efficacious,  since  animals  which  have  received  more  than  twice  the  fatal 
dose  succumb.  The  initial  destruction  of  the  leucoc3rfces  is  not  immediately 
prevented.  The  leucocytic  reaction,  however,  takes  place  earlier  and  to  a 
greater  extent  than  in  the  control  animals.  The  intense  congestion  which 
impedes  the  production  of  leucocytes  in  the  control  animals  is  much  less 
marked,  and  the  bone-marrow  shows  considerable  activity  at  the  end  of 
ten  hours.  Consequently,  the  antitoxic  serum  renders  the  leucocjrfces  less 
sensitive  to  the  noxious  action  of  the  toxine,  and  increases  the  reaction  of 
the  blood-forming  organs. 

When  the  serum  is  injected  after  the  toxine,  it  is  less  efficacious  in  pro- 
portion as  the  time  elapses  between  the  penetration  of  the  toxine  and  that 
of  the  serum  increases.  When  the  intoxication  of  the  elements  of  resistance 
is  too  advanced,  the  favourable  blow  produced  by  the  serum  no  longer 
occurs  with  the  same  power,  whence  the  indication  to  inject  the  serum  into 
man  as  early  as  possible.  This  essential  point  has  been  brought  out  in  all 
the  experimental  researches. 

The  duration   of   the  preventive  action   of   the   serum,   determined 


'rVlMlolD    DISKASKS  1720 

exporiinontally,  is  over  six  and  uiuler  liflcMMi  days.  Tlio  dunitioii  of  tho 
immunity  coiifi'iri'd  bv  an  injection  of  soruni  is  not  loiij^cr  thtin  ten  to 
twelve  days. 

Wo  hiivo  still  to  o.xiuuinc  tho  action  of  this  scrum  on  a  patient  witli 
typhoid  fever.  From  the  first,  however,  tlie  physician  must  bear  in  mind 
two  points  which  result  from  experimental  facts.  On  the  one  hand,  the 
serum  shows  its  full  power  only  when  it  acts  upon  an  organism  which  has 
all  its  forces,  and  which  is  not  profoundly  intoxicated,  whence  the  indica- 
tion to  intervene  as  early  as  possible  ;  on  the  other  hand,  in  the  case  of 
profound  intoxication,  it  does  not  appear  useful  to  inject  large  doses. 
Again,  we  must  be  afraid  of  preventing  the  reaction,  and  we  must  give  a 
small  dose  which  will  not  disturb  the  leucopoietic  apparatus,  which  is 
incapable  of  making  suddenly  too  great  an  effort.  The  recovery  of  the 
patient  will  be  slower,  but  it  will  result  from  the  assistance  given  to  the 
normal  processes  of  defence.  The  resistance  will  be  increased.  It  is 
evident  that  the  emplo}Tnent  of  this  serum  demands  accurate  clinical 
knowledge  on  the  part  of  the  physician,  as  well  as  a  knowledge  of  the  proper 
technique  and  of  the  resources  of  the  remedy.  We  must  remember  that  it 
is  chiefly  effective  against  the  cause  of  the  disease.  This  serum  is  anti- 
infectious  and  antitoxic,  but  less  so  than  in  the  case  of  antidiphtheritic 
serum  ;  and  therefore  the  toxic  symptoms,  properly  called,  should  be  treated 
with  cold  baths  in  addition  to  the  actual  serum.  The  two  modes  of  treat- 
ment are  not  exclusive,  but  rather  interdependent. 

The  treatment  of  typhoid  fever  by  serotherapy  and  by  cold  baths  has 
been  carried  out  in  Chantemesse's  wards  for  some  years  past.  Every 
patient,  without  exception,  to  the  number  of  350,  has  been  treated  by  this 
method.  Thirteen  died,  giving  a  total  mortality  of  less  than  4  per  cent. 
In  Josias's  wards  eighty  children  were  thus  treated  in  a  systematic  manner. 
Two  died — one  from  perforation  of  the  intestine,  on  the  same  day  as  the 
injection,  and  the  other  from  laryngo-typhus.  Patients  treated  before  the 
seventh  day  have  always  recovered,  and  the  fever  has  been  shorter  and  the 
cure  more  rapid  the  sooner  the  injection  of  serum  has  been  made  after  the 
onset  of  the  disease.  We  thus  become  reconciled  to  the  experimental  results 
of  so-called  preventive  injection,  since  typhoid  fever  in  man  only  causes 
gradual  changes  in  the  organs. 

In  his  communication  to  the  Congress  of  Hygiene  at  Berlin  (1907), 
Chantemesse  gave  his  latest  figures.  In  six  years  1,000  cases  of  typhoid 
were  under  treatment  in  his  wards.  The  death-rate  was  43  per  cent. 
These  figures  are  conclusive. 

Independently  of  the  results  furnished  by  the  diminution  in  mortality, 
the  action  of  the  serum,  says  Chantemesse,  shows  itself  in  the  course  of  the 
various  symptoms.     In  sixty-one  cases  treated  on  the  fourth  or  on  the  fifth 


1730  TEXT-BOOK  OF  MEDICINE 

day,  apjrexia  resulted  in  a  few  days.  In  the  severe  forms  tlie  defervescence 
is  less  rapid,  but  it  is  exceptional  if  the  patient  cannot  begia  to  dispense 
with  baths  three  or  four  days  after  the  injection.  The  duration  of  the  cold- 
bath  treatment,  which  is  sometimes  very  long  in  patients  treated  by  the 
baths  alone,  is  thus  much  shortened.  After  the  injection  the  blood-pressure 
rises  and  the  quantity  of  urine  increases.  Accordingly,  it  is  necessary  with 
serum  to  stop  all  medication  which  increases  the  blood-pressure,  and 
especially  cafEeine.  The  serum  does  not  cause  albuminuria.  The  general 
condition  improves  as  soon  as  the  temperature  faUs.  Perforation  does  not 
occur  in  patients  who  receive  injections  before  the  seventh  day — at  least, 
it  has  never  been  seen  in  the  large  number  of  persons  thus  treated. 

The  bridle  action  of  the  serum  on  the  course  of  typhoid  fever  is  seen 
with  great  clearness  in  relapses.  After  twelve  days,  the  benefit  of  immunity 
secured  by  treatment  disappears,  and  a  relapse  occurs.  A  fresh  injection 
of  serum  then  prevents  its  development  or  moderates  it,  giving  rise  to 
defervescence  by  lysis.  A  fact  worthy  of  notice  was  present  nine  times  in 
350  cases.  Some  patients  suffering  from  typhoid  fever  were  given  serum 
at  the  commencement  of  the  disease — about  the  fourth  or  the  sixth  day. 
The  disease  ended  in  less  than  a  week,  the  temperature  fell  to  normal,  and 
the  recovery  was  apparently  perfect. 

Nevertheless,  after  two  months  in  two  cases,  three  months  in  three  cases, 
and  six  months  in  four  cases,  following  a  chUl,  overwork,  or  poisoning  by 
tainted  meat,  the  typhoid  fever  reappeared,  and  ran  quite  a  benign  course. 
This  example,  in  which  the  microbes  were  checked  and  rendered  latent  by 
the  injection  of  serum,  deserves  attention  from  the  point  of  view  of  the 
pathological  physiology  of  the  disease. 

Following  on  researches,  made'  for  the  most  part  in  Germany,  Vincent 
has  recently  proposed  to  use  as  a  vaccine  the  autolysate  of  liying  typhoid 
bacilli.  This  is  obtained  by  maceration  of  living  typhoid  and  paratyphoid 
bacilli  in  physiological  serum ;  after  centrifugalization  the  clear  liquid  is 
collected  and  sterilized  with  ether.     This  vaccine  is  still  under  trial. 

II.  TYPHUS  FEVER. 

etiology. — The  principal  centres  of  typhus  in  Europe  are  Ireland  and 
SUesia.  The  disease  readily  spreads  from  Ireland  to  England,  where  typhus 
and  typhoid  fever  are  both  found.  From  SUesia  it  spreads  to  neighbouring 
countries,  and  the  epidemics  of  typhus  in  Berlin  were,  in  Virchow's  opinion, 
due  to  this  source.  We  have  had  typhus  in  France  at  different  times,  but 
it  was  imported  from  abroad.  In  1856  it  followed  the  return  of  our  soldiers 
from  the  Crimea. 

It  has  appeared  several  times  in  Brittany  since  1870  :  at  Riantec  (1870- 
1872),  Rouisson  (1872-1873),  the  Isle  of  Molene  (1878),  the  Isle  of  Tudy  (1891); 


TYI'IIOID   DISEASES  1731 

lastly,  iu  1891-1892,  it  broke  out  in  the  prison  of  Nantene,  and  lioui  there 
spread  to  Paris.  Some  months  previously  Leloir  had  seen  cases  at  Lille, 
and  its  presence  was  ultimately  notified  at  Beauvais,  Amiens,  Havre,  etc. 

Typhus  is  both  epidemic  and  contagious.  The  contagion  has  been 
proved  on  many  occasions.  In  the  Crimea  the  mortality  from  typhus 
was  12*88  per  cent,  among  the  medical  staff,  while  it  was  only  0"47  per  cent, 
among  the  combatant  officers  (Laveran).  In  the  last  epidemic  in  Paris  the 
hospital  attendants  especially  suffered.  Netter  believes  that  the  contagion 
is  effected  by  contact,  but  Chantemesse,  on  the  other  hand,  puts  it  down 
chiefly  to  drying  of  the  sputum  and  to  the  inhalation  of  the  dust  thus 
produced. 

Hava  (1888)  traced  the  development  of  typhus  to  a  strepto-bacillus,  but 
Comil  and  Babes  think  that  it  is  only  an  organism  of  secondary  infection. 
Calmette  and  Thoinot,  in  the  epidemic  of  the  Island  of  Tudy,  found  in  the 
blood  from  the  heart  and  from  the  spleen  abnormal  elements,  including 
mobile  granules  and  threads  which  were  mobile  or  united  with  the  red 
blood-corpuscles.  These  elements  resemble  those  found  in  the  blood  of 
patients  suffering  from  t3^hoid  fever,  erysipelas,  anaemia,  and  even  of 
healthy  persons.  It  is  possible  that  they  are  formed  at  the  expense  of  red 
corpuscles  .in  process  of  destruction. 

T}^hus  breaks  out  among  armies  in  the  field,  in  convict  stations,  in 
prisons,  and  on  ships,  where  no  previous  cases  have  occurred.  Over- 
crowding, poverty,  dirt,  privation,  and  fatigue  are  generally  potent  factors 
in  the  hatching  of  typhus. 

Jaccoud,  in  a  remarkable  report  on  an  epidemic  of  typhus  which  he  saw 
during  a  long  voyage,  arrived  at  a  conclusion  "  that  the  accumulation  of 
animal  products  in  a  state  of  fermentation  or  decomposition  may  cause  an 
outbreak  of  typhus,  apart  from  any  human  overcrowding." 

Symptoms. — After  an  incubation  period  lasting  about  ten  days,  the 
disease  appears  suddenly  in  most  cases,  although  it  may  be  preceded  by  a 
prodromal  period. 

Invasion. — The  onset  is  sudden,  with  a  chUl,  immediately  followed  by 
headache,  tremors  in  the  limbs,  and  vertigo.  Vomiting  is  not  rare.  The 
prostration  is  extreme,  the  conjunctivae  are  injected,  the  pulse  frequent, 
and  the  temperature  may  reach  104°  F.  on  the  evening  of  the  first  or  of  the 
second  day.  Insomnia,  restlessness,  delirium,  and  suicidal  mania  may  be 
added  to  the  above  symptoms.  The  course  of  events  is  not  always  con- 
tinuous. Alternating  improvement  and  aggravation  may  occur.  Bronchial 
catarrh  is  often  added  to  the  nervous  complications  which  dominate  the 
clinical  picture.  We  sometimes  see  broncho-pulmonary  symptoms,  which 
may  induce  error  as  to  the  nature  of  the  disease.  The  temperature  shows 
but  a  slight  morning  remission. 


1732  TEXT-BOOK  OP  MEDICINE 

The  period  of  invasion  is  sometimes  preceded  by  prodromal  symptoms  : 
lumbar  pain,  headacne,  lassitude,  injection  of  the  face,  and  hesitation  in  speech. 

Eruption. — The  eruption  of  typhus  appears  between  the  third  and  fifth 
days,  commencing  in  the  abdomen,  and  invading  all  the  body,  except  the 
face.  It  is  characterized  by  flat  or  papular  rose-coloured  spots,  which  are 
usually  isolated,  being  confluent  only  in  rare  cases.  They  fade  for  a  moment 
on  pressure.  The  exanthem  changes  in  character  after  two  or  three  days, 
many  of  the  spots  being  transformed  into  small  petechiee,  which  do  not 
fade  on  pressure  (petechial  typhus).  In  some  cases  slight  desquamation 
follows  the  eruption.  In  certain  epidemics,  and  especially  in  mUd  cases, 
the  eruption  is  absent.  All  the  symptoms  increase  in  severity  at  the  time 
of  the  eruption.  "  Violent  delirium,  with  a  tendency  to  suicide  "  (Jaccoud), 
is  frequent  in  the  severe  forms  of  typhus,  though  very  exceptional  in  typhoid 
fever. 

A  typhoid  condition  of  torpor  and  stupor  follows  the  period  of  restless- 
ness. The  patient  lies  on  his  back,  hardly  recognizing  those  around  him, 
and  mumbles  in  an  unintelligible  manner.  Constipation  is  the  rule,  and  the 
abdominal  symptoms,  which  are  almost  constant  in  typhoid  fever,  are  absent 
in  typhus.     The  urine  is  scanty,  and  often  contains  albumin. 

Combemale  has  noticed  upon  the  skin  a  whitish  dust,  formed  of  dry  fatty 
acids,  in  those  patients  who  are  affected  with  acute  nephritis. 

Typhus  lasts  from  eight  to  ten  days  in  mild  cases,  and  from  twelve  days 
to  a  fortnight  in  severe  ones.  Defervescence  is  often  sudden,  and  takes 
place  within  twenty-four  hours.  It  is  accompanied  by  perspiration,  sleep, 
and  a  feeling  of  comfort — it  is,  in  fact,  a  true  crisis.  In  other  cases  defer- 
vescence takes  three  or  four  days.  Typhus  may  cause  various  complica- 
tions in  the  nervous  system ;  motor  troubles,  such  as  paresis  of  the  upper 
or  of  the  lower  limbs  ;  abolition  of  the  patellar  or  of  the  plantar  reflexes ; 
inco-ordination  of  movements  ;  and  trophic  troubles,  with  acute  bedsores. 
These  nervous  troubles  appear  to  be  due  to  spinal  lesions,  characterized  by 
microscopic  interstitial  haemorrhages,  and  by  a  vesicular  condition  of  some 
of  the  motor  cells  in  the  anterior  cornua. 

In  spite  of  the  sudden  return  to  health,  convalescence  is,  as  a  rule,  long, 
and  the  patient  is  liable  to  pleuro-pulmonary  inflammation,  multiple 
abscesses,  otitis  media,  gangrene  of  the  extremities,  parotiditis,  and  erysipe- 
las, which  may,  moreover,  supervene  in  the  course  of  typhus. 

Diagnosis — ^Prognosis. — The  principal  elements  in  the  differential 
diagnosis  between  typhus  and  typhoid  fever  are  the  sudden  onset  and  the 
stupor,  which  is  more  marked  than  in  typhoid  fever ;  the  absence  of 
meteorism ;  the  constipation  ;  the  abundance  and  the  general  distribution 
of  the  rash,  its  petechial  character,  and  the  rapid  recovery  which  often 
takes  place  by  crisis.     Further,  typhus  attacks  patients  at  a  more  advanced 


TV  n  loll)   DLSKASES  1733 

age  than  tyj)hf>id  fovor.  It  is  much  more  contiif^ious  than  the  hitter,  an<l  it 
especially  aflccts  vagrants,  prisoners,  and  armies  in  the  field.  Certain 
malignant  eruptive  fevers  (measles,  scarlatina)  are  accompanied  by  adynamia 
as  marked  as  in  typhus,  but  the  distribution  of  the  eruption  and  the  course 
of  the  disease  difTer  sulHciently  to  prevent  error.  Sero-diagnosis  (Widal), 
described  in  detail  in  the  preceding  section,  will  remove  all  doubts,  and 
clinch  the  diagnosis. 

The  mortality  of  typhus  varies  according  to  the  epidemic,  and  to  the 
circumstances  which  have  given  rise  to  the  disease,  thus  explaining  why 
the  mortality  varies  from  15  per  cent,  to  the  high  rate  of  50  per  cent.  Every 
degree  of  severity  is  seen  between  the  benign  cases,  which  recover  in  a  few 
days,  and  the  severe  forms  to  which  I  have  alluded  in  my  description. 
Death  usually  occurs  about  the  end  of  the  second  week,  but  in  severe 
epidemics  malignant  cases  are  seen,  causing  death  as  early  as  the  third  day 
(typhus  siderans). 

Pathological  Anatomy. — The  lesion  of  Peyers  patches  is  a  change 
special  to  tvphoid  fever.  Typhus  presents  no  characteristic  anatomical 
lesions.  The  spleen,  as  in  all  cases  of  severe  pyrexia,  is  enlarged,  the  mus- 
cidar  fibres  are  degenerated,  and  the  same  change  is  seen  in  the  heart  muscle, 
which  is  flabby  and  pale.     The  blood  is  abnormally  fluid. 

Treatment. — Prophylactic  treatment  must  be  rigorously  employed. 
Patients  must  be  isolated  in  well-aired  apartments,  and  all  contaminated 
media  thoroughly  disinfected. 

The  treatment  of  typhus  may  be  summed  up  in  tonics,  alcohol,  cold 
sponging,  sedatives,  and  restricted  diet.  Warm  baths  at  90°  F.  give  good 
results.     Injections  of  artificial  serum  may  be  employed  with  advantage. 

III.  RELAPSING  FEVER. 

Relapsing  fever  is  a  specific,  contagious,  and  epidemic  malady  proper 
to  man.  It  is  due  to  the  presence  of  a  micro-organism  of  the  blood — Ober- 
meier's  spirillum — and  is  characterized  clinically  by  the  succession  in  a  well- 
defined  cycle  of  two  acute  febrile  attacks,  with  a  regular  temperature  curve. 

History. — The  old  descriptions  confounded  relapsing  fever  with  the  other  continuous 
fevers,  and  in  particular  with  typhus,  to  which,  indeed,  it  has  some  relation  ;  the  chief 
centres  of  both  diseases  are  found  in  the  same  regions,  and  their  epidemics  are  almost 
always  associated.  Thej'  differ  clinically  in  numerous  points,  and  there  is  not  the  least 
doubt  as  to  the  specific  nature  of  relapsing  fever  at  the  present  time,  because  we  know 
the  infectious  agent  concerned. 

Craigie  and  Henderson,  of  Edinburgh,  definitely  separated  this  disease  from  typhus 
during  the  Scotch  epidemic  of  1843.  Since  that  time  recurrent  fever  has  been  studied 
by  Irish,  Scotch,  German,  and  Russian  physicians,  who  have  been  able  to  watch  it  in 
the  countries  where  it  is  especially  prevalent.  The  discovery  of  the  spirillum  by  Ober- 
meier  has  been  followed  by  numerous  experimental  researches,  which  I  shall  have 
occasion  to  quote  in  the  course  of  this  section. 

II.  110 


1734  TEXT-BOOK  OF  MEDICINE 

JEilologS- — Recurrent  fever  lias  a  special  geographical  distribution.  Its 
chief  endemic  centre  is  Ireland,  and  it  has  been  imported  thence  in  epidemic 
form  into  Scotland  in  1843,  into  England,  and  even  into  the  United  States. 
Another  more  extensive  centre  comprises  the  shores  of  the  Baltic,  Finland, 
the  Western  Provinces  of  Russia,  Poland,  and  the  North-East  of  Germany. 
From  this  centre  certain  epidemics  invaded  G-alicia,  Bohemia,  Saxony,  and 
Bavaria,  spreading  to  the  banks  of  the  Rhine,  and  appearing  even  in  the 
Belgian  portion  of  Flanders.  At  the  present  time  the  number  of  cases  seen 
in  Germany  is  constantly  diminishing,  and  France,  Switzerland,  Italy,  and 
Spain  have  so  far  remained  free  from  the  disease.  The  malady  is,  further- 
more, endemic  in  the  South  of  Russia,  on  the  borders  of  the  Black  Sea, 
and  in  Roumania.  It  has  also  been  seen  in  Egypt,  Abyssinia,  India,  China,  etc. 

Numerous  proofs  of  the  great  contagiousness  of  this  disease  are  furnished 
by  aU  these  epidemics.  The  contagion  appears  to  proceed  either  directly 
from  the  patient  or  by  contact  with  clothes,  linen,  and  other  articles. 
During  the  Edinburgh  epidemic  of  1843  the  physicians  and  the  hospital 
attendants  sufEered  to  a  marked  degree.  During  epidemics  it  is  common 
to  see  small  centres,  limited  to  a  house  or  to  a  family,  which  show  clearly 
the  mode  of  contagion.  Overcrowding  and  famine  were  looked  upon  by 
Murchison  as  the  cause  of  this  afEection  (famine  disease),  but  they  are  only 
predisposing  factors,  preparing  the  soil  for  the  infective  germ,  which  must 
enter  the  organism  in  order  to  produce  the  disease. 

Symptoms. — Recurrent  fever  is  chiefly  seen  in  young  people,  and  its 
onset  is  extremely  violent.  A  healthy  individual  is  seized  with  a  sharp 
chUl,  and  feels  sudden  general  malaise,  which,  as  it  were,  roots  him  to  the 
spot.  He  is  sometimes  quite  incapable  of  standing  upright.  He  suffers 
from  ^aolent  headache,  severe  backache,  and  acute  pains  iu  the  trunk  and 
in  the  limbs.  Nausea  and  vomiting  appear,  the  skin  is  burning  hot,  the 
face  is  injected,  the  pulse  is  quickened,  and  the  temperature  rapidly  rises 
to  104°  F. 

The  nature  of  the  attack  is  clearly  marked  upon  the  first  day  of  the 
disease.  The  headache  and  the  pains  in  the  limbs  are  persistent  and 
intense,  producing  most  troublesome  insomnia.  The  patient  is  anxious,  and 
sometimes  restless.  The  mental  powers,  however,  are  clear,  and  the  con- 
dition of  stupor  present  in  typhus  and  typhoid  fever  is  not  seen,  although 
in  a  few  days  transient  delirium  may  supervene.  Nausea  and  vomiting  of 
bUe  may  be  only  slight.  Constipation  is  the  rule.  The  patient's  face  is 
red  and  injected,  and  his  eyes  are  bright.  The  respiration  is  at  times 
slightly  quickened,  the  tongue  remains  moist,  and  is  covered  with  a  thin 
fur,  and  some  vesicles  of  herpes  may  in  rare  cases  appear  upon  the  lips. 
The  skin  is  dry  and  burning  ;  t^he  pulse  is  full,  bounding,  and  rapid,  the  rate 
being  about  120. 


TYPHOTD  DISEASES  1735 

No  eruption  is  seen,  but  a  few  insignificant  petochiaB  or  rose-coloured 
spots  may  appear  upon  the  abdomen.  Tlie  epigastric  region  is  particularly 
tender  on  palpation,  ospe(!ially  near  the  border  of  the  ribs,  both  on  the 
right  and  left  sides.  The  spleen  undergoes  rapid  and  marked  increase  in 
size.  It  can  be  felt  below  the  false  ribs.  The  stethoscope  may  reveal  a 
soft  systolic  murmur.  The  liver  is  but  slightly  increased  in  size.  Auscul- 
tation of  the  lungs  sometimes  reveals  the  signs  of  pulmonary  congestion. 

The  urine  is  of  a  dark  colour,  and  the  excretion  of  urea  is  much  increased. 
In  about  a  third  of  the  cases  albuminuria  is  found,  and  the  microscope 
shows  red  corpuscles  and  cylindrical  casts,  which  are  said  to  be  fairly 
common  (Obermeier).  Kannenberg  has  found  the  spirillum  in  the  urine. 
Jaundice  is  frequent,  and  is  usually  seen  in  severe  cases  accompanied  by 
delirium.  It  commences  on  the  third,  fourth,  or  fifth  day,  appearing  first 
in  the  conjunctivse,  and  rapidly  becoming  general,  but  it  diminishes  very 
quickly,  and  soon  disappears.  It  is  sometimes  accompanied  by  a  general 
bilious  condition,  with  vomiting  of  greenish  and  blackish  matter.  It  is 
important  to  remember  that  the  jaundice  is  not  due  to  retention.  The  bile 
continues  to  flow  iilto  the  intestine,  and  the  stools  remain  coloured. 

During  this  time,  whether  jaundice  is  or  is  not  present,  the  temperature 
remains  between  104°  F.  and  106°  F.  It  may  even  reach  107°  F.  The  morning 
remission  is  slight,  and  does  not  exceed  1°.  There  is  often  recrudescence 
of  fever  before  the  appearance  of  the  phenomena  which  will  mark  the 
terminal  crisis  of  the  attack.  The  thermometer  may  then  show  a  reading 
of  108°  F. 

These  symptoms  usually  last  a  week,  but  the  attack  may  last  only  three 
days,  or  may  be  as  long  as  twelve  days.  The  final  crisis  then  takes  place 
as  suddenly  as  the  onset  of  the  attack  appeared  :  profuse  sweating,  abundant 
urine,  and  a  fall  of  temperature  to  98°  F.,  or  sometimes  to  95°  F.  The 
pulse  becomes  normal,  the  pains  disappear,  and  the  patient  experiences 
only  a  somewhat  marked  feeling  of  fatigue.  The  appetite  returns,  and 
after  two  or  three  days  the  patient  thinks  that  he  is  cured.  The  spleen 
may  have  diminished  in  size,  but  it  often  remains  much  hypertrophied 
(Griesinger). 

A  fresh  phase,  which  is  quite  characteristic,  and  which  has  given  the 
disease  its  name,  appears  five,  six,  or  seven  days  after  the  end  of  the  crisis 
(sometimes  earlier — viz.,  two  or  three  days ;  sometimes  later,  as  long  as 
two  weeks).  The  patient  is  again  seized  with  a  chill,  extreme  malaise, 
headache,  pain,  and  nausea.  The  pulse  is  quickened,  and  the  temperature 
rapidly  rises  to  104°  F.  This  second  attack  is  an  exact  reproduction  of  the 
first  attack.  As  a  general  rule,  the  second  attack  does  not  last  so  long  as 
the  first  one,  and  after  three,  four,  or  five  days  the  terminal  crisis  appears 
suddenly. 

110—2 


1736  TEXT-BOOK  OF  MEDICINE 

The  crisis  of  the  second  attack  in  most  cases  means  the  end  of  the  disease. 
The  fever  has  been  once  recurrent,  and  there  has  been  only  a  single  relapse. 
In  some  cases,  however,  after  a  fresh  period  of  apyrexia,  a  second  relapse 
occurs,  which  is  shorter  than  the  first  one.  Four  or  five  successive  attacks 
may  be  seen  in  exceptional  cases  (Moszutkowsky). 

Recurrent  fever  generally  ends  in  recovery,  and  death  only  results  from 
complications.  The  immunity  acquired  by  a  first  attack  is  not  always 
lasting,  as  recurrence  may  be  seen  after  some  months.  In  this  case  there  is 
sometimes  only  a  single  attack. 

Forms — Bilious  Typhoid  Fever  of  Hot  Countries.— Griesinger,  who 
has  studied  this  affection  during  an  epidemic  in  Egypt,  has  shown  its  relation 
to  relapsing  fever,  and  has  demonstrated  that  it  is  a  form  thereof,  modified 
by  the  appearance  of  certain  severe  typhoid  symptoms,  with  jaundice. 
The  onset  is  as  sudden  as  in  the  ordinary  form,  and  the  jaundice  appears 
about  the  fourth  or  the  fifth  day,  being  accompanied  by  nervous  symptoms. 
The  patient  soon  falls  into  a  state  of  prostration.  The  tongue  and  lips  are 
dry,  and  covered  with  sordes,  diarrhoea  appears,  the  pulse  becomes  slow, 
and  death  usually  takes  place  in  a  typhoid  condition,  'being  often  due  to 
the  complications  so  frequent  in  this  form. 

Complications — Prognosis. — Epistaxis,  cutaneous  haemorrhage,  bleeding 
from  the  gastro-intestinal  tract,  cerebral  haemorrhage,  and  metrorrhagia 
may  occur  in  the  course  of  relapsing  fever.  Uterine  haemorrhages  are 
especially  serious  in  pregnant  women.  Detachment  of  the  placenta  and 
miscarriage,  which  is  a  characteristic  feature  of  relapsing  fever,  may  be 
followed  by  profuse  and  fatal  haemorrhage,  and  the  foetus  almost  always 
succumbs. 

During  convalescence  we  may  see  ocular  symptoms,  which  are 
usually  unilateral  (Mackenzie),  and  comprise  retinitis  and  iridochoroiditis, 
which  are  transient  affections,  receding  slowly,  but  leaving  no  other 
results. 

Acute  myocarditis  may  cause  fatal  syncope.  Rupture  of  the  spleen  is 
another  complication  special  to  relapsing  fever,  and  worthy  of  notice  because 
it  accounts  for  20  per  cent,  of  the  fatal  cases.  The  patient  dies  from  intra- 
peritoneal haemorrhage.  In  other  cases  the  presence  of  small  abscesses  in 
the  tissue  of  the  spleen  produces  general  peritonitis. 

The  other  complications  are  sacral  bedsores,  subcutaneous  abscesses, 
diffuse  cellulitis,  parotiditis,  arthritis,  etc. ;  they  are  due  to  common  secondary 
infection.  It  is  necessary  to  dwell  upon  the  complications  which  may  arise 
in  the  respiratory  tract.  In  12  per  cent,  of  the  fatal  cases  oedema  of  the 
glottis  results  from  laryngeal  perichondritis,  but  broncho-pneumonia,  and 
more  often  lobar  pneumonia,  are  fatal  in  relapsing  fever,  and  about  20  per 
cent,  of  deaths  must  be  attributed  to  them  (Ponfick).     Pneumonia  generally 


TYT'TTOTT)  DTSEASES  17:i7 

appears  about  tlie  end  of  the  tirst  attack,  uud  thi-n  runs  its  own  course  in  a 
soil  which  is  profoundly  weakened. 

It  is  well  to  remeinher  that  all  these  complications  are  exceptional  in 
the  ordinary  form,  and  that  the  prognosis  of  recurrent  fever  is  rarely  grave 
except  in  the  delirious  form  of  tropical  countries.  The  mortality  varies 
much  in  diffei^'ut  epidemics,  of  which  some  are  remarkably  benign,  while 
others  are  very  fatal  (St.  Petersburg,  1864,  10  per  cent.).  The  mean  mor- 
tality is  given  as  from  2  to  5  per  cent.,  and  the  German  statistics  show  that 
these  ligures  have  a  tendency  to  progressive  diminution. 

Pathological  Anatomy. — Post-mortem  examinations  of  persons  who 
have  died  from  relapsing  fever  show,  in  the  first  place,  lesions  which  have 
been  the  direct  cause  of  death  (pneumonia,  broncho-pneumonia,  laryngeal 
lesions,  etc.).  At  times  small  foci  of  cerebral  hajmorrhage,  hsemorrhagic 
lesions  in  the  stomach  and  in  the  small  intestine,  and  exceptionally  in  the 
large  intestine,  are  also  found.  But  the  lesions  special  to  relapsing  fever 
affect  other  organs.  The  kidneys  are  large  and  soft,  and  the  medullary 
substance  is  of  a  greyisli  colour.  The  myocardium  is  flabby,  friable,  and 
of  a  dirty  grey  colour,  like  that  of  dead  leaves.  The  other  striated  muscles 
show  similar  changes.  Small  yellowish,  softened  nodules  are  found  in  the 
bone-marrow.  The  liver  is  large  and  altered  in  colour,  but  the  most 
characteristic  lesions  are  found  in  the  spleen. 

The  spleen  is  commonly  five  or  six  times  larger  than  normal.  The 
capsule  is  stretched,  and  sometimes  torn  near  the  hilum.  On  section,  the 
parenchyma  is  softened,  of  a  bright  red,  and  studded  with  grey  or  with 
yellowish  points,  which  are  the  corpuscles  of  Malpighi.  The  appearance 
is,  therefore,  somewhat  analogous  to  that  of  the  typhoid  spleen.  These 
little  yellowish  points  are  sometimes  true  miliary  abscesses.  Hsemorrhagic 
infarcts  (attributed  to  obliteration  of  the  vessels  by  masses  of  degenerated 
cells)  may  also  be  found,  and  may  end  in  suppuration,  with  the  formation 
of  large  abscesses. 

The  spleen  in  relapsing  fever  shows  two  kinds  of  histological  changes — 
hypertrophy  of  the  corpuscles  of  Malpighi,  and  formation  of  leucocytic 
masses  in  the  spleen  pulp.  The  cells  of  the  corpuscles  of  Malpighi  multiply 
exceedingly.  Those  in  the  centre  sometimes  undergo  degeneration,  which 
results  in  the  formation  of  a  small  miliary  abscess.  The  leucocytic  masses 
(inflammatory  lymphomata  of  Roudnef),  which  are  scattered  through  the 
pulp,  and  are  very  variable  in  size,  are  said  to  appear  in  each  attack  (Son- 
dakewitch).  They  are  considered  by  Ponfick  as  characteristic  of  relapsing 
fever.  In  some  cases  they  disappear,  but  in  others  their  centre  necroses  (in 
40  per  cent,  of  the  cases,  according  to  G-riesinger),  and  in  this  manner  other 
small  abscesses  are  formed.  The  spirillum  is  very  abundant  in  all  these 
foci. 


1738  TEXT-BOOK  OF  MEDICINE 

Diagnosis. — The  sudden  onset,  with  prostration,  general  pain,  rapid  rise 
of  temperature,  marked  swelling  of  the  spleen,  absence  of  eruption,  co- 
existence of  jaundice,  attacks  of  apyrexia,  and  relapse,  are  such  charac- 
teristic sjonptoms  that  there  can  scarcely  be  doubt  in  the  diagnosis  of 
relapsing  fever,  especially  during  an  epidemic.  In  the  absence  of  any 
epidemic,  however,  the  sudden  onset  may  be  set  down  to  influenza,  dengue, 
gastric  trouble,  etc.  Attacks  of  intermittent  fever  also  commence  with  a 
severe  chUl,  and  the  spleen  is  large  and  hard,  but  inquiry  into  the  patient's 
past  history  at  once  decides  the  question  of  malaria.  The  coexistence  of 
jaundice,  especially  in  warm  climates,  may  closely  simulate  the  biliary  form 
of  malaria  or  even  of  yellow  fever.  Typhus  is  especially  liable  to  be  con- 
founded with  relapsing  fever,  and  this  is  the  more  likely,  because  both 
diseases  are  seen  in  the  same  regions,  and  epidemics  of  them  are  usually 
associated.  And  yet  the  distinction  is  not  really  a  matter  of  difficulty. 
The  onset  of  typhus  is  less  violent,  and  is  preceded  by  slight  prodromata. 
The  temperature  reaches  a  high  degree  much  less  rapidly ;  the  abdominal 
rash  is  generally  present  on  the  fourth  or  on  the  fifth  day ;  the  spleen  is 
rarely  enlarged  ;  lastly,  the  temperature  curve  is  different,  and  the  duration 
of  the  disease  is  longer. 

Besides,  in  any  doubtful  case  the  diagnosis  can  be  readily  established 
by  examination  of  the  blood,  in  which  the  spirOla  swarm  during  the 
attacks. 

Bacteriology  and  Pathological  Physiology.— During  an  epidemic  of 
relapsing  fever  in  Berlin  ia  1868  Obermeier  discovered  the  pathogenic 
parasite  in  the  blood  of  patients  examined  during  the  febrile  attack.  This 
was  the  first  discovery  of  a  pathogenic  microbe  in  man.  It  was  only  in 
1873,  however,  on  the  occasion  of  a  fresh  epidemic,  that  Obermeier  pub- 
lished his  discovery.  He  pointed  out  the  filiform  appearance,  spiral  shape, 
and  great  mobility  of  this  micro-organism,  and  remarked  that  it  is  only 
met  with  during  the  febrile  attack,  and  that  it  disappears  in  the  apyretic 
stage. 

Obermeier's  discovery  has  been  verified  by  numerous  observers,  and  the 
parasite  has  been  constantly  found  in  relapsing  fever,  and,  as  it  is  present 
in  no  other  disease,  its  special  pathogenic  action  is  therefore  established 
beyond  a  doubt.  Cohn  gave  it  the  name  of  SpirochcBta  Ohermeieri,  or 
Spirillum  Ohermeieri,  because  the  morphological  characters  of  this  organism 
place  it  in  the  bacterial  family  of  the  spirochsetse. 

To  confirm  the  diagnosis  of  recurrent  fever  by  discovery  of  the  spirillum, 
it  is  necessary  to  examine  the  blood  during  the  febrile  attacks.  After 
puncture  with  a  needle,  we  can  make  two  sets  of  preparations,  which  are 
examined  in  the  fresh  state  without  staining,  and  also  after  drying  and 
staining.      In  the  former  the  parasites  which  remain  aUve  preserve  their 


TYPHOID  DISEASES  1739 

mobility.  We  see  under  tho  mioroscopo,  among  the  clomonts  of  the  blood, 
long  hhiments  of  remarkable  fineness,  varying  in  length  from  15  to  45  /* 
(from  two  to  ten  times  the  diameter  of  a  red  corpuscle),  twisted  in  spirals, 
with  eight  to  twenty  turns,  exceedingly  mobile,  altering  their  position  by 
turning  on  their  long  axis,  moving  laterally,  and  pursuing  the  corpuscles 
which  are  in  their  way.  At  a  temperature  of  37°  C.  the  spirilla  preserve 
their  mobility  for  a  fairly  long  period.  When  the  spirilla  are  scanty,  pre- 
parations dried  in  air  thould  be  examined.  Giinther's  method  is  the  best. 
A  5  per  cent,  solution  of  acetic  acid  is  employed  for  a  few  seconds  to  dissolve 
the  hsemoglobin  of  the  red  corpuscles,  and  is  then  neutralized  by  exposure 
to  ammonia  vapour.  The  preparation  is  stained  with  aniline  gentian  violet 
for  a  long  time.  The  red  corpuscles  remain  unstained,  but  the  nuclei  of 
the  leucocytes  and  the  spirilla  appear  of  a  violet  colour.  The  latter  are 
very  numerous,  clearly  outlined,  and  are  sometimes  isolated,  or  at  other 
times  interwoven  in  groups. 

By  these  methods  we  can  foUow  from  hour  to  hour  the  presence  of  the 
spirilla  in  the  patient's  blood.  It  has  also  been  proved  that,  speaking 
generally,  the  spirilla  are  found  in  the  blood  of  the  peripheral  veins  only 
during  the  febrile  phase.  They  are  found  at  the  onset  of  the  attack,  and 
sometimes,  indeed,  a  few  hours  before,  their  number  increasing  up  to  the 
last  day,  and  attaining  its  maximum  on  the  day  of  the  crisis,  sixteen  hours 
before  the  sweating  stage.  They  diminish  rapidly  in  numbers,  and  dis- 
appear at  the  moment  of  the  precritical  hyperthermia.  Half  an  hour  after 
the  onset  of  the  sweats  they  are  no  longer  visible,  although  some  authors 
have  found  them  during  the  stage  of  apyrexia.  During  the  relapse  they 
reappear  again  in  large  numbers,  and  disappear  afresh  after  the  final  crisis. 

Every  attempt  to  preserve  cultures  of  the  spirillum  has  so  far  failed, 
and  we  are  therefore  ignorant  as  to  the  phases  of  its  development.  Metch- 
nikoff,  however,  has  seen  reproduction  by  transverse  di\asion,  without  any 
formation  of  spores.  Its  habitat  is  also  unknown,  but  Klebs  thinks  that 
the  parasites  (fleas,  bugs,  etc.)  so  frequent  in  the  rooms  or  the  night-shelters 
occupied  by  the  usual  victims  of  relapsing  fever  play  a  part  in  the  trans- 
mission of  the  spirillum.  Tiktine  has  found  the  spirillum  in  the  digestive 
tube  of  bugs.     Klebs's  opinion,  however,  remains  hypothetical. 

Apart  from  the  usual  contagion,  the  mechanism  of  which  still  evades 
our  knowledge,  the  pathogenic  action  of  Obermeier's  spirillum  in  the  blood 
of  patients  has  been  proved  by  a  series  of  accidental  and  experimental  dis- 
coveries. Pricks  received  at  the  autopsy  of  patients  who  have  died  from 
this  disease  have  been  sufl&cient  to  cause  it.  We  may  remember  the  fact 
that  the  phase  of  incubation — or,  in  other  words,  the  interval  between  the 
prick  introducing  the  spirillum  into  the  blood  and  the  clinical  onset  of 
symptoms — varies  from  three  days  and  a  half  to  eight  days  and  a  half. 


1740  TEXT-BOOK  OF  MEDICINE 

Munch,  in  1874,  after  inoculating  himself  with  the  blood  of  a  patient  in  the 
stage  of  pyrexia,  was  attacked  by  relapsing  fever.  Moszutkuwsky,  in  1876, 
performed  inoculation  upon  a  number  of  lunatics.  The  results  were  in 
every  case  positive,  and  the  mean  period  of  incubation  was  from  five  to 
eight  days. 

Relapsing  fever  is  seen  spontaneously  only  in  man.  The  various  labora- 
tory animals  are  refractory  to  inoculation.  Monkeys  have  been  successfully 
inoculated  (Koch,  Carter,  Metchnikoff,  Soudakewitch,  etc.),  and  experi- 
mental studies  with  this  animal  furnish  very  interesting  information  as  to 
the  pathological  physiology  of  the  disease.  The  inoculation,  of  course,  only 
succeeds  if  made  with  blood  taken  during  the  febrile  phase.  After  an 
inoculation  period  of  about  four  days,  symptoms  analogous  to  those  of 
relapsing  fever  in  man  appear — the  same  sudden  onset,  high  temperature, 
etc. ;  but  the  attacks  are  shorter,  and  the  second  attack  or  relapse  is  very 
rare.  During  the  febrile  phase  the  blood  of  the  inoculated  animals  contains 
spirilla  in  large  numbers,  and  the  animals,  like  human  beings,  acquire  more 
or  less  lasting  immunity  after  the  first  attack. 

Metchnikoff,  by  killing  inoculated  monkeys  at  different  phases  of  the 
disease,  has  proved  the  action  of  phagocytosis  in  recurrent  fever,  and  the 
important  role  of  the  spleen  in  the  defence  of  the  organism  against  the 
infection.  Ponfick  was  of  opinion  that  if  the  spirilla,  which  are  so  numerous 
in  the  peripheral  veins  during  the  attack,  disappear  during  the  apyretic 
phase,  a  certain  number  of  them  are  lodged  in  the  abdominal  viscera  and 
especially  in  the  enlarged  spleen. 

Metchnikoff  has  proved  that  the  spleen  contains  a  very  large  number  of 
spirilla  at  the  end  of  the  attack  and  during  the  first  days  of  apyrexia,  but 
it  is  a  particularly  interesting  point  that  the  spirilla  are  then  included  in 
the  leucocytes.  During  the  attack  the  spirilla  are  extracellular,  and 
phagocytosis  does  not  appear  to  take  place  in  the  blood.  When  the  pre- 
critical  rise  of  temperature  occurs,  they  disappear  from  the  blood,  and 
crowd  into  the  spleen.  Although  alive  and  mobile,  they  are  engulfed  by 
the  microphages  (leucocytes  with  multilobular  nuclei,  etc.),  which  fight 
them,  and  bring  about  their  gradual  disappearance.  This  intrasplenie 
phagocytosis,  which  is  exceedingly  active,  may  bring  about  the  end  of  the 
attack.  Experimental  research  agrees  weU  with  the  facts  revealed  by 
histological  examination  of  the  spleen  in  fatal  cases  of  relapsing  fever,  and 
this  examination  has  shown  us  the  development  of  leucocytic  masses  in 
the  pulp,  and  the  proliferation  of  the  Malpighian  corpuscles,  which  are 
leucocytopoietic  organs,  and  assist  in  phagocytosis.  At  this  time  the  liver, 
kidneys,  glands,  and  bone-marrow  do  not  contain  spirilla.  The  spleen, 
therefore,  is  said  to  be  the  exclusive  seat  of  the  phagocytosis. 

Certain  spirilla,  however,  preserve  their  virulence  for  some  time  after 


TVI'IIUID  DISEASES  1741 

ingestion,  as  proved  by  the  positive  result  of  inoculiUion  of  a  Kiiiall  portion  of 
the  spleen  of  an  animal  killed  during  the  apyretic;  period  (MctchnikutT) ; 
these  active  spirilla  may  determine  the  second  attack  in  man. 

Soudakevvitch  has  eonfirnied  the  essential  role  of  phagocvto.sLs  in  the 
spleen  by  the  following  experiments  :  On  the  one  hand,  he  inoculated  nine 
monkeys  with  blood  containing  spirilla  ;  and,  on  the  other  hand,  nine 
monkeys,  in  which  splenectomy  had  been  performed,  with  blood  containing 
spirilla.  The  former  recovered,  but  the  latter  died,  and  their  blood  con- 
tained enormous  numbers  of  free  spirilla,  phagocytosis  being  absent. 

Tiktine,  on  the  other  hand,  has  shown  that  inociUated  monkeys  may 
recover,  even  after  previous  splenectomy,  and  that  animals  immunized  by 
a  previous  attack  preserve  their  immunity  even  after  removal  of  the  spleen. 
The  splenic  phagocytosis,  which  is  not  doubtful,  because  it  has  been  directly 
observed,  would  not,  therefore,  be  the  only  means  of  defence  of  the  organism 
against  the  spirillum. 

Gabritchewsky  of  Moscow  thinks  that  the  principal  role  in  this  struggle 
may  be  attributed  to  the  bactericidal  power  of  the  serum.  He  tries  to  prove 
the  presence  of  bactericidal  substances  by  test-tube  experiments.  He  has 
found  the  spirilla  immobile  and  deformed  one  to  four  hours  after  mixing  a 
drop  of  blood  taken  from  a  patient  during  the  crisis,  and  containing  spirilla, 
with  a  drop  of  serum  from  a  monkey  during  the  period  of  apjTexia.  He  has 
studied  the  coefficiency  of  this  bactericidal  power  with  regard  to  the  spirillum 
in  man,  and  also  the  different  phases  of  infection.  He  concludes  that  this 
coefficient  increases  during  the  disease,  especially  on  the  two  days  pre\'ious 
to  the  crisis,  and  that  it  reaches  its  maxim imi  during  the  crisis  by  a  prompt 
accumulation  of  bactericidal  substances.  According  to  Gabritchewsky, 
splenic  phagocjrtosis  commences  only  after  this  attenuation  by.  fluids,  al- 
though the  spirilla  may  be  already  modified  as  regards  their  vitality ;  certain 
germs,  moreover,  may  assist  in  producing  a  relapse,  favoured  by  the  rapid 
enfeeblement  of  the  bactericidal  power  of  the  serum  after  the  crisis.  This 
power  reappears  during  the  second  attack,  and  persists,  though  more  or  less 
weakened,  after  recovery  for  months  and  years.  In  order  to  complete  his 
theory  and  to  make  use  of  this  bactericidal  power,  Gabritchewsky  attempted 
serotherapy  by  means  of  a  serum  from  a  monkey  which  had  just  entered  the 
stage  of  defervescence,  and  in  which  the  blood  might  be  considered  to 
possess  this  immunizing  power.  Two  other  monkeys  were  simultaneously 
inoculated  with  blood  containing  spirilla  :  the  one  not  treated  by  serum  was 
sick  for  seventy-two  hours,  and  had  a  relapse  ;  the  other,  to  whom  serum 
had  been  given,  showed  in  forty-eight  hours  rapid  defervescence,  the 
spirilla  were  less  abundant  in  the  blood,  and  no  relapse  appeared. 

Metchnikofi  has  criticized  the  experiments  of  Gabritchewsky,  and 
thinks  that  they  are  not  sufficiently  clear  to  justify  the  conclusions  of  the 


1742  TEXT-BOOK  OF  MEDICIKE 

Russian  author ;  the  results  have  been  too  variable  to  allow  the  deduction 
of  general  laws  applicable  to  the  process  in  the  living.  Metchnikoff  has 
found  that  the  spirilla  do  not  lose  their  vitality  in  the  blood  before  the  crisis 
and  the  splenic  phagocjrfcosis.  He  considers,  therefore,  that  it  is  not  yet 
demonstrated  that  the  refractory  state  (immunity)  depends  on  the  bacteri- 
cidal power  of  the  serum.  Lastly,  it  may  be  remarked  that,  as  regards 
serotherapy,  we  cannot  deduce  general  results  from  the  single  experiment 
performed  by  Gabritchewsky. 

Treatment. — It  is  of  the  highest  importance  to  guard  against  contagion 
by  every  possible  means ;  hygiene  of  apartments,  isolation  of  the  sick, 
careful  disinfection  of  the  clothes,  of  the  hands,  of  the  linen,  and  of  the 
articles  which  have  been  in  contact  with  the  sick.  Although  further  re- 
searches are  necessary  before  we  are  in  possession  of  a  specific  treatment 
for  the  disease,  we  must,  nevertheless,  have  recourse  to  systematic  treat- 
ment, employing  analgesics  when  indicated  to  diminish  the  pain,  tonics  or 
alcohol  to  sustain  the  general  health,  and  cold  baths  to  reduce  the  hyper- 
pyrexia. 


CHAPTER  III 
INFECTIOUS   DISEASES   PROPER   TO   MAN 

I.— STREPTOCOCCAL  INFECTION  OF  THE  BLOOD. 

Clinical  Cases. — On  November  22, 1908,  a  youiig  man,  who  had  been  for  six  days  on 
the  surgical  side,  was  transferred  to  my  charge.  One  morning  ho  had  scratched  his 
right  thumb  ;  in  the  afternoon  he  felt  such  acute  pain  in  the  arm  and  axilla  that  he 
went  home,  when  he  was  taken  iU  with  chills,  fever,  and  headache,  and  passed  a  sleep- 
less night. 

Next  morning  the  arm  was  swollen,  ihe  axiUa  was  indurated,  and  the  patient  felt 
some  lumps  (enlarged  glands).  At  night  he  was  admitted  to  the  Hotel-Dieu  ;  the  tem- 
perature was  10J..°  F. ;  the  little  scratch  on  the  thumb  had  healed,  the  arm  was  swollen 
and  very  painful,  but  no  sign  of  lymphangitis  was  present. 

The  axilla  was  brawny  and  several  glands  could  be  felt.  Further,  a  diffuse  redness 
with  ill-defined  edges  and  starting  from  the  axilla,  was  invading  the  chest-wall.  TIih 
red  patch  was  very  painful,  but  no  fluctuation  could  be  felt. 

In  three  days  the  axiUary  cellulitis  cleared  up  without  surgical  intervention  ;  the 
patient  was  now  sent  over  to  my  ward.  On  examination  the  red  patch  was  disaj)pear- 
ing,  but  the  general  condition  showed  the  severity  of  the  infection  ;  temperature  over 
101°  F. ;  diy  red  tongue,  ballooning  of  the  beUy,  diarrhoea,  enlargement  of  the  spleen, 
and  delirium  (a  clinical  picture  much  like  that  of  typhoid  fever) ;  respiration  quickened, 
many  rales,  mucopurulent  blood-stained  expectoration.  Cryogenine  brought  down  the 
fever. 

In  a  few  days  the  erythema  of  the  thorax  and  axillary  swelling  disappeared,  but  a 
fresh  patch  of  redness,  streaked  with  veinules  and  marked  with  piu-puric  spots 
appeared  on  the  left  arm.  The  patch  was  not  erysipelas,  because  the  limit  between 
the  patch  and  the  healthy  skin  was  not  well  marked,  and  because  there  was  no  pro- 
minent edge,  due  to  oedema  and  to  accumulation  of  migratory  leucocytes ;  moreover, 
the  redness  disappeared  on  pressure,  which  does  not  obtain  in  erysipelas.  Considering 
the  erythema  and  the  cause  of  the  infection,  my  opinion  was  :  Sti-eptococcal  infection, 
the  wound  of  the  thumb  being  the  portal  of  entry.  Le  Play  found  the  streptococcus. 
in  cultures  from  the  blood,  in  a  pure  state,  no  other  organisms  being  present.  But  in 
this  case  the  Streptococcus  pyogenes  had  not  produced  i^us,  although  it  had  caused 
erythemata  ;  moreover,  erythema  is  one  of  the  manifestations  of  streptococcal  infec- 
tion, and  may  be  accompanied  by  j)urpura,  petechiae,  and  ecchymoses. 

The  mine  contained  albumin,  polynuclear  and  mononuclear  leucocytes  and  some 
chains  of  streptococci :  streptococcal  nephritis. 

The  erythematous  patch  on  the  left  arm  reached  the  shoulder  ;  two  days  later 
similar  erythema  appeared  on  the  left  thigh.  The  patient  now  complained  of  pain  in 
the  left  knee,  and  artluitis  developed.  An  eschar  then  appeared  on  the  right  buttock. 
The  situation  did  not  appear  too  grave,  considering  only  the  local  condition ;  but  the 
general  condition  was  very  grave ;    dyspnoea,  delirium,  loss  of  strength,  albuuiiuiu-ia, 

1713 


1744  TEXT-BOOK  OF  MEDICINE 

enlargement  of  the  liver  and  spleen,  obstinate  diarrhoea,  ballooning  of  the  belly,  and 
total  failure  of  the  remedies  employed.     The  prognosis  was  very  gloomy. 

Nevertheless,  during  the  latter  part  of  November,  the  temperature  did  not  exceed 
100°  F.  For  a  moment  a  halt  was  called ;  the  deliriiun  ceased,  the  tongue  became 
moist,  the  belly  was  supple,  the  diarrhoea  had  disappeared,  the  rales  were  much  less 
marked,  the  patient  took  his  milk  well,  and  improvement  was  manifest.  But,  during 
the  next  few  days,  collections  of  pus  rapidly  formed  in  the  arms  and  in  the  thighs ; 
they  were  opened,  and  the  streptococcus  was  found  in  a  pure  state. 

The  first  stage,  of  three  weeks'  dxiration,  was  marked  by  erythema,  somewhat 
resembling  erysipelas,  and  by  the  absence  of  pus  formation.  In  the  second  stage, 
abscesses  occurred  one  after  another,  and  the  situation  became  markedly  worse. 

Injections  of  antistreptococcal  serum  and  of  physiological  serum  gave  no  result. 
The  dyspnoea  was  intense.  Numerous  rales  and  bronchial  breathing  were  audible 
over  the  base  of  the  right  Itmg.  The  delirium  reappeared,  and  sedatives  had  no  effect. 
The  patient  died  in  collapse  after  an  illness  of  thirty-nine  days. 

The  autopsy  was  not  satisfactory,  because  it  was  not  performed  until  three  days 
after  death.     Still,  the  streptococcus  was  foun.d  in  the  blood  from  the  heart. 

Such  a  case  has  the  value  of  an  experiment.  A  healthy  man  scratched  his  thumb, 
and  streptococcia  immediately  developed.  The  mischief  ran  a  fulminant  course,  the  incu- 
bation period  lasted  but  a  few  hours,  and  was  then  followed  by  symptoms  of  invasion, 
high  fever,  and  rigors ;  by  night  the  axillary  glands  were  affected ;  the  next  day 
saw  the  phase  of  eruption,  and  the  morbid  cycle  ended  in  the  phase  of  suppuration 
with  multiple  abscesses.  Meanwhile  the  streptococcus  was  found  in  the  blood,  in  the 
urine,  and  in  the  pus. 

In  this  case  the  streptococcal  infection  followed  two  channels  ;  it  entered  the 
lymphatic  system,  and  affected  the  axillary  glands,  although  there  was  no  sign 
of  lymphangitis,  and  it  also  entered  the  capillaries  direct  in  the  neighbourhood  of  the 
original  wound.  The  thumb,  which  served  as  the  point  of  entry,  was  neither  painful 
nor  swollen.  It  would  have  been  better  if  it  had  been,  from  the  first,  the  seat  of  an 
abscess. 

Other  Cases. — Post-operative  Streptococcia. — A  woman  had  been  operated  upon,  six 
weeks  before,  for  a  tumour  of  the  left  breast.  She  was  seized  with  a  sharp  rigor,  and 
with  pain  on  the  right  side  ;  the  diagnosis  was  pneumonia.  On  her  admission  to  the 
Broussais  Hospital  some  days  later,  it  was  noticed  that  the  operation  scar  was  sur- 
rounded by  an  erysipelatous  patch.  Pleuritic  effusion  was  found  on  the  right  side, 
and  sero-purulent  fluid  was  obtained  on  puncture.  Arthritis  appeared  in  the  sterno- 
clavicular joint,  in  the  knee,  and  in  the  tibio-tarsal  joint. 

Double  parotiditis  appeared  :  the  prostration  was  extreme,  and  the  patient  died  in 
collapse.  Various  methods  of  treatment,  including  three  injections  of  anti-strepto- 
coccic  serum,  gave  no  result.  Cultures  made  during  life  revealed  the  streptococcus 
in  the  blood,  in  the  pleuritic  fluid,  and  in  the  pus  from  the  affected  joints. 

A  man,  fifty  years  of  age,  was  admitted  to  the  Boucicault  Hospital  for  tubercular 
glands  in  the  axilla.  The  glands  were  removed.  Next  day  the  temperature  rose 
to  105°.  Twenty-four  hours  later  the  march  of  events  was  so  rapid  that  the  patient 
was  comatose.  Tongue  dry,  temperature  104°  F.,  pulse  rate  120.  A  focus  of  sub- 
crepitant  rales  was  found  at  the  left  base.  Examination  of  the  blood  yielded  strep- 
tococci in"  pure  culture.  Five  centigrams  of  collargol  were  given  by  intravenous 
injection,  the  situation  improved,  and  the  patient  finally  recovered. 

Puerperal  Streptococcia. — A  woman,  eight  months  pregnant,  was  admitted  to  the 
Maternite.  On  the  day  after  her  delivery,  she  was  taken  iU  with  chiUs  and  fever ; 
during  the  next  few  days  pains  appeared  in  the  right  leg,  but  she  left  the  hospital. 
Phlebitis  soon  set  in,  and  she  was  admitted  to  the  Cochin  Hospital  under  Widal. 
She  had  phlegmatia   alba  doleus  of  the  right  leg ;    the   temperature  was  103°  F. 


INFECTIOUS  DISEASES  rROPKR  TO  MAN  1745 

Four  days  lator  phlohitis  appeared  in  tho  l(<ft  lej;,'.  Kxainiriiilion  of  Iho  blcjod  showed 
pure  eulturos  of  streplorocci.     Slie  ^'nidiially  recovered. 

A  woniaii,  whose  period  was  six  weeks  overdue,  lost  blood  and  passod  a  coini)lete 
ovum  as  bi^"-  as  ilie  list.  On  the  same  oveninff  sho  had  a  severe  ri^ror.  At  the  end  of 
livo  days  the  belly  was  distended  and  painful.  Intermittent  iever  ajijieared,  the 
ovenintr  rise  beinjjr  as  hi>jrli  as  lOl^  F.  A  murmur  was  heard,  and  the  diag-no.sis  of 
infec'live  endocarditis  was  made.  Cultures  from  the  blood  revealed  the  streptococcus. 
In  a  few  hours  the  loft  leg-  and  left  foot  became  painful,  livid,  and  cold.  Embolism  of 
the  popliteal  and  tibio-peroneal  vessels  was  suspected.  Death  occurred  four  days 
later. 

An  infant,  a  mouth  old,  was  admitt-ed  into  the  Enfants-Assistes  for  erysipola.s, 
which  luul  invaded  the  buttocks,  the  thighs,  the  penis,  and  the  scrotum.  A  small 
abcess  formed  at  the  ])oint  where  an  injection  of  anti-streptococcic  serum  had  been 
priven.  The  patient  died.  An  autopsy  was  made  tive  hours  after  death,  and  pure 
cultures  of  streptococci  were  obtained  from  blood  from  the  heart,  from  the  cerebro- 
spinal fluid,  and  from  the  liver  and  spleen  tissue. 

So  called  Medical  Streptococcia. — In  the  preceding  cases  the  breach 
in  the  economy  was  so  important  that  it  could  not  pass  unnoticed,  and  the 
streptococcal  infection  found  a  wide  portal  of  entry.  In  other  cases, 
however,  the  portal  is  so  small  that  it  may  escape  notice.  Two  cases  of 
this  nature  are  here  quoted: — 

In  the  first  case,  a  man  who  had  an  ulcerated  hasmorrhoid  was  seized  with  chills, 
and  fever ;  pain  appeared  in  the  right  thigh.  Painful  areas  of  redness  were  found  on 
the  right  thigh  and  on  the  left  leg.  The  urine  contained  albumin.  Two  days  later 
brawny  and  painful  red  nodules  appeared  at  the  elbow.  Pure  cultures  of  streptococci 
were  obtained  from  the  blood.  The  patient  died  from  streptococcal  infection  of  the 
blood,  the  portal  of  entiy  being  the  small  htemorrhoidal  ulcer. 

In  the  second  case,  the  infection  would  seem  to  have  entered  the  system  through 
an  inflamed  throat.  A  woman  with  mitral  stenosis  was  admitted  under  Widal. 
Two  days  later  she  complained  of  a  slight  sore  throat.  After  the  throat  got  better, 
the  evening  temperatui-e  rose  to  101^  P.,  and  shivering  fits  set  in.  Examination  of 
the  heart  revealed  the  old  stenosis  murmiu-,  and  also  a  long  diastolic  murmur  at  the 
aortic  orifice.  Examination  of  the  blood  revealed  the  streptococcus  in  pure  culture. 
The  diagnosis  of  strejitococcal  endocarditis  was  confirmed.  Pleuritic  efl'usion  developed 
on  each  side  of  the  chest ;  the  effusion  was  sero-fibrinous.  The  patient  died  suddenly. 
The  autopsy  showed :  long-standing  lesions  of  the  mitral  valve,  and  recent  vegetations 
upon  the  sigmoid  valves. 

I  have  quoted  cases  of  streptococcal  infection  of  the  blood  in  which 
the  point  of  entrance  was  at  times  evident,  at  other  times  more  or  less 
hidden.  We  see,  also,  cases  in  which  it  is  not  possible  to  find  the  portal 
of  entry.  We  may,  therefore,  ask  whether  streptococcal  infection  may  not 
occur  in  streptococci  carriers,  the  germs  remaining  harmless  for  a  time, 
and  later  becoming  so  virulent  as  to  produce  streptococcal  infection  with 
all  its  results.  Such  a  supposition  is  not  improbable,  and  such  cases 
would  be  comparable  to  the  well-proved  auto-infection  of  typhoid  fever. 
We  see,  as  a  matter  of  fact,  persons  who  were  carriers  of  harmless  bacilli, 
until  these  bacilli  became  virulent  to  the  point  of  causing  typhoid  fever. 


1746  TEXT-BOOK  OF  MEDICINE 

Symptoms — Diagnosis. — The  symptoms  of  streptococcal  infection  of 
the  blood  vary :  cutaneous  eruptions  (erythemata  in  patches  or  in  nodules, 
rashes,  petechiee,  purpura);  superficial  and  deep  suppuration  (abscess, 
cellulitis,  arthritis,  parotiditis,  empyema) ;  phlebitis,  lymphangitis,  endo- 
carditis, jaundice,  albuminuria;  conditions  simulating  typhoid  fever  (swell- 
ing of  the  spleen,  ballooning  of  the  beUy,  diarrhoea,  delirium,  headache, 
prostration)  :  such  are  the  many  symptoms  which  may  be  seen  in  patients 
suffering  from  streptococcal  s^ticsemia. 

Of  these  symptoms,  some  are  sufficiently  characteristic  to  lead  readily 
to  a  diagnosis.  For  example,  when  a  patient,  having  fever  and  the  look  of 
some  infectious  condition,  has  at  the  same  time  lymphangitis,  patches  of 
erythema,  arthritis,  and  abscesses,  the  condition  is  probably  streptococcal 
in  nature,  and  blood  cultures  will  confirm  the  clinical  diagnosis.  In  many 
cases  the  diagnosis  is  simplified  by  the  cause  which  has  given  rise  to 
the  infectious  condition.  Thus,  a  woman,  recently  delivered,  is  taken 
ill  with  attacks  of  fever,  while  slight  jaundice,  patches  of  erythema,  and 
joint  troubles  may  or  may  not  be  present ;  such  a  complex  should  direct 
attention  to  streptococcia.  Cultures  are  made  from  the  blood  and  the 
streptococcus  is  found  as  the  cause  of  the  infection.  If  a  new-born 
infant  is  attacked  by  erysipelas  of  the  umbilicus  or  of  some  other  part, 
with  concomitant  symptoms  of  infection,  it  is  natural  to  attribute  these 
symptoms  to  streptococcal  septicaemia. 

On  the  other  hand,  the  diagnosis  of  streptococcal  septicaemia  is  not 
always  obvious  from  the  first ;  the  reYealing  symptoms  may  be  absent, 
the  infection  runs  its  course,  without  the  appearance  of  erythematous 
patches,  without  the  formation  of  abscesses,  without  arthritis,  without  any- 
thino-  to  recall  the  external  signs  of  streptococcia,  and  we  find  ourselves 
face  to  face  with  an  infectious  condition  which  may  simulate  typhoid 
fever,  icterus  gravis,  or  malignant  endocarditis;  the  pathogenesis  of  this 
infectious  condition  cannot  be  clearly  elucidated  without  blood  cultures. 
To  quote  examples  : — 

A.  Tvoman.  previously  in  good  healtli,  "was  admitted  to  tlie  Cliarite  for  general 
malaise,  mth  fever,  lassitude,  h-eadaclie,  dizziness  and  obstinate  insomnia.  Considering 
these  symptoms  onlT,  tlie  condition  resembled  tbe  onset  of  typboid  fever.  Tbe 
temperature  was  10-i°  E.  Yomiting  of  bile  -with  profuse  diarrbcea  and  some  jaundice 
noTV  set  in.  Tbese  symptoms  somewbat  recalled  tbe  pictui-e  of  icterus  gravis.  And 
yet  tbe  condition  -was  neither  typboid  fever  nor  icterus  gi-avis.  Tbe  patient  died 
comatose. 

The  autopsy  did  not  reveal  tbe  nature  of  the  malady.  It  was  the  bacteriological 
examination  that  cut  tbe  knot.  Tubes,  inoculated  with  blood  from  the  heart,  and  with 
tissue  from  the  liver  and  spleen,  all  gave  the  streptococcus  in  pure  culture.  In  this 
ca&e  the  clinical  diagnosis  was  not  possible ;  no  sign  was  present  to  direct  the  attention 
to  the  hypothesis  of  a  streiotococcal  infection. 

A  boy  bad  been  iU  for  ten  days  with  malaise,  and  headache.     The  temperature  was 


INFECTIOUS  DISEASES  PROPER  To  MAN  1747 

104r  F. ;  tlie  belly  was  diskmilod.  Typhoid  lovnr  was  suspui-led..  Some  days  later,  the 
patient  hejriin  to  couj,'!!  and  marked  dysjinooa  appeared.  PercuHsion  gave  a  zone  of 
duLuess  over  tlie  median  part  of  the  left  lung-;  auscnltation  revealed  sub-crepitunt 
rules  and  tubidar  lireaihing-.  The  diagnosis  was  broucho-puoumonia.  Effusion  took 
place  into  tlio  ri.Lrht  pleural  cavity  and  puncture  removed  oitron-coloured  fluid.  The 
patient's  strength  rapidly  declined,  and  he  died  after  an  illnes.s  of  .six  wxMjks'  duration. 
The  lungs  were  splenized  and  the  two  pleiu-al  cavities  contained  al)oat  three  pints 
of  reddish  fluid.  At  the  base  of  the  brain,  over  the  optic  chiasma,  thei-e  was  a  patch  of 
Hrm  pus.  Bucteriologicid  examination :  the  pleuritic  fluid  contained  the  streptococcus 
alone,  the  juice  from  the  lungs  contained  .streptococci  and  some  staphylococci,  the 
meningeal  pus  showed  the  streptococcus  in  a  pure  state. 

These  two  cases  difier  absolutely  from  cases  of  classical  stieptococcia. 
We  find  none  of  tlie  cardinal  symptoms  which  put  us  on  the  track  of  the 
iliagnosis  :  erysipelas,  lymphangitis,  patches  of  erythema,  cutaneous  mani- 
festations, purulent  collections,  arthritis^^  phlebitis  were  all  absent.  The 
key  to  the  diagnosis  was  supplied  by  cultures.  According  to  the  pre- 
dominance of  various  symptoms,  streptococcal  infection  may  simulate 
typhoid  fever,  icterus  gravis,  acute  tuberculosis  and  staphylococcal  infection. 

Blood-Cultures. — In  any  doubtful  case  of  an  infectious  nature,  blood- 
cultures  systematically  made  are  of  the  greatest  importance.  Nevertheless, 
the  result  furnished  by  blood  cultures  is  a  criterion  which  is  at  times 
wanting.  Such  local  streptococcal  lesions  as  patches  of  erysipelas  and 
abscesses  are  rarely  followed  by  blood-infection.  At  times,  indeed,  in 
such  a  case,  the  defence  against  the  blood-infection  becomes  organized  on 
the  very  soil  of  the  inoculation.  "  The  leucocytic  and  cellular  defence  is 
energetic,  the  lesion  remains  local ;  it  runs  its  course  and  perishes  in  situ, 
extinguishing  the  germ-infection.  If,  on  the  other  hand,  the  virulence  of 
the  microbe  is  considerable,  the  colonization  and  the  multiplication  of 
the  streptococcus  take  place  rapidly  "  (Bluysen). 

The  presence  of  the  streptococcus  in  the  blood  can  be  recognized  before 
the  infection  has  reached  an  advanced  stage.  The  cases  quoted,  though 
very  different  in  their  clinical  course,  show  that  a  positive  diagnosis  was 
possible  by  making  blood-cultures  even  a  short  while  after  the  onset  of  the 
disease.     This  means,  then,  is  valuable  and  should  not  be  neglected. 

Proper  technique  is  necessary.  Direct  examination  of  slides  rarely 
show  the  streptococcus  ;  insemination  is  the  method  of  election,  the  blood 
being  taken  from  a  vein  in  the  arm,  and  5  c.c.  sown  on  200  grams  of 
culture-medium. 

Pathogenesis. — My  patient  in  the  Saint  Christopher  ward  died  from 
general  streptococcal  infection,  the  portal  of  entry  being  a  trifling  scratch 
on  the  thumb.  At  first  sight,  great  disproportion  would  seem  to  exist 
between  the  cause  and  the  effect.  To  die  from  a  scratch  on  a  finger  is, 
indeed,  sad.     But  this  disproportion  between  the  cause  and  the  effect  is 


1748  TEXT-BOOK  OF  MEDICINE 

oommon  in  streptococcic  and  staphylococcic  infections.  The  enemy  can 
enter  through  a  small  breach  in  the  skin  or  in  a  mucous  membrane.  This 
breach  may  be  so  small  as  to  pass  unnoticed ;  once  inoculation  has  taken 
place,  local  trouble  or  general  infection  may  follow. 

Treatment. — Let  us  first  consider  prophylactic  measures.  When  we 
remember  that  slight  abrasions  of  the  skin  or  of  the  mucous  membranes 
may  be  the  starting-point  of  streptococcal  infections,  we  must  never  treat 
these  small  lesions  with  indifference.  The  smallest  wound  of  the  skin 
should  be  most  carefully  cleansed  and  protected  from  the  entrance  of 
organisms.'  Too  much  care  cannot  be  exercised  when  we  are  making  an 
autopsy. 

When  streptococcal  infection  of  the  blood  is  present,  it  is  natural  to 
think  first  of  anti-streptococcic  serum,  but  the  results  obtained  from  this 
treatment  are  scarcely  encouraging.  If  I  had  had  Wright's  streptococcic 
vaccine  ready  to  hand,  I  should  certainly  have  used  it  in  the  first  case 
quoted,  because  I  have  employed  the  gonococcic  vaccine  in  cases  of  gono- 
coccic  infection  of  the  blood,  Intra-venous  injections  of  collargol  appear 
to  have  given  good  results  in  a  case  of  blood  infection  due  to  the  staphy- 
lococcus ;  I  do  not  know  of  any  similar  result  in  a  case  of  streptococcal 
infection.  Injections  of  a  hundred  grams  of  artificial  serum,  given  twice 
daily,  may  aid  the  organism  in  the  struggle.     Cold  baths  are  of  service. 

II.  EEYSIPELAS  OF  THE  FACE. 

Bacteriology. — The  infectious  nature  of  erysipelas  (IpvOpog,  red ;  TrlAXa, 
skin)  and  its  microbic  origin  are  well  known.  The  agent  which  produces 
it  is  the  streptococcus  (Nepveu,  Fehleisen). 

Description. — Facial  erysipelas  is  usually  ushered  in  by  chUls,  malaise, 
headache,  nausea,  vomiting,  and  high  temperature.  As  these  symptoms 
may  precede  the  appearance  of  the  erysipelatous  patch,  erysipelas  has  been 
compared  to  an  eruptive  fever  (Borsieri),  In  some  cases  erysipelas  is 
preceded  by  painful  enlargement  of  the  submaxillary  glands. 

Erysipelas  appears  as  a  red  and  sensitive  patch.  The  aperture  of  the 
nostrils,  the  angle  of  the  eye,  and  the  external  ear  are  the  usual  starting- 
points.  If  the  skin  of  the  face  or  the  scalp  presents  an  excoriation  (eczema, 
herpes),  erysipelas  usually  comm^ences  at  the  excoriated  spot.  The  patch 
soon  becomes  dark  red,  shiny,  and  painful.  The  skin  is  burning,  tense, 
prominent,  dry,  and  parchment-like.  The  redness  does  not  completely 
disappear  on  pressure,  as  in  erythema.  The  patch,  when  taken  between 
the  fingers,  cannot  be  raised  in  folds,  but  is  resistant  and  gives  a  sensation 
of  thickening,  due  to  the  invasion  of  the  dermis  and  of  the  subjacent  tissue. 

The  erysipelatous  patch  spreads  in  an  irregular  manner,  and  presents 


INFECTIOUS  DISKASKS  IMiol'KR  TO  MAN  1710 

at  its  invadiiij^  ed;;e  a  promiiKMit  Itorder,  clearly  maiked  against  the  hcaltliy 
parts.  When  the  border  disappears,  we  may  say  that  the  erysipelas  has 
reached  its  limit.  Its  course  is  more  or  less  rapid  in  different  cases.  When 
it  begins  at  the  root  of  the  nose,  it  extends  in  a  symmetrical  manner  to  the 
cheeks,  like  a  pair  of  spectacles.  In  its  progress  the  disease  dies  out  upon 
the  parts  first  invaded.  It  may  be  limited  to  a  part  of  the  face,  or  it  may 
affect  the  whole  face,  which  then  becomes  umrecognizable.  The  red  oede- 
matous  eyelids  cover  the  eyeballs,  the  swollen  and  deformed  nostrils  are 
almost  closed,  the  cheeks  are  swollen,  and  the  ears  are  red,  shiny,  and 
double  their  normal  size.  The  face  thus  deformed  recalls  the  appearance 
of  certain  Chinese  grotesques  (Raynaud).  The  forehead,  the  cranium,  the 
nape  of  the  neck,  and  the  neck  itself  are  sometimes  invaded.  Upon  the 
scalp  the  erysipelatous  tint  is  not  as  dark  as  upon  the  face,  but  the  pain 
is  more  acute. 

In  some  cases  the  skin  of  the  face  is  raised  by  a  serous  efEusion,  which 
collects  in  the  form  of  vesicles.  The  fluid  in  the  bullae  may  become  turbid, 
purulent,  or  haemorrhagic.  The  pus  collects  in  the  form  of  an  abscess. 
After  rupture,  the  blebs  become  covered  with  thick  yello^^^sh  crusts.  The 
skin  desquamates  in  patches,  and  the  hair  usually  falls  out  when  the  disease 
affects  the  scalp.  It  does  not  end  in  baldness,  although  the  scalp  is  some- 
times much  affected.     The  loss  of  the  eyebrows  may  be  permanent. 

The  disease  usually  lasts  from  six  to  ten  days.  The  fever  is  high  at 
night,  with  a  more  or  less  marked  morning  remission.  In  some  cases  it 
diminishes  gradually,  but  in  others  it  falls  suddenly  in  one  night.  In  some 
cases  erysipelas,  supposed  to  be  at  an  end,  revives.  The  fever  reappears, 
and  the  disease  lasts  from  a  fortnight  to  three  weeks. 

A  disordered  condition  of  the  digestive  tract,  with  anorexia  and  con- 
stipation, succeeds  the  gastric  troubles  of  the  onset ;  the  urine  is  scanty  and 
albimiinous ;  the  headache  is  severe  ;  and  the  restlessness  and  delirium  are 
sometimes  very  marked,  especially  when  the  scalp  is  affected. 

Erysipelas  of  the  Mucous  Membranes. — The  disease  usually  remains 
localized  to  the  face,  but  it  may  affect  the  mucous  membranes  either  before 
or  after  it  has  affected  the  face. 

Angina  and  Stomatitis. — The  mouth  is  rarely  invaded.  At  most,  it  is 
but  slightly  affected  by  erysipelas,  while  the  pharynx  is  one  of  the  most 
frequent  seats  of  the  disease.  Erysipelas  of  the  pharynx — or,  rather,  of 
the  throat  (Lasegue) — is  characterized  by  purple,  shiny  redness  and  severe 
angina.  It  is  sometimes  accompanied  by  bullae,  gangrene,  and  retro- 
pharyngeal abscess.  It  may  spread  to  the  face,  either  by  way  of  the  buccal 
mucous  membrane,  the  nasal  fossae,  or  the  lachrymal  ducts  (Peter). 

Respiratory  Tracts. — Erysipelas  often  begins  in  the  nasal  fossae.  The 
coryza  is  very  painful,  and  is  accompanied  by  acute  fever  and  by  adenitis 

n.  Ill 


1750  TEXT-BOOK  OF  MEDICINE 

of  the  cervical  glands.  In  some  cases  the  rhinitis  extends  to  the  middle  ear 
(deafness),  reaching  the  mastoid  cells  and  the  meninges. 

The  larynx  is  invaded  secondarily  by  erysipelas,  but  primary  laryngitis 
has  been  seen.  The  usual  symptoms,  when  the  larynx  is  afiected,  comprise 
great  swelling  of  the  mucosa  covering  the  tongue,  of  the  arjrtenoid  region, 
and  of  the  epiglottis  with  more  or  less  rapid  oedema,  and  severe  dyspnoea. 

Bronchopneumonia  is  well  recognized  since  Straus's  case  was  pub- 
lished : 

A  patient  suffered  from  a  mild  attack  of  facial  erysipelas,  and  the  fever  fell,  but  at 
the  same  time  pain  appeared  in  the  right  side  ;  erysipelatous  pharyngitis  and  pneumonia 
at  the  right  base  were  discovered ;  the  pneumonia  invaded  the  whole  lung ;  albuminuria 
appeared,  with  slight  jaundice  and  bleeding  from  the  nose.  The  patient  died.  I  have 
seen  a  similar  case  in  a  workman  who  was  taken  ill  with  pneumonia  during  the  decline 
of  facial  erysipelas.  In  Straus's  case  the  autopsy  proved  that  the  erysipelas  had  invaded 
the  trachea,  the  bronchi,  and  the  lung.  Histologically  the  pneumonic  exudate  was 
composed  solely  of  leucocytes  without  fibrin.  Rendu  has  reported  a  similar  case,  in 
which  benign  facial  erysipelas  had  commenced  at  the  angle  of  the  eye. 

In  Mosny's  case  the  pulmonary  erysipelas  was  primary.  A  servant  who  was  attend- 
ing her  master  suffering  from  erysipelas  took  bronchopneumonia,  which  proved  fatal. 
The  bacteriological  examination  revealed  the  presence  of  the  streptococcus. 

Complications — Nephritis. — Albuminuria  is  very  frequent  in  facial 
erysipelas ;  the  only  evidence  of  the  renal  lesion  is,  as  a  rule,  the  presence 
of  albuminuria,  of  casts,  and  sometimes  of  streptococci,  in  the  urine.  In 
other  cases  oedema  and  symptoms  of  acute  uraemia  may  also  be  present. 
Nephritis  in  erysipelas  recovers,  but  the  affected  kidney  may  at  some  later 
period  become  the  starting-point  of  Bright's  disease. 

Joint  troubles  are  rarely  associated  with  facial  erysipelas.  In  all  cases 
it  is  a  question  of  mild  pseudo-rheumatic  iufection.  Nevertheless,  sjmovitis 
of  the  tendon-sheaths  of  the  wrist  (Quinquaud)  and  suppurative  arthritis 
have  been  seen  (Aubree). 

Pericarditis  is  very  rare.  In  two  cases  with  effusion  streptococci  in 
chains  were  found  (Denucee). 

Endocarditis  is  more  common.  Although  it  is  usually  benign  and 
transient,  it  may  sometimes  assume  the  character  of  infective  endocarditis, 
and  may  lead  to  embolism,  aphasia,  and  gangrene. 

Streptococci  have  been  found  in  the  vegetations  of  the  endocardium 
(Achalme).  This  form  of  endocarditis  has  been  reproduced  experimentally. 
Erysipelas  appeared  in  a  rabbit  which  had  been  inoculated  with  the  strepto- 
coccus. The  erysipelas  recovered,  but  the  animal  died  from  endocarditis, 
and  at  the  autopsy  a  large  vegetation  containing  the  streptococcus  was 
found  upon  the  mitral  valve. 

Pleurisy  is  exceptional.  It  was  present  in  two  out  of  six  cases  which 
were  inoculated  by  Fehleisen. 

Erysipelas  sometimes  attacks  the  eye,  and  the  following  complications 


INFECTIOUS  DISEASES  PROPER  TO  MAN  1751 

have  been  seen  :  Conjunctivitis,  chemosis,  keratitis,  iritis,  suppuration  of 
the  eyelids,  and  atrophy  of  the  papilla,  following  obliteration  of  the  central 
artery  of  the  retina. 

The  ear  may  also  suffer  in  erysipelas,  which  causes  purulent  catarrh  of 
the  tympanic  cavity. 

Meningitis  is  extremely  rare.  In  three  cases  published  by  Roger  the 
fibrino-purulent  exudate  contained  the  pneumococcus,  with  or  without  the 
streptococcus.  Delirium  in  erysipelas  is,  therefore,  due  to  the  toxines  or  to 
alcoholism. 

Prognosis. — In  the  great  majority  of  cases  erysipelas  of  the  face  is  a 
benign  disease.  The  nervous  troubles  and  delirium  need  cause  no  alarm, 
and  recovery  is  the  rule.  In  fact,  in  about  a  third  of  the  cases  erysipelas  is 
extremely  slight  and  benign,  so  that  the  name  primary  attenuated  erysipelas 
has  been  given  to  this  form. 

Erysipelas,  however,  may  in  some  cases  be  extremely  serious.  Thus, 
erysipelas  of  the  face  may  become  ambulant,  reaching  the  trunk  or  the 
limbs,  and  causing  prostration  and  infection  of  the  patient. 

It  must  not  be  forgotten  that  erysipelas  of  the  face  may  attack  the 
pharynx,  the  larynx,  the  bronchi,  or  the  lung,  and  cause  severe  inflamma- 
tion of  these  organs,  which  justifies  Coiml's  assertion  that  erysipelas  which 
goes  in  is  more  severe  than  erysipelas  which  comes  out. 

When  erysipelas  occurs  in  cachectic  people,  or  in  those  suffering  from 
Bright's  disease,  diabetes,  abuse  of  alcohol,  pneumonia,  diphtheria,  or  typhoid 
fever,  the  prognosis  is  often  grave,  because  of  their  impaired  constitution, 
and  the  same  remark  applies  to  erysipelas  contracted  during  the  puerperium 
or  in  surgical  operations. 

The  streptococcal  infection  may,  then,  be  so  intense  that  it  shows  its 
malignant  nature  either  by  a  tendency  to  diffuse  suppuration  and  gan- 
grenous inflammation  or  by  a  typhoid  condition,  with  ataxo-a dynamic 
symptoms.  In  these  infective  cases  of  erysipelas  the  tongue  is  dry,  the 
pulse  is  quickened,  the  patient  m  prostrated,  the  delirium  is  more  or  less 
violent,  and  retention  or  incontinence  of  urine  is  present.  These  cases  are 
very  contagious.  They  may  become  the  origin  of  epidemic  foci.  Trous- 
seau, with  his  marvellous  sagacity,  anticipatiijg  the  explanation  which 
bacteriological  researches  have  now  given,  wrote  a  most  lucid  description 
of  the  pathogenesis  of  these  malignant  cases.  "  At  the  commencement  of 
1861,  when  a  terrible  epidemic  of  puerperal  fever  broke  out  in  nearly  every 
lying-in  hospital,  facial  erysipelas,  which  is  generally  so  slight,  assumed 
severe  proportions  in  a  fair  number  of  cases."  This  malignant  character 
of  erysipelas  is  also  frequent  when  the  contagion  is  transmitted  from  trau- 
matic or  surgical  erysipelas.  As  a  matter  of  fact,  surgical  erysipelas  is, 
practically  speaking,  no  longer  seen,  owing  to  the  wonderful  progress  of 

111—2 


1752  TEXT-BOOK  OF  MEDICINE 

antiseptic  surgery  ;  but  if  we  refer  to  former  times,  many  persons  liave  paid 
heavy  tribute  to  facial  erysipelas  in  the  practice  of  surgery. 

Erj^sipelas,  in  some  exceptional  cases,  has  appeared  to  be  a  fortunate 
complication,  which  brought  about  recovery  in  certain  chronic  diseases  of 
the  skin.  Thus,  in  tubercular  scrofula  and  ulcerative  lupus  an  improve- 
ment, and  even  recovery,  have  been  brought  about  by  erysipelas.  The 
injection  of  streptococcal  toxines  has  caused  a  definite  improvement  in  the 
local  condition  of  lupus  (Hallopeau  and  Roger). 

As  regards  the  prognosis  of  erysipelas,  the  blood-count  (Chantemesse 
and  Rey)  gives  important  results.  In  severe  cases  we  find  general  leucocy- 
tosis,  so  that  the  number  of  white  corpuscles  always  exceeds  12,000  per  cubic 
millinietre,  and  also  an  excessive  proportion  of  polynuclear  leucocytes,  which 
may  exceed  92  per  cent.  "  The  degree  of  leucocytosis,  and  especially  the 
increase  in  the  number  of  polynuclear  ceUs,  is  in  direct  relation  with  the 
severity  of  the  disease.  On  the  other  hand,  the  formation  of  numerous 
abscesses  indicates  a  favourable  prognosis.  In  6,000  cases  of  erysipelas 
Chantemesse  never  saw  death  occur  when  abscesses  supervened ;  in  1,000 
cases  with  spontaneous  abscesses,  or  with  abscess  following  the  use  of 
Marmorek's  serum,  recovery  was  the  rule  ;  in  300  fatal  cases  observed  by 
Chantemesse  death  did  not  supervene  by  reason  of  suppuration.  Abscesses 
are,  therefore,  an  indication  of  recovery,  and  may  be  compared  to  the 
abscesses  of  fixation,  playing  the  part  of  the  curative  abscess  which  Trousseau 
described  in  erysipelas  of  the  new-born. 

Diagnosis. — The  idea  of  erysipelas  at  once  enters  the  mind  if  an  indi- 
vidual presents  a  reddish  and  swollen  patch  upon  the  face.  The  face  may 
show  the  gross  appearance  of  erysipelas  in  other  conditions — erythema 
produced  by  the  application  of  carbolic  acid,  or  by  the  emanation  from 
thapsia  plaster,  dental  inflammation,  conjunctivitis,  dacryocystitis,  boils 
upon  the  lips  and  nose,  urticaria,  and  impetigo.  In  aU  these  conditions 
some  portion  of  the  face  may  simulate  erysipelas  by  reason  of  its  redness 
and  swelling. 

The  diagnosis,  however,  rests  upon  the  following  signs :  Erysipelas  begins 
with  fever,  and,  further,  the  erysipelatous  patch  has  special  characters. 
It  is  shiny,  painful,  and  thickened,  while  it  is  also  red,  without  intervals 
of  healthy  skin.  This  redness  does  not  disappear  on  pressure,  like  that  of 
erythema  ;  and,  lastly,  an  essential  point  is  that  the  limit  of  the  erysipe- 
latous patch  is  clearly  marked  from  the  healthy  skin  by  a  prominent 
edge,  which  is  not  found  in  erythema.  Moreover,  the  streptococcus  is  the 
pathogenic  agent. 

Eczema  rubrum,  which  is  accompanied  by  redness  and  swelling  of  the 
face,  at  first  sight  resembles  erysipelas  ;  but  the  disease,  instead  of  gradually 
spreading,  at  once  invades  almost  the  whole  of  the  face.     The  redness  blends 


INFECTIOUS  DISEASES  riiUi'Eli  To  MAN  1753 

insensibly  with  Llio  healtliy  j^arts.  We  can  almost  always  discovei-  some 
siiuill  vesicles,  which  itch  acutely ;  the  fcvor  is  absent  or  very  slight 
(Hardy). 

etiology.-  Krysipclas  is  contagious  and  epidemic.  Any  streptococcus 
[)(Kss(^ssing  sp(*cial  virulence  may  cause  erysipelas,  the  more  sureh'  if  it 
grows  on  a  soil  favourable  to  its  development.  Consequently,  it  is  not  only 
erysipelas  which  may  produce  erysipelas.  Erysipelas  may  also  arise  from 
]nierj)cral  infection,  lymphangitis,  and  collections  of  pus.  The  pathogenic 
streptococcus  may  be  conveyed  by  the  fingers,  by  the  linen,  or  by  articles 
of  any  kind,  and  the  germ  enters  more  easily  if  the  skin  presents  chafes, 
cracks,  or  abrasions.  The  flakes  of  skin  in  erysipelas  are  not  virulent 
(Achalme). 

The  old  name  of  idiopathic  erysipelas  should  be  preserved,  because 
erysipelas,  like  many  infectious  diseases,  may  arise  spontaneously.  I  must, 
however,  explain  this  statement.  Streptococci  devoid  of  virulence  are 
present  in  the  mouth,  in  the  nasal  cavities,  in  the  saliva,  and  in  the  skin. 
Under  the  influence  of  known  or  unknown  causes,  these  inoffensive  microbes 
may  acquire  a  virulence  which  renders  them  pathogenic,  as  has  been  proved 
by  experiments. 

Further,  our  economy,  our  phagoc}^es,  and  our  cells  are  not  always  in 
a  proper  state  of  defence  against  the  hostile  microbe.  Consequently,  on 
the  one  hand,  exaltation  of  virulence  in  an  inoffensive  agent,  and,  on  the 
other  hand,  weakness  of  the  defence  (overwork,  diabetes,  B right's  disease, 
menstruation,  etc.),  are  the  factors  which  explain  the  development  of  so- 
called  spontaneous  erysipelas. 

A  similar  explanation  is  applicable  to  many  infectious  diseases,  such  as 
typhoid  fever,  pneumonia,  and  perhaps  diphtheria.  Morbid  spontaneity, 
therefore,  rises  phoenix-like  from  its  ashes,  and  will  continue  to  occupy  its 
place  in  the  pathogenesis  of  diseases  after  a  momentary  eclipse. 

Erysipelas  does  not  confer  immunity,  and  other  attacks  are  frequent. 
"  The  persistence  of  the  micro-organism  of  erysipelas  in  the  tissues  is  as 
clear  as  that  which  is  met  with  in  old  cultures,  and  its  presence  at  a  certain 
moment  in  the  organism,  where  it  is  fixed,  explains  the  pathogenesis  of 
periodical  erysipelas  "  (Leroy).  Menstruation  and  the  puerperal  condition 
favour  the  return  of  erysipelas  {erysifele  d  repetition).  Experimentally, 
vasomotor  paralysis  favours  the  rapid  arrival  of  phagoc}i;es,  and  opposes 
the  development  of  erysipelas,  while  section  of  the  sensory  nerves  favours 
infection. 

Pathological  Anatomy. — The  coloration  has  almost  disappeared  from 
the  skin  of  the  cadaver,  and  the  peripheral  edge  is  but  little  prominent, 
although  the  skin  is  slightly  oedematous,  and  preserves,  the  imprint  of  the 
finger.      The  skin  is  thickened  and  adherent  to  the  subcutaneous  fatty 


1754  TEXT-BOOK  OF  MEDICINE 

tissue,  over  which  it  no  longer  moves.  We  find  under  the  microscope  that 
the  skin  is  infiltrated  with  white  corpuscles,  the  vessels  are  dilated,  the  flat 
cells  of  the  connective  tissue  are  swollen  and  granular,  and  their  nuclei  are 
divided.  The  adipose  tissue  takes  part  in  the  iaflammation,  l5rmphangitis 
is  frequent,  but  not  constant,  and  "  the  absence  of  abundant  fibrinous 
exudate  constitutes  in  ordinary  cases  a  very  important  difference  between 
erysipelas  and  inflammation  of  the  skin  "  (Renaut). 

Erysipelas  is  an  oedematous  dermatitis.  The  streptococci,  after  pene- 
trating the  derma,  produce,  either  by  themselves  or  by  their  toxines,  the 
following  phenomena  :  dilatation  of  the  small  vessels,  diapedesis  of  the 
white  corpuscles,  phagocytosis,  proliferation  of  the  fixed  cells  of  the  con- 
nective tissue,  infiltration  of  the  cutis  by  serous  fluid  containing  a  small 
amount  of  fibrin,  and  changes  in  the  epidermis.  The  streptococci  are  found 
in  the  lymphatic  spaces,  in  the  channels  at  the  base  of  the  papillse,  and  in 
the  crevices  of  the  derma,  as  well  as  in  the  connective  spaces  of  the  sheaths 
of  the  hair-follicles  (Cornil  and  Babes). 

Fehleisen  has  described  three  zones  in  the  patch  of  erysipelas.  The  zone 
external  to  the  edge,  or  the  peripheral  zone,  has  almost  the  appearance  of 
normal  skin,  in  which  the  streptococci  are  numerous.  They  prepare  the 
soil,  but  have  not  as  yet  caused  phagocytosis,  accumulation  of  wandering 
cells,  dermatitis,  or  oedema.  The  lesion  is  found  in  full  activity  at  the 
edge  of  the  patch.  A  considerable  accumulation  of  migratory  cells,  with 
oedema,  takes  place  there,  the  edge  in  erysipelas  being  produced  through 
the  separation  of  the  connective  tissue  bundles  by  the  oedema  and  the 
leucocytes.  The  central  zone  of  the  patch  shows  the  process  in  retrogres- 
sion. The  streptococci  are  no  longer  present  in  the  derma,  or,  at  least, 
only  in  very  small  numbers. 

The  epidermis  also  undergoes  multiple  lesions.  The  cells  which  form  its 
various  layers  become  separated  and  degenerated,  and  yield  to  the  pressure 
of  the  oedema,  forming  a  bleb.  In  some  cases  the  lesion  ends  in  abscess,  in 
inflammation,  or  in  gangrene. 

Treatment. — Until  recent  times  the  treatment  of  erysipelas  was  absolutely 
empirical,  and,  it  must  be  said,  unsatisfactory.  The  topical  remedies 
variously  advised  to  arrest  the  progress  of  the  disease,  such  as  collodion, 
iodine,  solutions  of  nitrate  of  silver,  mercurial  ointment,  boric  lotions,  and 
solutions  of  mercury,  have  really  no  action.  Compresses  soaked  in  soothing 
applications,  and  frequently  renewed,  are  the  best  topical  applications,  and 
give  the  patient  some  relief. 

An  emetic  or  a  saline  purgative  is  employed  for  gastric  trouble ;  opium, 
bromides,  chloral,  .and  sedative  draughts  are  given  for  restlessness  and 
delirium ;  tonics,  such  as  extract  of  cinchona  and  champagne,  are  indicated 
if  adynamic  symptoms  predominate. 


INFECTIOUS  DISEASES  PROPER  TO  MAN  1755 

Cbautemesse  advises  the  ap])lication  of  serum  mixed  with  lanoliue  to 
the  erysipelatous  patch.     This  local  serotherapy  gives  good  results. 

III.  STAPHYLOCOCCAL  INFECTION  OF  THE  BLOOD. 

Clinical  Cases.  A  boy  who  fell  from  a  bicycle  struck  his  right  hip  violeully  and 
Rorulrliod  his  liancls  in  several  ]»lacos.  Some  daj's  later  ho  was  taken  ill  with  Hharji 
pain  iu  the  loins  ;  the  general  ctmdition  became  serions,  with  fever,  epistunin,  headache 
and  insomnia.  He  was  admitted  under  Letulle  ;  he  lay  comatose  in  bed  ;  the  nostrils 
were  dry,  the  belly  was  distended  and  painful ;  gurgling  was  present  in  the  right 
iliac  fossa.  The  temperature  was  104°  F.  In  the  presence  of  these  .symptoms,  the 
diagnosis  leant  towards  typhoid  fever,  but  Widal's  test  was  negative.  Sharp  pain 
soon  appeared  in  the  right  buttock,  and  in  the  back  of  the  thigh.  An  aortic  murmur 
of  insufficiency  was  audible. 

Blood  cultures  revealed  the  Staphylococcus  av/revs  in  a  pure  state.  The  diagnosis, 
llierefore,  was  staphylococcal  septicaemia. 

The  buttock  was  incised,  much  pus  being  evacuated ;  the  abscess  had  started  from 
the  iliac  bone.  The  pus  contained  the  Staphylococcus  aurexis.  Intravenous  injeftions 
of  collargol  (5  centigrams)  were  given  some  days  apart.  The  patient  recovered,  except 
that  the  aortic  murmur  still  persisted.  In  this  case  the  injury  favoured  the 
staphylococcic  infection. 

A  girl,  sixteen  years  of  age,  was  admitted  to  the  Cochin  Hospital  for  sore 
throat  with  rigors,  headache  and  vomiting.  Examination  of  the  throat  showed 
general  redness  but  neither  exudate  nor  ulceration.  The  submaxillary  and  cervical 
glands  were  enlarged.  Next  day  the  condition  suddenly  grew  worse ;  the  temperature 
rose  to  105°  F.,  the  headache  was  intense,  the  throat  was  very  red,  the  glands  were 
much  enlarged  and  very  painful.  Profuse  diarrhoea  came  on  and  the  belly  was 
t^Tupanitic.  Sero-diagnosis  proving  negative,  typhoid  fever  was  excluded.  Blood 
examination  yielded  pure  cultures  of  the  Staphylococcus  aureus.  The  patient  died 
after  an  illness  of  twelve  days'  duration.  The  post-mortem  showed  miliary  abscesses  in 
the  Uver  and  in  the  kidneys.  Pus  from  the  liver  gave  pure  cultures  of  Staphylococcias 
aureus.    In  this  case  the  sore  throat  was  the  starting-point  of  the  general  infection. 

In  the  following  case  it  was  impossible  to  find  the  point  of  entrance  of  the  infective 
agent.  A  girl  had  been  taken  ill  three  weeks  before  with  a  sharp  chill.  Since  that 
time  the  chills  were  frequently  repeated  and  the  breathing  was  much  embarrassed.  On 
admission  to  hospital  double  pleuritic  effasion  and  an  aortic  murmur  were  discovered. 
Slight  jaundice  appeared.  The  Staphylococcus  aureus  was  obtained  in  pm-e  culture 
from  the  blood.  The  diagnosis,  therefore,  was  staphylococcal  septicaemia.  The  case 
was  fatal. 

At  the  autopsy  a  bunch  of  vegetations  was  found  on  the  aortic  valves.  Above  these 
vegetations  was  an  ulcer  which  established  a  communication  between  the  aorta  and  the 
right  auricle.  An  abscess  as  large  as  a  pea  was  found  in  the  myocardium  of  the 
septum  between  the  right  auricle  and  the  aorta.  The  other  organs  were  healthy. 
The  Staphylococcus  aureus  was  obtained  in  pure  culture  from  the  liver,  pericardium, 
and  endocarditic  vegetations.  The  pus  from  the  abscess  in  the  heart  gave  the 
Staphylococcus  aureus,  the  Bacillus  celi,  and  some  large  rods. 

Diagnosis. — These  cases  help  us  to  compare  staphylococcal  with 
streptococcal  infection.  They  have  characteristics  in  common,  and  also 
points  of  difference.  In  many  respects  they  resemble  each  other;  thus 
they  may  both  show  a  symptom -complex,  somewhat  resembling  typhoid 
fever.     They   may   both   cause  suppuration.     Nevertheless,   suppuration. 


1756  TEXT-BOOK  OF  MEDICINE 

abscesses,  cellulitis  purulent  arthritis,  lymphangitis,  and  phlebitis  are 
nearly  always  the  appanage  of  streptococcal  infection.  Osteomyelitis 
is  most  commonly  seen  in  staphylococcal  infections.  Endocarditis,  usually 
of  the  infective  type,  is  seen  equally  in  both  forms  of  infection. 

Looking  only  at  these  symptoms  and  these  lesions,  the  difference 
between  staphylococcal  and  streptococcal  infections  is  not  always  clear.  It  is 
more  marked  if  we  consider  the  cutaneous  manifestations.  Thus,  exclud- 
ing erysipelas,  which  is  always  due  to  the  streptococcus,  it  is  especially 
streptococci  infection  that  causes  patchy  erythema,  erythema  with  purpura, 
and  erythema  simulating  erythema  nodosum.  And  yet,  in  spite  of  these 
distinctive  signs,  it  is  not  always  possible  to  differentiate  clinically  between 
streptococcic  and  staphylococcic  infections  ;  hence  the  absolute  rule  to 
make  cultures  from  the  blood.     In  this  way  many  errors  wiU.  be  avoided. 

As  regards  treatment,  injections  of  Wright's  staphylococcic  vaccine 
appear  to  be  indicated. 

IV.  MUMPS. 

In  the  first  place,  it  is  necessary  to  establish  a  well-marked  difference 
between  parotiditis  and  mumps.  This  difference  is  not  exclusively  based 
upon  the  anatomical  position  of  the  lesion,  since  in  both  cases  the  cellular 
tissue  of  the  parotid  gland  may  be  as  much  involved  as  the  glandular  tissue. 
The  difference  lies  in  the  nature  of  the  disease  itself. 

The  term  parotiditis  is  applied  to  inflammations  which  sometimes 
supervene  during  the  course  or  during  the  decline  of  severe  fevers  and 
infectious  diseases,  such  as  scarlatina,  measles,  variola,  typhoid  fever, 
dysentery,  diphtheria,  puerperal  fever,  and  appendicitis.  These  cases  of 
parotiditis,  which  often  end  in  Suppuration,  in  necrosis,  or  in  gangrene  of 
the  gland,  are  the  indication  and  the  result  of  general  ill-health,  and  their 
appearance  is  generally  of  gloomy  augury.  There  are  also  cases  of  paroti- 
ditis which  are  associated  with  stomatitis  (mercurial  stomatitis),  in  which 
the  inflammation  is. purely  local,  and  spreads  through  Stenson's  duct  to  the 
gland.  These  inflammations,  though  of  different  origins,  are  due  to  the  ordi- 
nary microbes  of  suppuration,  and  have  nothing  in  common  with  mumps. 

Mumps,  which  has  justly  been  compared  with  the  eruptive  fevers,  may 
be  placed  among  the  infectious  diseases.  It  is  a  specific,  epidemic,  and 
contagious  disease. 

Description.— Mumps  is  characterized  by  enlargement  of  the  parotid 
glands,  and  usually  of  the  salivary  glands  in  general,  for  the  submaxillary 
and  subliagual  glands  are  often  affected.  The  incubation  period  varies  from 
two  to  three  weeks  in  general,  and  then  the  mumps  commences  on  one  side, 
and  speedily  invades  the  opposite  one.  It  is  usually  ushered  in  with  more 
or  less  pain  in  the  parotid  region,  mastication  becomes  difficult,  the  secretion 


INFECTIOUS  DISEASES  TROPER  T<)  MAX  17^7 

of  saliva  is  decreased,  tlie  swelling'  allects  tlic  i)arolid  ro<,'iuu,  and  sonu'tiiueH 
invades  the  neck  and  face,  so  as  to  disfigure  the  patient.  It  may  even 
extend  to  the  tonsils  and  pharynx.  In  some  cases  the  angina  and  the 
swelling  of  the  tonsils  precede  the  affection  of  the  parotid  gland.  The 
skin  ttf  the  face  preserves  its  colour,  or  may  be  slightly  reddened. 

In  some  instances  rigors,  headache,  lassitude,  and  insomnia  precede  the 
local  sjTnptoms  of  mumps.  In  the  stationary  stage,  especially  in  children, 
we  often  see  fever  accompanied  by  vomiting,  and  lasting  twenty-four  or 
forty-eight  hours.  The  disease  declines  about  the  fourth  day,  and  recovery 
supervenes  between  the  sixth  and  eighth  days. 

Orchitis. — In  young  people  and  in  adults,  more  often  than  in  children, 
as  soon  as  the  swelling  of  the  parotid  disappears,  whether  the  disease  have 
been  slight  or  severe,  we  may  see  orchitis,  which  is  so  frequent  that  it  may 
be  regarded  as  a  symptom  and  not  as  a  complication.  Simple  or  double 
orchitis  has  been  noted  156  times  in  432  cases  of  mumps  in  soldiers  (Laveran). 
The  frequency  of  orchitis  varies  in  different  epidemics.  Thus,  at  Digne,  in 
1892,  it  was  noted  four  times  in  nine  cases  of  mumps,  and  at  Saintes,  during 
the  same  year,  six  times  in  ninety-three  cases.  At  Libourne,  in  1889, 
orchitis  was  noticed  once  in  forty  cases  of  mumps,  and  at  Epinal,  during  the 
same  year,  it  was  found  eight  times  in  twenty-six  cases.  In  the  Paris  epidemic 
of  1892  Catrm  saw  orchitis  forty-three  times  in  159  cases  of  mumps. 

The  orchitis  may  present  every  degree  of  severity.  We  see  congestions 
of  the  testis  which  do  not  deserve  the  name  of  orchitis.  The  epididymis  or 
the  testis  is  slightly  painfid  and  swollen,  but  fever  is  absent  or  trifling,  and 
these  abortive  cases  are  of  particidar  interest,  because  they  are  not  followed 
by  atrophy  of  the  organ  (Catrin).  More  often  the  orchitis  is  associated  with 
high  fever  and  sharp  pain  in  the  testes,  which  may  swell  to  three  or  four 
times  their  normal  size  ;  the  skin  of  the  scrotum  is  red  and  tense.  In  four 
or  five  days  the  swelling  diminishes,  and  resolution  speedily  occurs. 

Lastlv,  orchitis  may  be  ushered  in  with  acute  fever,  restlessness,  delirium, 

and  a  typhoid  condition,  forming  the  febris  testicidaris  of  Morton.     I  may 

mention  here  a  case  quoted  by  Trousseau  : 

"  In  1832,"  says  Trousseau,  "  I  was  attending  a  man,  thirty-five  years  of  age,  who 
was  suffering  from  mumps.  The  disease  ran  a  regular  course,  the  pain  had  diminished, 
and  the  sweUing  in  the  parotid  region  was  beginning  to  decrease.  I  saw  the  patient  in 
the  morning,  and  he  was  as  well  as  I  could  expect,  but  at  the  end  of  the  day  I  was  called 
in  haste.  I  found  him  in  the  greatest  distress — pale,  drawn  face  ;  small,  frequent,  and 
irregular  pulse  ;  cold  extremities.  He  had  neither  vomiting,  diarrhcea,  nor  any  appreci- 
able lesions  in  the  heart  and  lungs.  I  acted  as  the  emergency  suggested,  and  gave  ether, 
warm  drinks,  and  ordered  mustard  plasters,  anxiously  awaiting  the  issue  of  a  disease 
which  showed  itself  imder  such  gloomy  auspices.  Next  morning  I  was  agreeably  sur- 
prised to  find  the  patient  with  marked  fever,  full  pulse,  and  free  perspiration  ;  his  face 
was  of  good  colour,  and  his  appearance  was  Uvely.  The  scrotum,  however,  was  swollen, 
and  one  of  the  testes,  and  especially  the  epididvmis,  was  enlarged  and  painful,  so  that 


1758  TEXT-BOOK  OF  MEDIOIKE 

the  symptoms  were  those  of  acute  orcMtis.  I  recalled  tlie  case  reported  by  Borsieri, 
and  the  febris  testicularls  of  Morton,  and  felt  satisfied.  I  felt  respect  for  the  local 
manifestation  which  had  freed  the  economy  from  the  menacing  symptoms,  and  a  few 
days  sufficed  for  the  cure  of  this  metastatic  complication  and  for  complete  recovery." 

Occasionally  orchitis  and  mumps  appear  at  the  same  time,  and  in  rare 
cases  the  former  may  precede  the  appearance  of  the  latter.  In  some 
instances  the  orchitis  is  the  sole  symptom  of  the  disease,  parotid  troubles 
being  absent.  These  cases  are  more  or  less  frequent  ia  difierent  epidemics, 
and  I  may  here  quote  an  excellent  example  of  defaced  mumps  reported  by 
Trousseau  : 

"  In  1853 1  was  called  by  Moynier  to  see  a  youth,  seventeen  years  of  age,  whose  case 
caused  him  the  greatest  anxiety.  The  young  man  had  suddenly  been  taken  ill  with 
severe  fever,  rapid  pulse,  tendency  to  syncope,  dehrium,  carphology,  vomiting,  and 
involuntary  defascation.  The  case  thus  resembled  the  dread  period  of  the  third  week  in 
putrid  fever,  or  the  onset  of  malignant  scarlet  fever,  which  kills  patients  in  a  few  hours. 
You  will  readily  imderstand  the  anxiety  of  the  family  and  of  the  physician  in  the 
presence  of  such  formidable  symptoms.  Andral  had  seen  the  young  man  in  the  early 
part  of  the  attack,  and,  like  Moynier,  had  observed  the  danger,  without  being  able  to 
account  for  it.  These  two  gentlemen  felt  that  it  was,  before  all,  essential  to  relieve  the 
threatening  symptoms,  and  with  excellent  judgment,  had  prescribed  small  doses  of 
opium,  with  sulphate  of  quinine,  in  fairly  large  doses,  and  cardiac  tonics. 

"  Next  day,  when  I  met  my  colleagues  ia  consultation,  there  was  no  evident  change 
in  the  patient's  condition,  though  perhaps  he  was  not  quite  so  ill.  We  were  told  of  a 
complication  which  had  appeared  during  the  night — namely,  that  the  scrotum  was 
swollen,  and  that  one  of  the  testes  was  enlarged  and  painful.  This  was  the  only  organic 
lesion  to  be  found,  and  it  was  scarcely  of  such  a  nature  as  to  account  for  the  alarming 
symptom -complex  present.  The  history  of  my  other  patient  came  back  to  my  mind, 
and  I  told  it  to  my  colleagues.  I  ran  the  risk  of  giving  a  somewhat  less  gloomy  prognosis, 
on  the  supposition  that  the  case  might  be  one  of  metastasis  in  mumps.  The  parents 
and  the  principal  of  the  institution,  on  being  questioned,  rephed  that  the  patient  had 
shown  no  signs  of  mumps  during  the  last  few  days.  I  was  therefore  obliged  to  yield 
in  the  face  of  such  clear  statements,  and  the  same  treatment  was  continued.  Next  day 
the  swelling  of  the  testis  and  of  the  epididymis  was  much  more  marked ;  the  delirium 
had  ceased,  as  well  as  the  vomiting  and  the  diarrhoea.  The  fever  was  stiU  acute,  but 
the  pulse  was  fuller  and  the  skin  was  moist. 

"  After  a  few  days  the  patient  went  home  in  good  health.  We  questioned  him  care- 
fully, and  he  told  us  that  two  or  three  days  before  the  onset  of  the  severe  symptoms  he 
had  felt  out  of  sorts,  with  pain  in  the  throat  and  swelling  between  the  ear  and  the  angle 
of  the  jaw,  and,  further,  that  he  had  been  for  a  walk  in  the  forest  of  Saint-Germain, 
when  he  was  seized  with  a  chiU.  The  swelling  had  diminished  on  the  next  day,  and 
the  day  after  the  alarming  compH cations  noted  above  became  manifest." 

As  regards  the  localization  of  the  orchitis,  we  should  be  wrong  in  saying 
that  it  is  always  limited  to  the  testis.  It  may  be  limited  to  the  epididymis, 
and  even  in  the  numerous  cases  in  which  the  testis  appears  to  be  alone 
invaded  the  .epididymis  is  as  a  rule  slightly  afiected.  In  forty-three  cases 
reported  by  Catrin  epididymitis  was  always  coexistent  with  the  orchitis. 

Although  the  orchitis  is  only  a  transient  affection,  it  is  followed  at  times 
by  atrophy  of  the  testis,  which  occurs  slowly  and  progressively,  and  may 
lead  in  some  persons  to  impotence  and  to  signs  of  feminism.     When  the 


INFECTIOUS  DISEASES  PROPER  TO  MAN  1759 

atrophy  is  coniplote,  the  testis  ia  reduced  to  a  more  shell,  being  soft  and  of 
the  size  of  a  beau.  It  preserves  its  shape,  and  does  not  prevent  either  the 
iiitluration  or  the  irreguhir  character  of  the  syphilitic  testis. 

Very  trilling  orchitis  (simple  congestion  of  the  organ)  is  never  followed 
by  atrophy,  but  siicli  is  not  the  case  in  severe  orchitis.  It  is  interesting  to 
know  what  happens  in  these  cases  of  atrophy  months  and  years  later,  and 
we  often  see  that  the  testes  recover  their  consistency  and  their  size  after  a 
prolonged  period  of  atrophy.  Catrin  re-examined,  seven  to  eleven  months 
after  orchitis,  thirty-eight  out  of  forty-three  soldiers  who  had  suffered  from 
testicular  atrophy.  In  thirteen  the  testes  were  absolutely  normal,  in  sixteen 
marked  atrophy  was  present,  in  five  the  change  was  slight,  and  in  the  re- 
maining four,  although  the  testes  remained  atrophied  for  several  months, 
they  finally  recovered  their  functional  integrity. 

Malassez  had  occasion  to  examine  an  atrophied  testis.  The  epididymis 
was  healthy ;  the  seminiferous  tubules  were  reduced  to  half  of  their  size ; 
some  were  converted  into  cords,  while  others  presented  some  epithelial 
debris  at  their  centre ;  so  that  the  lesion  was  a  kind  of  parenchymatous 
orchitis,  the  vessels  and  connective  tissue  being  practically  spared. 

Writers  have  quoted  cases  of  mumps  in  which  the  breasts,  the  ovaries, 
and  the  labia  majora  showed  congestion. 

The  preceding  description  applies  to  the  classical  form  of  mumps,  with 
or  without  orchitis,  but  the  so-caUed  mumps  fever  does  not  always  answer 
to  the  description  just  given.  We  see  here,  as  in  aU  epidemic  diseases, 
slight  or  abortive  forms,  which  are  none  the  less  very  contagious.  Some 
individuals  during  an  epidemic  of  mumps  have  only  slight  malaise  and 
swelling  of  the  parotid  gland,  which  may  pass  almost  unnoticed.  In  other 
cases  the  parotid  glands  remain  free,  and  the  congestion  is  localized  to  the 
submaxillary  and  sublingual  glands.  This  clinical  picture  is  fairly  common. 
We  might  well  think  of  submaxillary  adenitis  when  we  see  the  submaxillary 
region  swollen  and  painful,  but  here,  as  in  other  forms,  orchitis  may  appear. 

Complications. — Mumps  is  sometimes  followed  by  compHcations. 
Albuminuria  may  be  severe  (Stoicesco).  Its  frequency  varies  in  different 
epidemics,  and  it  is  nearly  always  the  sign  of  slight  and  transient  nephritis, 
although  in  some  cases  the  nephritis  may  be  so  severe  as  to  cause  death 
from  uraemia.  The  infection  in  mumps  may  in  some  cases  become  the 
origin  of  Bright' s  disease. 

I  may  mention  among  the  nervous  complications  of  mumps  cerebral 
troubles  of  the  preorchitic  stage,  with  delirium,  contractures,  convulsions, 
And  even  coma,  which  disappear  when  the  orchitis  appears.  The  paralyses 
and  the  aphasia  have  been  considered  by  Comby  as  related  to  hysteria. 
Finally,  mumps  may  be  followed  by  peripheral  neuritis,  with  sensory 
troubles,  flaccid  paralysis  of  the  limbs,  complete  loss  of  the  muscular  sense, 


1760  TEXT-BOOK  OF  MEDICINE 

total  abolition  of  the  reflexes,  slight  atrophy,  and  reaction  of  degeneration 
(Gallavardin). 

Some  patients  suffer  from  slight  pericarditis  or  from  endocarditis  during 
the  course  of  the  fever ;  others  show  pseudo-rheumatic  joint  troubles,  which 
appear  chiefly  durmg  the  decline  of  the  disease.  They  are  subacute,  causing 
but  little  pain  and  swelling  of  the  joints,  and  they  never  suppurate. 

In  some  epidemics  oedema  of  the  larjmx,  bronchial  catarrh,  and  con- 
gestion of  the  lungs,  have  been  seen.  Suppuration  in  the  salivary  glands 
is  exceptional.  We  may  see  infection  of  the  lachrymal  gland,  with  dacryo- 
cystitis, which  resolves  after  a  few  days. 

Fournie  has  carefuUy  studied  the  auricular  complications  in  mumps,  and 
Eloy  has  given  an  excellent  description  of  them.  "  The  lesion  is  a  special 
one,"  writes  Fournie,  "  and  is  due  to  direct  infection  of  the  auditory  centres." 
However  this  may  be,  the  resulting  deafness  is  generally  incurable.  It  may  be 
unilateral  or  bilateral ;  it  appears  suddenly  and  at  an  early  date ;  it  may  or  may 
not  be  accompanied  by  vertigo,  buzzing  in  the  ears,  vomiting,  and  insomnia. 
The  fits  of  giddiness  may  increase  in  severity  and  persist  indefinitely. 

iEtiology. — The  numerous  examples  of  contagion  prove  that  mumps  is 
essentially  a  contagious  disease.  It  is  hardly  ever  transmitted  to  a  distance 
by  a  third  person  or  by  inanimate  objects.  The  contagion  is  nearly  always 
direct,  and  may  take  place  at  any  period  of  the  disease,  but  it  is  perhaps 
more  active  during  the  onset,  before  the  appearance  of  the  swelling  in  the 
glands.  The  disease  chiefly  afiects  infants  and  young  people.  Boarding- 
schools,  colleges,  orphanages,  and  barracks  are  generally  the  centres  of 
epidemics.  The  epidemic  does  not  strike  down  a  large  number  of  persons 
at  once  ;  it  extends  by  successive  outbursts.  A  first  attack  generally  confers 
immunity,  but  second  attacks  are  fairly  frequent. 

The  researches  of  Laveran  and  Catrin  indicate  progress  in  the  bacteriology 
of  mumps.  They  have  collected  serum  from  the  parotid  gland  and  from  the 
testis,  as  well  as  the  oedematous  fluid  and  the  joint  secretion  in  cases  of 
rheumatism.  In  sixty-seven  out  of  ninety- two  patients  they  found  diplo- 
cocci,  and  more  rarely  micrococci,  united  in  fours  or  in  zooglsea.  The  micro- 
cocci measure  from  1  to  1'5  /x,  and  are  mobile,  but  their  movements  are 
slight.  They  stain  readily  with  the  usual  dyes,  but  do  not  take  Gram's 
stain.  A  culture  placed  in  the  oven  at  35°  C.  becomes  turbid  in  twenty 
hours,  and  the  turbidity  increases  during  the  next  few  days.  On  plates  of 
gelatine  the  colonies  only  appear  after  forty-eight  hours.  They  are  puncti- 
form,  whitish,  spread  slowly,  and  only  liquefy  gelatine  at  a  very  late  period. 
The  colonies  are  white  on  agar,  potato,  carrot,  and  serum.  Mumps  has  never 
been  reproduced  by  inoculation.  Moreover,  the  disease  is  unknown  in  animals. 

Prognosis. — Mumps,  though  benign  as  a  rule,  may  in  some  exceptional 
cases  assume  the  malignant  or  typhoid  form.     The  prognosis,  however,  is 


INFECTIOUS  DISEASES   TKOPKl:  To  MAX  ITOl 

exceediiif^ly  beni;4ii  if  we  only  n^moinber  Lluit  in  tlie  Eionch  army,  Kinco 
18S7,  only  three  ileuths  luive  tiikcn  place  out  of  33,445  cases  (Catriu). 

Diagnosis  and  Treatment.  Mumps  will  not  bo  confounded  with  cases 
of  parotiditis,  although  the  diagnosis  of  mumps  from  certain  cases  of  toxic 
jiarotiditis  may  sometimes  be  a  delicate  matter.  Orchitis  in  mumps  is 
clearly  distinguished  from  blennorrhagic  epididymitis,  which  is  always  con- 
secutive to  a  urethral  discharge. 

During  epidemics  the  patients  must  be  isolated  as  far  as  possible,  and, 
when  the  disease  has  appeared,  rest,  milk  diet,  gentle  laxatives,  and  oint- 
ments applied  to  the  parotid  region,  form  the  basis  of  treatment. 

Antip\Tin  should  be  prescribed  for  pain.  An  ointment  composed  of 
ten  parts  of  vaseline  with  one  part  of  methyl  salicylate  should  be  rubbed 
into  the  painful  region. 

Orchitis  during  this  painful  stage  should  be  treated  by  compresses  soaked 
in  poppy-head  water,  or  inunction  of  the  salicylate  ointment  may  be  used. 
In  addition,  we  may  employ  leeches  over  the  cord  in  the  fold  of  the  groin. 
Sedative  draughts  or  hypodermic  injections  of  morphia  should  be  given  if 
necessary. 

We  must  not  forget  that  mumps  is  contagious  from  its  onset  until  three 
weeks  after  its  disappearance.  From  the  point  of  view  of  prophylaxis,  we 
cannot  be  too  energetic  in  our  disinfection,  for  the  germ  of  mumps  is  very 
tenacious  of  life,  and  is  exceedingly  resistant. 

Atrophy  of  the  testis  must  be  carefully  watched  for,  and  the  continuous 
current  employed,  as  this  method  has  given  excellent  residts.  Olivier  has 
published  a  very  interesting  paper  on  this  subject,  and  it  is  clear  that  in 
several  cases  atrophy  of  the  testis  has  been  arrested  by  the  treatment. 

Y.  CHOLERA. 

In  this  section  I  shall  describe  true  cholera,  which  has  received  the  name  of  Indian 
cholera,  from  its  place  of  origin. 

Cholera,  after  being  confined  to  India,  where  it  is  endemic,  invaded  several  countries 
in  Asia  in  1818.  Since  this  time  both  continents  have  frequently  been  visited  by  this 
terrible  scourge,  and  the  fearful  ravages  caused  by  cholera  in  France  in  the  epidemics 
of  1832,  1849,  and  1853  are  well  known.  For  some  years  past  cholera,  which  has  paid 
us  several  visits,  has  assumed  an  attenuated  form.  I  may  even  say  that  between  Indian 
cholera  and  cholera  nostras  a  kind  of  promiscuity  is  established,  which  bacteriological 
studies  have  not  been  able  to  clear  up. 

^Etiology. — In  India,  where  cholera  is  endemic,  it  is  probable  that  the 
poison  is  engendered  and  nourished  by  special  telluric  conditions  and  by 
infection  of  water.  From  these  endemic  centres  cholera  sometimes  appears 
in  epidemic  form,  and  the  epidemic  is  provoked  by  large  collections  of 
persons  living  under  defective  hygienic  conditions,  as  is  often  seen  during 
the  great  pilgrimages  of  the  Mohammedans. 

The  pilgrims  leave  the  epidemic  focus,  and  carry  the  cholera  with  them  by 


1762  TEXT-BOOK  OF  MEDICINE 

land  and  sea,  and,  as  it  were,  sow  it  in  tlieir  journeys  in  the  form  of  secondary 
epidemic  centres,  which  may  in  their  turn  become  the  origin  of  severe 
epidemics.  Cholera  may  be  transmitted  by  numerous  agents.  Patients 
suffering  from  cholera  or  from  specific  diarrhoea,  linen  and  articles  of 
clothing  or  bed-clothes  fouled  by  the  dejecta,  are  the  most  important. 
When  a  focus  of  cholera  is  established,  drinking-water  and  cesspools 
are  active  agents  in  its  diffusion,  while  the  atmosphere  has  only  a  very 
limited  action.  These  peculiarities  explain  why  alluvial  soil,  which  is  readily 
permeated  by  water  and  by  organic  matter,  is  more  favourable  to  the 
diffusion  of  cholera  than  hard  ground.  Thes»-  telluric  conditions  are  of 
great  importance  when  they  concern  the  superficial  layers  of  the  soil,  which 
are  in  close  relation  with  houses  and  dwelling-places. 

An  epidemic  of  cholera  may  reappear  in  the  same  locality  months  and 
even  years  apart.  These  recrudescences  are  explained  by  the  survival  of 
the  germ  in  the  drinking-water  and  in  the  soil  of  the  affected  locaKties.  In 
1893  Blachstein  and  Sanarelli  found  the  bacillus  of  cholera  in  the  waters  of 
the  Seine  eight  months  after  the  termination  of  the  epidemic. 

SmaU  epidemics  of  autochthonous  cholera,  developing  in  situ,  apart  from 
any  apparent  contagion,  have  been  noted.  The  frequent  presence  of  vibrios 
in  water  (Metchnikoff),  so  often  recognized  of  late  years,  even  apart  from 
any  choleraic  constitution,  accounts  for  the  origin  of  these  epidemics,  which 
at  first  sight  appear  to  arise  in  an  incomprehensible  manner.  The  vibrios 
come  from  the  intestine.  They  are  poured  into  the  water  by  man  and  by 
domestic  animals,  who  may  often,  while  in  good  health,  carry  them  as 
saprophytes  in  their  digestive  canal. 

"We  find  refractory  localities,  where  cholera  may  only  produce  isolated 
cases,  and  not  epidemics.  Lyons,  and  especially  Versailles,  are  well  known 
for  their  immunity.  In  1893,  however,  Sanarelli  often  found  the  comma 
bacillus  in  water  from  the  spring  of  Versailles,  and  Metchnikoff  has  seen 
typical  cholera  in  man  after  ingestion  of  water  containing  this  microbe. 
The  comma  bacillus  does  not  comprise  the  whole  aetiology  of  cholera.  In 
addition  to  predisposing  causes,  such  as  the  physiological,  pathological,  and 
social  condition  of  the  individual,  as  well  as  poverty,  alcoholism,  intestinal 
troubles,  overcrowding  in  asylums  and  prisons,  etc.,  we  must  also  reckon 
with  a  predisposing  cause  which  has  its  origin  in  the  intestinal  flora  of 
individuals  living  in  certain  regions.  Metchnikoff  has  shown  that  receptivity 
in  cholera  results  from  the  association  of  microbes.  The  vibrio  remains 
inactive  or  becomes  dangerous  according  as  it  meets  with  an  unfavourable 
or  favourable  microbic  flora  in  the  alimentary  canal.  Metchnikoff  has  also 
found  that  young  rabbits,  prepared  by  the  ingestion  of  favourable  microbes, 
such  as  the  torula,  sarcinse,  and  the  coliform  bacillus,  die  much  more  readily 
when  they  are  subsequently  made  to  ingest  the  cholera  bacillus. 


I.YFECTIOUS  DISEASES  PKOPEi:  TO  MAX  1763 

Bacteriology.— The  e])i(lomic  of  cholera  which  allocted  Ej^pt  and  part 
of  Eurojto  some  years  ago  furnished  an  opportunity  of  finding  the  micro- 
organism of  this  disease.  Koch  found  in  the  contents  of  the  small  intestine, 
as  well  as  in  its  walls,  a  slightly  curved  and  short  bacillus,  known  as  the 
comma  bacillus.  This  bacillus  is  found  in  large  numbers  in  the  stools  of 
cholera  patients,  and  stains  very  readily  either  with  Ziehl's  fuchsin  or  with 
gentian  violet.  It  may  be  seen,  though  unstained,  with  very  high  mag- 
nification. It  then  shows  extreme  mobility.  It  has  not  always  the  curved 
form,  the  yoimg  bacilli  being  nearly  straight.  The  comma  bacilli,  placed 
end  to  end,  form  the  letter  S.  In  old  cultures  several  bacilli,  when  placed 
end  to  end,  present  the  picture  of  the  choleraic  spirillum.  The  conmaa 
bacillus  presents  at  its  extremities  waving  cilia,  which  vary  in  number  in 
different  epidemics. 

The  bacillus  of  cholera  can  be  cultivated  in  milk,  broth,  agar,  potato, 
and  gelatine.  The  culture  on  the  latter  medium  is  characteristic.  Tubes 
kept  in  the  oven  at  22°  C.  show  a  kind  of  air-bubble  on  the  surface  of  the 
gelatine,  which  becomes  liquefied  in  a  funnel-shaped  form.  Colonies  with 
a  fringe-like  lower  edge  develop  in  the  deep  part  of  the  gelatine.  The 
liquefaction  of  the  gelatine  is  complete  at  the  end  of  six  or  seven 
days. 

The  cholera  bacillus  acquires  its  maximimi  vitality  between  30^  and 
37°  C,  but  it  can  also  be  cultivated  in  spite  of  cold.  This  fact  explains 
the  appearance  of  epidemics  at  any  season  of  the  year. 

The  reaction  of  indol  nitrate,  still  called  cholera-roth,  is  very  typical. 
A  rosy  violet  colour  is  seen  on  the  addition  of  pure  sulphuric  or  hydrochloric 
acid. 

The  bacillus  is  present  in  the  rice-water  fluid  of  the  small  intestine, 
especially  in  fulminant  or  very  acute  cases.  When  the  disease  is  less  acute, 
and  the  patient  dies  in  the  algid  stage,  the  bacillus  is  associated  with  other 
micro-organisms,  which  render  its  discovery  more  difficult.  Moreover,  the 
longer  the  duration  of  the  disease,  the  greater  is  the  number  of  foreign 
microbes  present.  The  comma  bacillus  may  even  completely  disappear  in 
the  period  of  reaction.  The  bacillus,  at  first  confined  to  the  intestinal  fluid, 
subsequently  penetrates  the  mucous  membranes,  after  the  epithehum  has 
disappeared.  It  may  then  reach  the  liver  or  the  lungs,  but  it  is  very  rarely 
present  in  the  blood. 

Koch  was  not  only  able  to  isolate  and  cultivate  the  cholera  bacillus, 
but  also  to  produce  choleraic  symptoms,  by  causing  various  animals  to 
ingest  the  bacillus  after  the  contents  of  the  stomach  had  been  rendered 
alkaline.  Guinea-pigs  are  sensitive  to  the  intraperitoneal  injection  of  the 
comma  bacillus,  and  die  in  less  than  twenty-four  hours,  with  progressive 
lowering  of  the  internal  temperature.     Post  mortem,  the  intestine  is  found 


1764  TEXT-BOOK  OF  MEDICINE 

to  be  of  a  hydrangea  colour,  with  a  deposit  of  fibrin  on  the  liver.  The  serous 
fluid  in  the  peritoneum  contains  the  bacillus, 

Haffldne,  by  applying  the  method  of  exaltation  and  attenuation  of  the 
virus  used  in  the  study  of  anthrax  and  of  chicken  cholera  to  the  Asiatic 
disease,  has  been  able  to  obtain  a  remarkable  attenuation  of  the  bacillus  by 
cultivating  it  in  a  constantly  aerated  atmosphere  at  a  temperature  of  39°  C. 
A  guinea-pig,  after  two  inoculations  of  this  attenuated  virus,  is  immune  to 
the  infection  of  cholera,  iu  spite  of  every  attempt  to  produce  the  disease. 
The  animal  is,  therefore,  vaccinated.  This  method,  formerly  indicated  by 
Ferran  in  Spain,  is  still  under  study  as  regards  man. 

In  the  laboratory  the  virulence  of  the  vibrio  is  governed  by  inoculation 
of  cultures  into  the  cellular  tissue,  and  especially  into  the  peritoneum  of 
guinea-pigs.  The  peritonitis  thus  produced  rapidly  briugs  about  the  death 
of  the  animal. 

We  have  seen  how  Metchnikoff  succeeded  in  causing  intestinal  cholera 
in  young  rabbits  by  mixed  infection. 

Bacteriologists  who  have  lately  studied  the  vibrios  isolated  during  the 
course  of  epidemics  in  different  parts  of  the  world  (India,  Cochin-China, 
Massowa,  Constantinople,  Rome,  Hamburg,  Paris,  etc.)  have  found  morpho- 
logical and  biological  differences  between  them.  In  addition  to  the  small, 
short,  curved  type  described  by  Koch  in  India,  slightly  curved  as  well  as 
thin  elongated  types  have  been  met  with.  The  number  of  cilia  varies.  The 
vibrios  at  Hamburg  and  at  Courbevoie  had  only  one  cilium ;  those  at  Mas- 
sowa and  Calcutta  had  four  cilia.  The  characters  of  cultures  on  gelatine 
may  present  variations.  The  \drulence  in  animals  is  by  no  means  constant, 
so  that  every  intermediate  form  is  found  between  the  vibrio  at  Massowa, 
which  was  extremely  virulent,  and  that  at  Rome  or  Lisbon,  which  was 
practically  harmless.  The  cholera-roth  reaction  may  in  exceptional  cases 
be  absent.  The  microbe  of  cholera,  therefore,  is  not  always  of  a  uniform 
nature,  Like  Eberth's  baciUus.  It  presents  certain  modifications,  according 
to  the  epidemic  soil,  but  this  fact  does  not  destroy  the  bacteriological  unity 
of  cholera.     The  different  specimens  are  merely  races  of  the  same  species. 

The  cholera  bacillus  is  formidable  by  reason  of  the  poison  which  it 
elaborates.  In  this  respect  it  resembles  the  bacilli  of  diphtheria  and  of 
tetanus,  which  also  elaborate  toxines.  "  Cholera  is  an  acute  poisoning,  due 
to  the  absorption  of  a  special  substance  elaborated  in  the  intestine  by  Koch's 
comma  bacillus  "  (Metchnikoff,  Roux,  and  Taurelli-Salimbeni). 

Petri,  Hueffe,  and  Gamaleia  have  described  various  toxines  in  cholera, 
Pfeiffer  has  recently  maintained  that  the  cholera  toxine  was  adherent  to 
the  body  of  the  vibrio,  and  that  it  only  made  its  exit  after  the  death  of  the 
vibrio.  Behring  and  Ransom  have  stated,  on  the  other  hand,  that  the 
poison  secreted  by  the  microbe  is  soluble  and  diffusible  during  its  life.     In 


INFECTIOUS  DKSEASKS  rUUPEK  TO  MAN  17G5 

a  remarkable  work,  full  of  therapeutic  promise,  Metchnikoff,  Roux,  a«d 
Taurelli-Salimbeui  have  clearly  pointed  out  the  difference.  They  succeeded 
in  making  the  bacilli  of  cholera,  enclosed  in  capsules  of  c(»llo(lion,  live  in  the 
peritoneum  of  guinea-pigs,  and  they  have  sho\vn  that  the  toxine  alone  was 
diffused  through  the  organism,  killing  it,  without  any  microbic  action. 
This  capsule  is  practically  an  artificial  coil  of  bowel,  in  which  they  have 
produced  a  simplified  cholera,  without  the  presence  of  microbes,  and  apart 
from  the  action  of  the  digestive  juices.  This  experiment  proves  the  exist- 
ence of  a  soluble  poison  in  cholera,  and  teaches  us  that,  in  order  to  obtain 
an  efficient  serum  against  experimental  infection,  we  must  employ  an  anti- 
toxic serum,  as  in  diphtheria,  and  not  an  antimicrobic  one.  These  authors 
have  obtained  such  a  serum  by  progressive  injections  in  horses  of  an  active 
toxine  produced  by  a  vibrio  with  exalted  virulence.  The  most  minute  dose 
of  this  serum  not  only  cures  choleraic  peritonitis  in  guinea-pigs,  but  prevents 
intestinal  cholera  in  young  rabbits,  although  no  other  senim  had  so  far 
accomplished  this  end. 

Bacteriological  Diagnosis  of  Cholera. — This  diagnosis  is  a  matter  of 
extreme  importance.  In  a  suspected  case  we  must  first  examine  the  stools 
for  the  bacUlus,  and  then  make  cultures  on  broth  or  upon  peptonized  agar  and 
glycerine  (Koch).  Upon  broth  a  thin  cloud  containing  curved  bacilli  in 
abundance  forms  after  twelve  hours,  the  temperature  being  37°  C.  The 
culture  on  agar  is  less  characteristic,  but  develops  almost  as  quickly.  On 
gelatine  we  obtain,  after  two  or  three  days'  exposure  in  the  oven  at  22°  C, 
the  special  aspect  already  mentioned. 

The  variation  in  character  of  the  cholera  bacillus  in  different  epidemics 
shows  that  the  bacteriological  diagnosis  is  often  difficult.  Is  the  \'ibrio 
obtained  from  the  intestine  of  a  patient  at  the  onset  of  an  epidemic,  or 
perhaps  obtained  from  drinking-water,  a  true  cholera  bacillus  ?  Koch  has 
lately  recommended  us  to  rely  upon  two  points  in  order  to  prove  the  diag- 
nosis :  the  reaction  of  cholera-roth  and  the  reaction  of  immunity  in  vac- 
cinated animals  ;  but  in  exceptional  cases  the  former  reaction  may  be 
absent,  and  we  have  dwelt  above  on  the  variation  of  the  virulence  according 
to  the  origin  of  the  microbe. 

Pfeifier  and  Issaef  have  expressed  their  belief  in  a  specific  character  in 
the  reaction  of  immunity  of  gmnea-pigs  previously  vaccinated.  If  fresh 
guinea-pigs  are  vaccinated  with  a  true  \abrio,  the  immunity  lasts  for  about 
three  months.  If  an  animal,  vaccinated  three  months  pre\"iously  by  inocula- 
tion with  a  cholera  bacillus,  does  not  prove  resistant  to  the  intraperitoneal 
injection  of  the  suspected  %'ibrio,  the  latter  should  not  be  considered  as 
cholerigenous ;  if,  on  the  other  hand,  the  animal  proves  resistant,  the  \abrio 
in  question  is  that  of  cholera.  In  the  peritoneum  of  the  inoculated  animal 
the  vibrios  become  agglutinated  and  form  small  masses.  According  to 
II.  112 


1766  TEXT-BOOK  OF  MEDICINE 

PfeifEer  and  Issaef,  the  serum  of  a  guinea-pig  vaccinated  against  an  authentic 
cholera  vibrio  should  confer  immunity  against  aU  vibrios  which  are  choleri- 
genous  in  nature.  This  reaction  constitutes  Pfeiffer's  phenomenon,  which 
may  render  the  greatest  service  in  the  diagnosis  of  the  cholera  bacillus,  but 
its  certainty  is  not  absolute.  The  Massowa  vibrio,  which  has  become 
classical  by  reason  of  its  toxicity,  kills  guinea-pigs  treated  by  preventive 
inoculation  of  serum  from  an  animal  immunized  against  the  Hamburg 
vibrio.  If  we  recognize  Pfeiffer's  law,  we  should  exclude  the  active  Massowa 
bacillus  from  the  group  of  cholerigenous  vibrios.  By  reason  of  the  variety 
of  races  of  the  cholera  vibrio,  the  reaction  of  immunity  is  not  as  exact  as  in 
typhoid  fever,  where  the  bacillus  is  always  of  the  same  nature. 

Asiatic  Cholera  and  Cholera  Nostras. — Until  1892  the  distinction 
between  these  two  diseases  appeared  to  be  very  clear.  Asiatic  cholera  was 
contagious,  epidemic,  and  fulminant ;  it  was  characterized  by  the  presence 
of  the  comma  bacillus  in  the  stools  and  in  the  intestinal  contents.  Cholera 
nostras,  on  the  other  hand,  was  as  a  rule  benign,  rarely  causing  death, 
being  but  little  contagious,  and  never  epidemic,  although  endemic  in  our 
countries  during  very  hot  weather,  and  appeared  to  be  due  either  to  Finkler 
and  Prior's  bacillus,  to  the  B.  coli  communis  (Girode  and  Gilbert),  or  to 
Thiercelin's  enterococcus. 

The  question  has  become  more  obscure  since  the  epidemic  of  Paris  in 
1892,  and  I  shall  quote  cases  in  proof  of  this  assertion  : 

At  the  end  of  May,  1892, 1  saw  four  cases  of  cholera  at  the  Necker  Hospital.  Three 
of  the  patients  survived,  and  the  fourth  died.  Renon  examined  the  stools  and 
the  intestinal  contents  in  these  four  patients,  and  on  two  occasions  found  the 
B,  coli  communis  alone,  the  comma  bacillus  once,  and  in  the  fourth  case  these  two  baciUi 
in  association.  I  should  have  thought  that  the  case  due  to  the  comma  bacillus  would 
be  more  severe  than  those  due  to  the  B.  coli  communis.  Such  was  not  the  case,  and 
the  symptoms  were  equally  grave  in  both  cases.  Clinically,  no  difference  existed, 
and  in  the  patient  who  died  the  Bacillus  coli  was  foxmd  without  the  comma  bacillus. 
At  the  same  time  Netter  saw  numerous  deaths  among  choleraic  patients  in  whom  the 
B.  coli  communis  was  alone  present.  In  1893  Giraudeau  and  Renon,  who  examined 
nearly  aU  the  cases  of  cholera  in  Paris  and  the  suburbs,  did  not  find  in  two  months  and 
a  half  a  single  case  due  to  the  comma  bacillus.  In  all  their  patients  the  B.  coli  communis 
was  found,  and  several  died  with  the  symptoms  and  lesions  of  Indian  cholera.  Giraudeau 
and  Renon  have  seen  a  case  of  contagion,  which  I  wiU  report  briefly :  A  patient,  who  came 
from  Nantes,  where  cholera  was  raging,  was  admitted  to  hospital,  and  died.  A  very 
virulent  Bacillus  coli  was  found  in  the  stools  and  the  bowel,  since  it  killed  a  guinea-pig 
in  eight  hours.  The  attendants  who  nursed  this  patient  died  of  cholera  two  days  later, 
and  here  again  the  Bacillus  coli  was  found  alone  in  the  dejecta  and  in  the  bowel. 

Cholera  due  to  the  Bacillus  coli  may  kill  as  surely  and  as  rapidly  as 
cholera  due  to  the  comma  bacillus.  The  former  is  as  contagious  as  the 
latter. 

The  study  of  the  relations  between  cholera  due  to  the  B.  coli  and  cholera 
due  to  the  comma  bacillus,  and  especially  the  assisting  action  of  the  former 


INFECTIOUS  DISEASES  rilOrER  To  MAN  1707 

microbe  on  the  latter,  have  enabled  Renon  to  throw  some  light  on  this 
obscure  question.     He  formulates  the  following  conclusions  : 

"  This  assisting  action  of  the  B.  colt  communis  on  the  comma  bacillus  may 
occur  just  as  readily  outside  as  inside  the  organism,  since  it  is  proved  that 
we  can  give  asylum  to  the  comma  bacillus  and  the  B.  ti/pfiosus  without  being 
absolutely  doomed  to  cholera  or  to  typhoid  fever.  The  assisting  action  of  the 
B.  coli  commanis  becomes  still  more  clear  and  immediate  if  its  virulence  has  been 
reinforced  by  causes  which  we  cannot  as  yet  appreciate,  causing  choloriform  diar- 
rhoea or  cholera  nostras.  If,  however,  we  absorb  with  the  ingesta  a  comma  bacillus, 
wiiose  virulence  is  exalted  by  successive  passages  through  the  human  organism,  such 
as  occurs  in  large  epidemics,  the  B.  coli  is  not  necessary  to  produce  cholera. 
The  invasion  is  rapid,  and  the  course  is  fulminant.  These  considerations  as  to  the 
jetiologic  relations  between  these  two  varieties  of  cholera  may  be  summed  up  in  the 
following  statement :  Cholera  nostras  prepares  the  way  for  Indian  cholera.  The 
pathogenic  data  of  a  bacteriological  nature  are  thus  in  perfect  accord  with  the  epidemi- 
ology and  with  the  clinical  facts. 

"  In  the  cases  observed  during  the  epidemic  of  1892  the  action  of  the  B.  coli 
communis  was  clear  and  precise,  since  the  most  severe  cases  were  those  in  which  both 
pathogenic  agents  were  found.  In  the  epidemic  of  1893  the  absence  of  the  comma 
bacillus,  noted  by  all  authorities,  coincided  with  the  benign  nature  of  this  epidemic, 
which  would  have  become  terrible  if  the  comma  bacillus  had  also  been  present,  seeing 
that  the  Bacillus  coli  alone  acquired  a  fatal  virulence.  These  data  account  for  the 
immunity  of  certain  towns  against  cholera,  as  Metchnikoff  had  remarked.  They 
explain  why  cholera  does  not  always  exist  where  the  comma  bacillus  is  present. 
SanareUi,  in  the  benign  epidemic  of  1893,  found  the  comma  bacillus  almost  constantly 
present  in  the  water  of  the  Seine,  and  yet  only  one  case  of  cholera  due  to  the  comma 
bacillus  was  discovered  at  Saint-Denis.  In  conclusion,  these  data  explain  the  clinical 
importance  of  premonitory  diarrhoea  which  occurs  when  the  comma  baciUus  alone  has 
not  acquired  sufficient  virulence  to  produce  Indian  cholera." 

Pathological  Anatomy.— Rigor  mortis  is  always  very  pronounced,  and 
the  cyanotic  tint  is  as  marked  as  it  was  during  the  last  hours  of  life.  All 
the  tissues  are  bloodless,  and  this  dryness  becomes  the  more  striking  when 
we  examine  a  vascular  organ,  such  as  the  liver  or  the  kidneys.  The  small 
quantity  of  blood  contained  in  the  vessels  and  in  the  heart  is  viscid,  brownish, 
and  fluid,  or  clotted  in  soft  black  coagula. 

The  intestinal  lesions  are  constant,  but,  according  to  Kelsch  and  Vaillard, 
no  relation  exists  between  their  severity  and  the  duration  of  the  disease. 
They  chiefly  occupy  the  small  intestine,  and  become  the  more  marked  the 
nearer  they  are  to  the  caecum.  The  mucous  membrane  is  pale  and  colour- 
less, or,  on  the  other  hand,  shows  in  spots  a  clear  hydrangea  tint.  The 
ramifications  of  the  bloodvessels  are  well  marked  in  this  membrane.  Its 
free  surface  is  studded  with  small  transparent  projections  of  the  size  of  a 
millet-seed,  coUapsing  on  puncture.  They  contain  colourless  fluid.  This 
psorenteria,  regarded  as  characteristic  of  cholera  by  Serres,  is  common  to 
every  severe  diarrhoea.  In  some  cases  the  intestinal  mucous  membrane 
presents  scattered  ecchymoses,  which  may  reach  the  submucous  coat,  and 
may  occupy  a  fairly  large  extent. 


1768  TEXT-BOOK  OF  MEDICINE 

The  epithelium  is  detached,  and  floats  in  the  contents  of  the  intestine, 
thus  producing  the  rice- water  appearance.  This  desquamation  is  some- 
times the  prelude  of  small  ulcerations,  which  destroy  the  mucous  coat  to  a 
greater  or  less  extent.  It  is  sometimes  appreciable  to  the  naked  eye,  but 
at  other  times  it  is  visible  only  with  the  microscope  (Kelsch  and  Vaillard). 
The  superficial  ulcerations  are  necrobiotic  in  nature,  since  they  always 
follow  thrombosis  of  the  vessels.  We  find  the  capillaries  and  small  arterioles 
of  the  mucosa  filled  with  corpuscles,  which  are  more  or  less  altered  in  shape, 
while  the  cells  covering  the  walls  of  these  ulcerations  show  granulo-fatty 
degeneration. 

Lieberkiihn's  and  Brunner's  glands  are  healthy  (Jaccoud),  but  the  closed 
follicles  are  swollen  and  infiltrated  with  leucocytes.  The  integrity  of  the 
large  intestine  contrasts  with  the  lesions  in  the  small  bowel.  The  spleen  is 
always  atrophied  and  bloodless  (Kelsch  and  Vaillard).  The  follicles  of 
Malpighi  are  increased  in  size,  and  present  at  their  centre  an  irregular 
vitreous  mass,  which  is  cracked  upon  its  surface,  and  formed  at  the  expense 
of  the  artery  and  of  the  lymphatic  tissue  of  the  follicle. 

Straus  and  Eoux  have  described  in  the  liver  greyish  anaemic  areas,  which 
are  also  found  in  a  number  of  infectious  states,  and  which  have  been  attri- 
buted by  Doyen  to  an  arrest  in  the  local  circulation.  This  assertion  appears 
true,  for  the  bloodvessels  are  obliterated  by  leucocytes  and  by  fibrin. 
According  to  Doyen,  this  coagulation  is  consecutive  to  the  arrest  of  the 
cholera  microbes.  Hanot  and  Gilbert  have  found  in  many  of  the  liver  cells 
a  change  characterized  by  swelling  of  the  nucleus  and  by  difi&culty  in  staining 
the  protoplasm.  They  have  given  to  this  change  the  name  of  transparent 
swelling.  Apart  from  these  hepatic  lesions,  aU  authors  have  insisted  on  the 
distension  of  the  bile-ducts,  and  especially  of  the  gall-bladder,  by  thick, 
almost  colourless  bile.  Hayem  and  Winter  have  found  a  toxic  alkaloid  in 
this  fluid. 

The  kidneys  are  fairly  often  increased  in  size  and  congested.  They 
sometimes  show  an  early  stage  of  parenchymatous  nephritis.  The  cells  of 
the  tubuli  contorti  have  undergone  a  kind  of  cloudy  infiltration  (Doyen), 
and  the  straight  tubules  are  filled  with  hyaline  casts. 

Description. — The  incubation  period  of  cholera  is  from  thirty-six  to 
fifty-six  hours,  and  the  course  of  the  symptoms  in  an  ordinary  case  may 
be  divided  into  three  periods  :  period  of  premonitory  diarrhoea,  algid  stage, 
and  the  period  of  reaction. 

1.  Premonitory  Diarrhoea. — The  diarrhoea  commences  suddenly,  with- 
out colic  or  tenesmus.  It  is  characterized  by  stools  which  are  at  first 
faecaloid,  but  which  later  become  bilious  and  serous,  and  accompanied  by 
borborygmi.  Fever  is  either  slight  or  absent ;  the  appetite  is  good,  except 
in  cases  of  gastric  catarrh ;  the  stools  are  frequent ;  the  patient  feels  ex- 


INFECTIOUS  DTSKAiSKS  I'lIOl'Ki;  T<  i   MAX  17i;9 

ceodiiij^'ly  tired  ;  and  after  a  period  of  from  tliroo  to  .seven  days  tlio  di.seaR« 
is  well  marked.  Let  me  state  that  this  premonitory '  diarrhoea  is  not 
constant,  being  absent  in  a  third  of  the  cases,  and,  on  the  other  hand,  it 
may  be  the  only  manifestation  of  very  mild  rholera. 

2.  Algid  Stage. — The  dejecta  of  the  preceding  period  change  in  character, 
and  become  exceedingly  frequent.  The  stools  have  no  faecal  odour ;  they 
are  serous,  and  com])osed  of  a  watery,  colourless  fluid,  in  which  whitish 
flakes  of  epithelial  debris  float  (rice-water  stools).  The  stools  contain  the 
bacilli  previously  described. 

Cramps  now  appear,  with  vomiting  of  watery  matter,  repeated  every 
few  minutes,  and  aocompanicd  by  precordial  distress.  The  thirst  is  intense  ; 
the  belly  is  retracted ;  the  pulse  is  small ;  the  face  is  shrunken ;  the  eyes  become 
hollow  ;  the  nose  is  cold  and  pinched  ;  the  voice  sinks  to  a  whisper  ;  the  skin 
of  the  hands  grows  pale,  dry,  and  wrinkled  ;  the  limbs  become  as  cold  as 
ice  ;  the  nails  are  blue ;  and  the  feet  and  hands  are  covered  with  a  purple 
mottling.  During  the  algid  stage  the  temperature  of  the  hands  or  of  the 
mouth  is  10°  or  12°  F.  below  normal,  while  the  internal  temperature  rises,  thus 
explaining  the  sensation  of  heat  felt  by  the  patient.  If  this  period  ends 
fatally,  the  respiration  becomes  embarrassed,  and  the  patient  falls  into  a 
state  of  stupor,  and  dies  in  collapse. 

Most  of  these  s}'Tnptoms  are  due  to  the  toxines  and  the  thickening  of 
the  blood,  deprived  of  its  watery  elements  by  the  incessant  loss  result- 
ing from  the  stools  and  vomiting.  The  circulatory  organs  fail,  the 
secretions  diminish,  and  hsematosis  is  at  a  standstill.  This  stage,  which 
in  some  cases  lasts  only  two  or  three  hours,  scarcely  ever  exceeds  thirty 
hours. 

3.  Period  of  Reaction. — If  the  patient  does  not  die  in  the  algid  stage, 
the  cyanosis  disappears,  the  skin  grows  warm  again,  the  rectal  temperature 
falls  and  the  secretion  of  urine  is  re-established.  The  first  urine  passed  is 
albuminous,  and  poor  in  urea  and  chlorides.  The  different  functions 
gradually  become  normal  and  recovery  takes  place  in  a  few  days.  The 
period  of  reaction  does  not  always  run  this  favourable  course.  It  is  some- 
times incomplete,  and  after  various  oscillations  the  patient  may  recover  or 
may  pass  again  into  the  algid  stage.  At  other  times  the  reaction  oversteps, 
as  it  were,  the  normal  line  ;  congestion  of  the  chief  organs,  and  especially  of 
the  brain,  occurs  and  the  fever  reappears.  The  chances  of  recovery,  how- 
ever, are  not  hopeless  ;  and  if  improvement  supervenes,  it  generally  does  so 
after  a  short  period  of  from  twenty-four  to  forty-eight  hours. 

The  length  of  convalescence  varies  in  proportion  to  the  severity  of  the 
disease.  It  is  sometimes  interrupted  by  dyspepsia  and  paralyses,  and  the 
patient  is  not  free  from  the  risk  of  a  second  attack,  because  cholera  does 
not  confer  immunity. 


1770  TEXT-BOOK  OF  MEDICINE 

Rare  Forms. — The  above  description  of  cholera  applies  in  the  majority 
of  cases.  It  comprises  the  slight  forms  which  have  been  called  cholerine, 
and  which  are  characterized  by  the  first  period — namely,  that  of  premoni- 
tory diarrhoea.  Between  these  slight  and  severe  forms  we  see  every  inter- 
mediate form,  and  as  regards  severity,  they  practically  correspond  to  the 
preceding  description. 

Rare  forms  are,  however,  seen :  cholera  fulminans  and  cholera  sicca. 
True  cholera  fulminans  is  excessively  rare,  although  it  has  been  seen  in 
India  ;  but  we  may  often  see  in  certain  epidemics  rapid  forms,  in  which 
the  patients  may  or  may  not  suffer  from  premonitory  diarrhoea  and  are 
carried  oS  in  less  than  twenty-four  hours. 

The  form  which  is  not  accompanied  by  alvine  evacuations  is  called 
cholera  sicca.  In  this  form  the  fluid  is  not  expelled  from  the  intestine, 
probably  because  of  the  paralysis  of  the  gut. 

Diagnosis  and  Prognosis.— Cholera  nostras  has  nothing  in  common  with 
Indian  cholera.  The  evacuations  are  bilious  and  serous,  but  not  like  rice- 
water,  because  the  epithelial  flakes  are  absent.  Vomiting  and  marked 
coldness  of  the  body  are  not  seen,  and  the  disease  is  essentially  one  of 
seasons  (summer  and  autumn  diarrhoea),  and  presents  no  gravity.  If  the 
reader  wlU  refer  to  the  remarks  at  the  commencement  of  this  section,  he 
wiU  see  that  in  many  cases  clinically,  anatomically  and  bacteriologically, 
cholera  nostras  and  Asiatic  cholera  are  often  difficult  to  differentiate  from 
one  another,  and  here,  as  in  pernicious  choleraic  fever,  the  clinical  diagnosis 
depends  upon  bacteriology  and  sero-diagnosis. 

Sero-Diagnosis. — The  phenomenon  of  agglutination  of  the  microbes  by 
serum  is  most  typically  seen  among  animals  in  choleraic  infection.  It  will, 
perhaps,  furnish  the  elements  for  the  sero-diagnosis-  of  cholera  in  man,  as, 
indeed,  the  researches  of  Achard  and  Bensaude  lead  us  to  hope. 

The  prognosis  of  cholera  is  so  grave  that  in  some  epidemics  the  mor- 
tality exceeds  60  per  cent. 

Treatment. — Prophylactic  measures  should  be  rigorously  observed,  in 
order  to  prevent  the  importation  and  dissemination  of  cholera.  Quarantine 
is  not  as  efficacious  in  cholera  as  in  yellow  fever,  which,  by  reason  of  its 
origin,  can  only  be  imported  by  sea.  Cholera  spread  by  land  in  the  first 
two  epidemics  which  ravaged  Europe.  The  usefulness  of  sanitary  cordons 
is  undoubted,  but,  unfortunately,  these  measures  are  difficult  to  put  mto 
execution.  We  must  prevent  any  great  exodus  of  the  population  (pil- 
grimages and  caravans),  which  is  liable  to  spread  the  disease. 

The  usual  measures  employed  to  prevent  the  spread  of  cholera  are  : 
Patients  and  their  attendants  must  be  absolutely  isolated ;  pans  in  which 
the  dejecta  are  received,  latrines,  linen,  bed-clothes,  and  flooring  must  be 
disinfected  with  a  solution  of  sulphate  of  iron  or  of  sulphuric  acid.     The 


INFECTIOUS  DISEASES  PROPER  TO  MAN  1771 

physician  should  change  his  clot  lios  and  wash  his  hands  in  carbolic  lotion 
after  visiting  a  patient. 

People  who  live  in  an  epidemic  centre  should  drink  only  hoiled  water 
or  table  waters.  They  must  avoid  all  excess  or  fatigue,  and  the  slightest 
intestinal  symptoms  are  to  be  rigorously  checked. 

What  is  the  treatment  for  cholera  ?  In  the  first  stage,  our  efforts  must 
be  directed  to  checking  the  diarrhoea  by  administration  of  subnitrate  of  bis- 
muth, and  opium  and  its  preparations.  Rice-water  forms  an  excellent  drink. 
Champagne  and  iced  drinks  may  be  given  for  vomiting.  At  the  very  first 
sign  of  the  algid  stage  the  patient  must  be  rubbed  with  cold  aromatic 
lotions  or  with  tampons  of  wool  soaked  in  chloroform  liniment.  Lactic 
acid  in  doses  of  3  drachms  daily  has  given  good  results  (Hayem).  Intra- 
venous injection  of  artificial  serum  was  recommended  by  Hayem  in  1884, 
and  was  much  used  in  1892.  It  showed  a  larger  measure  of  successes  than 
had  been  previously  obtained. 

If  the  reaction  is  too  acute,  we  must  employ  mustard  plasters,  cold 
compresses  to  the  head  and  diaphoretics. 

VI.  INFLUENZA. 

Description. — Influenza  is  a  contagious  microbic  disease  affecting  chiefly 
the  respiratory  system,  but  presenting  in  addition  a  variety  of  local  mani- 
festations and  symptoms,  which  vary  in  character  and  severity  in  different 
epidemics. 

Influenza  arises  after  a  very  short  period  of  incubation,  varying  from  a 
few  hours  to  a  day.  The  onset  is  often  sudden.  An  individual  in  good 
health  is  struck  down  by  violent  headache,  pains  in  the  joints,  chills,  fainting- 
fits, hallucinations,  and  syncope.  The  onset  is,  however,  less  sudden  in 
most  cases  and  the  disease  begins  as  common  cold, 

I  shall  describe  two  forms  of  influenza — the  one  mild  or  of  moderate 
intensity,  the  other  severe,  though,  of  course,  every  intermediate  degree 
may  be  seen. 

The  mild  form  resembles  an  attack  of  bronchitis,  in  which  the  general 
symptoms  assume  an  unwonted  severity.  The  entire  economy  is  invaded, 
as  in  the  severe  fevers.  For  several  days  muscular  weakness  and  malaise 
are  felt,  with  intense  frontal  or  occipital  headache,  pains  awakened  by  every 
fit  of  coughing  and  repeated  cramps  in  the  limbs  and  chills.  Ocular,  nasal, 
and  pharyngeal  catarrhs  appear.  In  some  cases  these  local  s}Tnptoms  are 
wanting,  and  the  influenza  begins  with  catarrhal  laryngitis  or  bronchitis, 
accompanied  by  hoarseness  of  the  voice  and  very  painful  fits  of  coughing. 
The  expectoration  is  at  first  aerated,  but  later  becomes  more  thick  ;  the 
chest  is  full  of  snoring  and  whistling  rhonchi ;  the  fever  is  high  at  night, 


1772  TEXT-BOOK  OF  MEDICINE 

and  falls  in  the  morning.  In  some  cases  the  fever  is  slight,  and  yet  the 
headache,  pains  in  the  muscles  of  the  neck,  in  the  spine,  in  the  sides,  and  in 
the  lumbar  region,  as  well  as  in  the  neighbourhood  of  the  joints,  may  be 
of  marked  severity  during  the  whole  disease.  In  some  patients  the  chief 
symptoms  are  nausea,  vomiting,  gastric  catarrh,  and  biliousness.  After 
about  a  week  or  a  fortnight,  recovery  is  ushered  in  by  a  crisis,  with  sweating, 
diarrhcea,  bleeding  from  the  nose,  and  herpes  on  the  lips. 

The  severe  form  of  influenza  is  characterized  by  the  exaggeration  of  the 
symptoms  just  described,  with  a  tendency  to  delirium  and  syncope,  or  by 
the  predominance  of  lesions  and  symptoms  which  lend  a  special  character 
to  each  epidemic. 

Moreover,  most  epidemic  diseases,  such  as  tj^hoid  fever,  whooping- 
cough,  dysentery,  scarlet  fever,  mumps,  etc.,  are  subject  to  these  sympto- 
matic variations,  which  impress  their  special  hall-mark  on  the  epidemics 
{genie  epidemique),  and  which  are  dependent  upon  the  climatic,  telluric,  or 
atmospheric  conditions  (drcumfusa),  whereby  the  virulence  of  the  patho- 
genic agents  is  modified  or  increased.  The  varied  nature  of  the  lesions  and 
symptoms  in  different  epidemics  and  individuals  has  led  authors  to  describe 
severe  forms  of  influenza  of  a  nervous,  thoracic,  or  of  an  abdominal  type. 

Nervous  Influenza. — In  some  cases  the  cerebral  or  cerebro-spinal  symp- 
toms are  so  marked  that  they  seem  to  comprise  the  whole  disease.  The 
headache  may  be  intense,  dull,  stabbing,  or  like  the  blows  of  a  hammer, 
with  orbital  pains  and  a  feeling  of  constriction  in  the  temples.  The  pain  in 
the  head  is  sometimes  accompanied  by  vomiting,  somnolence,  and  photo- 
phobia, so  that  meningitis  is  naturally  thought  of.  In  most  cases  this 
lesion  is  not  present,  and  the  condition  is  only  a  pseudo -meningitis.  In 
some  cases,  however,  true  meningitis  develops  and  the  patient  dies  in  a 
few  days.  This  influenzal  meningitis  generally  results  from  suppurative 
otitis  (Weichselbaum),  pneumonia,  or  broncho-pneumonia,  the  pathogenic 
agents  primarily  localized  to  the  nose,  to  the  ear,  or  to  the  lung,  having 
spread  to  the  brain. 

Influenza  may  cause  polyneuritis,  ascending  paralysis,  meningo-myelitis, 
and  polymyelitis.  The  numerous  cases,  some  of  which  have  been  followed 
by  post-mortem  examination,  permit  the  clear  description  of  these  nervous 
complications.  Mosse  quotes  three  cases  which  prove  that  patients  suffer- 
ing from  influenza  may  show,  either  in  the  course  of  the  disease  or  during 
convalescence,  nervous  symptoms  due  to  peripheral  neuritis,  symptoms  of 
bulbo-spinal  meningo-myelitis,  which  specially  affect  the  dorso-lumbar 
enlargement  of  the  spinal  cord,  and  progressive  ascending  paralysis  of  a 
mixed  type,  both  polyneuritic  and  spinal,  which  ends  in  general  spinal 
paralysis. 

Polyneuritis  due  to  influenza  is,  however,  more  frequent  than  myelitis. 


INFECTIOUS  DISEASES  PRUl'EK  TO  MAN  177:'. 

The  norvous  complloations,  which  appear  a  'priori  to  be  of  spinal  orij^in, 
most  often  end  in  nM-overy,  even  though  they  may  be  very  marked.  Paralysis 
of  the  bladder,  rachialgia,  and  severe  trigeminal  neuralgia  also  belong  to 
the  nervous  disorders. 

We  see  in  some  persons  symptoms  of  depression  and  pro.stration,  which 
at  first  sight  simulate  coma  ;  others  sufTer  from  headache,  fainting-fits,  and 
SNTicope.  I  have  also  seen  delirium,  restlessness,  hallucinations,  and  acute 
mania.     Mental  alienation  following  influenza  has  also  been  noted. 

The  innervation  of  the  heart  may  be  affected,  so  that  patients  are  seized 
with  arrh}i;hmia,  collapse  and  pains  like  those  of  angina  pectoris. 

Thoracic  Influenza. — Broncho-pulmonary  complications  play  a  large 
part  in  the  mortality  from  influenza.  These  complications  include  capillary 
bronchitis,  inflammation  of  the  chest,  broncho-pneumonia,  or  pneumonia ; 
they  are  usually  rare  at  the  commencement  of  an  epidemic.  The  severe 
broncho-pulmonary  lesions  appear  later,  when  the  epidemic  is  at  its  height. 
Capillary  bronchitis  may  rapidly  become  purulent. 

Inflammation  of  the  chest  in  influenza  is  often  serious.  It  is  accom- 
panied by  blood-stained  sputum,  with  intense  dyspnoea,  and  the  multiple 
localizations  described  under  Inflammation  of  the  Chest. 

Broncho-pneumonia  is  one  of  the  most  terrible  manifestations  of  influ- 
enza. It  is  characterized  bacteriologically  by  the  presence  of  the  strepto- 
coccus, with  which  the  pneumococcus,  the  pneumobacillus  and  the  staphy- 
lococcus are  often  associated.  Broncho-pneumonia  arises  in  the  course  of 
influenzal  bronchitis  and  its  description  is  precisely  similar  to  the  classical 
form.  In  the  terrible  epidemic  of  1837  many  persons  died  from  capillary 
bronchitis  and  from  broncho-pneumonia  (Nonat). 

Lobar  pneumonia  is  also  one  of  the  manifestations  of  influenza.  It  is 
due  to  the  pneumococcus,  and  may  be  accompanied  by  pleurisy,  endo- 
carditis, pericarditis,  and  meningitis.  "  On  the  one  hand,  the  study  of 
previous  epidemics  shows  us  that  pneumonia  is  not  simply  a  complication ; 
it  may  appear  in  the  primary  form,  thus  forming  a  coincident  epidemic ; 
and,  on  the  other  hand,  in  the  influenzal  pneumonia  seen  this  year  [1886], 
we  have  been  able  to  demonstrate  the  presence  of  the  pneumococcus  in  the 
sputum,  in  the  hepatized  lung  after  death,  and  in  the  blood  during  life. 
We  may,  therefore,  conclude  that  influenza  and  pneumonia  are  two  inde- 
pendent diseases,  although  presenting  marked  affinities.  The  one  predisposes 
to  the  other,  and  both  appear  to  be  favoured  by  the  same  causes"  (Menetrier). 

At  other  times  the  respiratory  tracts  are  almost  unaffected,  and  yet  the 
dyspnoea  is  acute,  early,  and  sudden  (Graves,  epidemic  in  Ireland,  1830), 
as  though  the  nervous  system  was  directly  affected  by  the  poison.  This 
nervous  dyspnoea,  formerly  called  sine  materia,  is  similar  to  that  seen  in 
the  malignant  forms  of  certain  diseases,  such  as  scarlatina. 


1774  TEXT-BOOK  OF  MEDICIIsT: 

Pleurisy  is  by  no  means  rare  in  influenza,  being  either  sero-fibrinous  or 
purulent,  and  due  to  the  streptococcus  or  to  the  pneumococcus.  It  is 
sometimes  interlobar,  and  is  always  associated  with  lesions  of  the  lungs 
and  bronchi. 

Gangrene  is  certainly  the  gravest  of  the  pulmonary  complications.  It 
may  appear  during  the  acute  phase  of  influenza,  or  much  later  during  con- 
valescence. This  terrible  complication,  whether  it  is  circumscribed  or 
diffuse,  and  whether  it  is  or  is  not  accompanied  by  pyopneumothorax,  is 
nearly  always  fatal. 

Gastro-Intestinal  Influenza. — In  some  cases  influenza  takes  the  form  of 
a  severe  gastric  disorder,  with  vomiting,  absolute  intolerance  of  the  stomach, 
pain  in  the  epigastric  region,  and  dry,  red  tongue.  Erythema  of  the  pharynx, 
alveolo-dental  periostitis,  and  aphthous  or  ulcerative  stomatitis  are  some- 
times added  to  these  symptoms.  In  some  cases  the  symptoms  of  sore 
throat  are  predominant.  The  patient  complains  of  acute  dysphagia,  violet 
patches  are  seen  on  the  velum  palati  and  on  the  pharynx,  and  the  tonsils 
are  affected  by  suppurative  inflammation.  The  spleen  is  often  enlarged 
and  painful. 

The  intestinal  troubles  are  characterized  by  bilious  and  foetid  diarrhoea, 
with  colic,  tenesmus,  meteorism,  vomiting  of  bile,  epistaxis,  and  prostra- 
tion— symptoms  resembling  those  of  typhoid  fever.  The  epidemic  which 
broke  out  in  Vienna  in  1775  was  remarkable  for  the  predomiaance  of  biliary 
phenomena,  with  vomiting,  anorexia,  diarrhoea,  and  jaundice,  affecting  the 
conjunctivae  and  skui  (Stoll).  In  the  Paris  epidemic  of  1830  the  cramps 
and  intestinal  troubles  were  so  marked  that  they  closely  resembled  cholera 
(Hardy  and  Behier). 

Influenzal  Nephritis. — Nephritis  is  a  frequent  complication  of  influenza, 
and  here,  as  in  other  infectious  diseases,  it  may  assume  the  most  diverse 
characters.  The  nephritis  is,  as  a  rule,  slight  and  transient.  The  change 
ia  the  epithelium  is  shown  only  by  more  or  less  severe  and  prolonged  albu- 
miauria,  without  other  symptoms.  Sometimes,  however,  oedema,  puffiness 
of  the  face,  and  swelling  of  the  lower  limbs  are  seen  in  addition  to  the  albu- 
minuria. At  other  times  influenzal  nephritis  becomes  of  considerable  im- 
portance. The  urine  is  scanty  and  blood-stained,  and  the  patient  suffers 
from  slight  symptoms  of  uraemia,  viz.,  headache,  dyspnoea,  and  diarrhoea. 
As  these  symptoms  are  often  blended  with  similar  troubles  due  to  the  influ- 
enza itself,  their  true  cause  may  be  unnoticed  in  the  absence  of  careful 
examination.  Lastly,  influenzal  nephritis,  especially  in  its  severe  form, 
may  pass  into  the  subacute  and  chronic  stage,  and  give  rise  to  Bright's 
disease,  especially  if  the  kidneys  have  been  previously  damaged  by  other 
infectious  diseases.  ■  I  have  several  times  seen  all  these  forms  of  influenzal 
nepliritis.     I  have  known  60  to  70  grains  of  albumin  to  be  passed  in  the 


INFECTIOUS  DISEASES  PROPETl  TO  MAN  177r. 

tweuty-four  hours.  I  have  also  nvvn.  syiiiptoiiis  of  ur.i-rnia  which  dominated 
the  scene,  and  I  cannot  count  the  cases  in  which  l^rif^Mii's  disease  has  had 
influenza  for  its  primary  cause. 

Other  Local  Manifestations. — I  must  call  attention  to  certain  local 
manifestations  wiiich  are  of  great  importance.  The  organs  of  the  senses 
are  often  invaded,  and  the  nasal  form  of  influenza,  which  shows  itself  by 
rhinitis,  epistaxis,  and  by  discharge  from  the  nose,  may  be  complicated  by 
inflammation  of  the  frontal  sinuses  and  of  the  meninges. 

Otitis,  previously  almost  unmentioned,  was  so  frequent  in  the  epidemic 
of  1889-90  that  much  was  written  on  the  subject  (Loewenberg).  The 
condition  is  one  of  acute  otitis  media,  accompanied  by  pain  and  more  or 
less  prolonged  discharge  of  pus.  The  pain  ceases  after  perforation  of  the 
membrane.  The  most  usual  microbes  found  in  these  cases  are  the  strepto- 
coccus and  the  pneumococcus.  In  some  cases  the  mastoid  cells  are  invaded, 
in  which  case  it  is  necessary  to  trephine  the  bone. 

Ocular  paralyses  which  are  not  unlike  those  of  diphtheria  have  been 
described. 

Cystitis,  urethritis,  orchitis,  epididymitis,  and  vaginalitis  have  also  been 
seen  in  influenza.     Exanthematous  and  pustular  eruptions  are  frequent. 

In  certain  epidemics  a  hsemorrhagic  form  may  be  seen.  It  is  accom- 
panied by  metrorrhagia  (Law,  1779),  hsematuria  (Voisin,  1837),  purpura  and 
epistaxis.     This  form  was  very  common  in  the  epidemic  of  1889-90. 

etiology. — Influenza  is  an  epidemic  disease,  which  usually  spares 
children  and  by  choice  afiects  adults,  and  a  first  attack  does  not  confer 
immunity.  It  is  at  present  impossible  to  state  the  causes  which  favour  its 
development,  because  it  appears  to  disregard  conditions  of  climate,  season, 
and  temperature  (Graves).  It  swoops  down  upon  a  town  or  a  country, 
lays  low  a  half,  two-thirds,  or  three-quarters  of  the  inhabitants,  and  after 
a  duration  of  some  weeks  it  disappears,  thus  affecting  immense  areas, 
although  its  course  has  not  always  a  definite  direction  (Gintrac). 

Nevertheless,  epidemics  of  influenza  usually  travel  from  north  to  south 
and  from  east  to  west.  The  original  seat  of  the  disease  is  said  to  be  in 
Siberia  by  some  authorities  and  in  Persia  by  others.  At  any  rate,  it  is 
certain  that  influenza  is  endemic  in  Moscow  and  St.  Petersburg,  where  it 
appears  every  year  in  the  autumn  and  spring,  and  is  the  result  of  conditions 
as  yet  unknown.     It  assumes  an  epidemic  or  pandemic  character. 

Our  severe  epidemic  of  1889-90  furnished  material  for  studying  its 
conditions  of  diffusibility.  Influenza  does  not  exceed  in  its  diffusion  the 
quickness  of  human  communications.  It  usually  breaks  out  in  a  large  toAvn, 
and  then  spreads  to  smaller  communities.  There  are,  however,  exceptions 
which  remain  inexplicable.  Why,  for  example,  did  not  the  London  epidemic 
in  May,  1890,  spread  to  the  Continent  ? 


1776  TEXT-BOOK  OF  MEDICIXE 

The  contagioTis  nature  of.  influenza,  wHch  liad  long  been  doubted,  must 
be  definitely  accepted,  for  tbe  proofs  of  contagion  are  clear.  Influenza 
appears  to  be  transmissible  by  direct  contact  and  by  foniites. 

Bacteriology. — The  various  organisms  met  with  in  influenza,  such  as 
the  Streptococcus  'pyogenes,  which  is  most  common,  the  pneumococcus,  the 
pneumobacillus,  and  the  staphylococcus,  are  only  secondary  agents.  They 
are  not  the  prime  cause  of  influenza. 

PfeiSer  discovered  the  influenza  bacUlus  in  1892.  It  is  found  in  abun- 
dance in  the  sputum.  Its  presence  is  revealed  by  the  usual  bacterial  stains, 
but  care  must  be  taken  to  expose  the  slide  to  the  stain  for  at  least  ten 
minutes,  because  the  influenza  bacillus  is  slow  to  take  the  dye. 

Pfeiffer's  bacillus  does  not  stain  well  with  aniline  dyes.  It  is  preferable 
to  use  diluted  Ziehl's  stain.  It  does  not  take  Gram's  stain.  After  staining, 
the  bacillus  appears  among  the  shreds  of  mucus  and  the  leucocytes,  or  some- 
times in  the  leucocytes  themselves.  It  has  the  shape  of  an  extremely  thin 
rod ;  it,  indeed,  is  thinner  than  any  other  bacillus.  It  is  very  short,  and 
only  about  twice  as  long  as  it  is  broad,  so  that  it  sometimes  has  the  appear- 
ance of  a  cocco-baeilius.  When  these  rods  are  in  pairs  they  simulate  a 
diplococcus,  and  when  three  or  four  are  joined  end  to  end  they  resemble  a 
streptococcus. 

The  bacillus  of  Pfeiffer  is  cultivated  with  difiiculty  on  the  ordinary 
media.  It  grows  best  on  agar  to  which  a  few  drops  of  blood  have  been 
added.  A  mixture  of  haemoglobin  and  agar  gives  the  same  results.  If 
the  agar  is  impregnated  with  blood,  and  placed  in  the  oven  at  37°  C,  we 
find  after  twenty-four  hours  very  smaU  colonies,  which  are  visible  with  the 
lens.  They  have  the  appearance  of  smaU  transparent  drops,  which  show 
no  tendency  to  become  confluent  (Kitasato). 

The  bacillus  may  live  from  fifteen  to  eighteen  days  on  blood  agar,  and 
from  thirty  to  forty  days  on  haemoglobin  agar. 

If  we  sow  Pfeifler's  bacillus  on  agar  covered  with  blood,  making  stabs 
with  the  Staphylococcus  aureus  at  intervals,  the  culture  of  the  influenza 
bacillus  is  assisted  in  a  remarkable  manner.  Around  the  fertilizing  colonies 
of  the  staphylococcus  we  find  the  development  of  giant  colonies,  which  may 
be  twenty  times  as  large  as  those  of  a  pure  control  culture.  This  cultural 
satellitism  (Meunier)  must  be  employed  in  order  to  find  Pfeifler's  bacillus 
in  pathological  exudates.  Excellent  satellite  cultures  of  the  influenza 
bacillus  are  obtained  in  twenty-four  hours. 

Diagnosis. — The  diagnosis  of  influenza  is  not  always  simple.  It  may 
at  first  sight  simulate  typhoid  fever,  measles,  rheumatism,  meningitis,  or 
acute  tuberculosis,  either  by  reason  of  well-marked  lesions  in  a  particular 
system  or  by  reason  of  the  general  symptom-complex.  The  diagnosis  from 
meningitis  is  the  more  indefinite  because  influenzal  meningitis  is  also  seen. 


INKECTIUUS  1>1:dEAHK.S  miUi'KU  To   MAX  1777 

J  would  refer  the  roadcr  for  further  details  to  the  Meet  ion  on  Cerebro-Spinal 
Meningitis.  When  inlluenza  siinuhites  typhoid  fever,  sero-diagriosi.s  (Widal) 
will  remove  all  doubts. 

Treatment.  -It  is  not  possible  to  state  any  treatment  for  a  disease  which 
is  so  iliiloreut  in  its  course  and  appearance.  We  may  emjiloy  antiphlogistic 
measures  for  the  inflammatory  complications  and  antispasmodics  for  the 
nervous  symptoms.  Emetics  are  of  use  in  the  bilious  forms.  Slight  cases 
of  influenza,  which  are  happily  the  most  frequent,  should  be  treated  in  the 
same  manner  as  acute  bronchitis. 


MI.  YELLOW  FEVER— VOMITO  NEGRO. 

JEtiology. — Yellow  fever  has  been  classed  both  among  telluric  diseases 
and  typhoid  maladies,  but  it  should  certainly  find  a  place  among  the  in- 
fectious diseases  of  microbic  origin. 

We  are  not  yet  in  possession  of  precise  data  as  to  the  microbe  of  yellow 
fever.  Lacerda  has  foimd  in  most  of  the  viscera  a  microscopic  fungus, 
which  he  regards  as  specific.  Carmona  and  Domingo  Freire  have  described 
a  proto-organism  from  which  they  have  prepared  vaccine.  Babes  has  foimd 
in  the  liver  and  kidneys  micro-organisms  which  have  not  been  verified  by 
other  authors.  Sanarelli  thinks  that  the  B.  icteroides  is  the  pathogenic 
agent  of  yellow  fever. 

Reed,  Caroll,  and  Agramante  have  attributed  yellow  fever  to  a  microbe 
belonging  to  the  class  of  invisible  microbes  which  pass  through  the  pores 
of  filtering  candles.  This  microbe  is  carried  by  a  special  mosquito,  the 
Cidex  faseiatus,  which  is  classed  by  Theobald  in  the  genus  Stegomya  {Stego- 
niya  fasciata).  "  Healthy  men,  living  with  those  sufiering  from  yeUow 
fever,  and  exposed  to  the  bites  of  mosquitoes,  which  settle  alternately  upon 
the  patients  and  the  healthy,  have  contracted  the  disease.  This  fact  alone 
explains  whv  the  scourge  remains  limited  in  most  cases  to  the  seashore  and 
to  low-lying  districts.  The  habits  of  the  Stegomya  control  the  spread  of  the 
disease,  which  is  only  met  with  in  an  epidemic  condition  where  the  insects 
themselves  are  found.  The  parasite  in  question  swarms  only  in  the  low, 
damp,  and  warm  shores  of  intertropical  countries.  Moreover,  these  diptera 
are  not  found  on  high  ground  above  the  600-metre  line  or  outside  the  zone 
in  which  the  diminution  of  the  barometric  pressure  considerably  interferes 
with  their  flight  "  (Bogey). 

Chantemesse  and  Borel  speak  as  follows  in  their  communication  to  the 
Academy  of  Medicine  (1905)  : 

The  mission  of  the  Pasteur  Institute,  composed  of  Drs.  Marchoux, 
Simond,  and  Salimbeni,  has  confirmed  and  extended  these  views.  It  is 
now  settled  that  the  existence  of  yellow  fever  and  the  presence  of  the 


1778  TEXT-BOOK  OF  MEDICINE 

Stegomya  are  absolutely  reciprocal.  Although  this  mosquito  is  widely 
scattered,  its  habitat  has  something  special  in  that  it  is  clearly  determined 
by  the  forty-third  north  and  south  parallels,  and  this  is  the  reason  why 
every  region  external  to  these  two  parallels  remains  free  from  yellow  fever. 
The  forty-third  parallel  just  touches  the  South  of  France.  It  enters  at  the 
Department  of  the  Basses-Pyrenees,  passes  through  Argeles,  Saint-Girons, 
and  Eoix,  and  reaches  the  coast  a  little  above  La  Nouvelle.  The  only  port 
of  any  note  in  this  region  is  Port-Vendres.  The  same  parallel  passes  through 
the  islands  of  Hyeres,  and  then  through  the  north  of  Corsica.  It  would, 
therefore,  be  unwise  to  send  soldiers  coming  from  countries  infected  with 
yellow  fever  to  the  islands  of  Hyeres,  which  have  formerly  been  used  as  a 
quarantine'station.  On  the  other  hand,  all  our  colonies,  except  Saint-Pierre 
and  Miquelon,  are  in  the  country  of  the  Stegomya. 

YeUow  fever  is  endemic  upon  the  shores  of  the  Gulf  of  Mexico,  in  the 
Antilles,  in  Brazil  (Visca),  and  on  the  West  Coast  of  Africa,  etc.  It  may 
be  imported  from  these  centres,  and  appear  in  epidemic  form  in  both  hemi- 
spheres, as  the  multiple  epidemics  in  America  and  Europe  (Gibraltar,  1828  ; 
Lisbon,  1847  ;  Saint-Nazaire,  1861)  prove. 

YeUow  fever  only  leaves  its  endemic  centres  for  the  purpose  of  invading 
other  regions  by  reason  of  importation,  which  is  always  caused  through 
ships.  In  some  cases  the  vessel  has  shipped  passengers  who  are  already 
infected,  and  in  whom  the  disease  appears  during  the  voyage.  At  other 
times  the  whole  crew  is  quite  well  on  starting,  but  the  ship  harbours  the 
mosquito  in  the  holds,  and  an  epidemic  appears  some  days  after  sailing. 

Experience  has  shown  that  infection  occurs  chiefly  after  sunset  and  at 
night.      Physicians,  therefore,  visit  their  patients  about  midday. 

The  disease  does  not  spread  rapidly,  but  remains  at  first  limited  to 
certain  houses  or  to  a  single  street.  Visca  has  noted  the  interesting  fact 
that  the  invasion  often  takes  place  by  excentric  zones,  which  spread  from 
the  primary  centre.  The  epidemic,  like  the  endemic  form,  shows  little 
tendency  to  invade  places  remote  from  the  sea-coast  and  elevated  regions. 
The  incubation  of  yellow  fever  lasts  from  three  to  six  days. 
Description. — Prodromata  do  not,  as  a  rule,  occur  in  yellow  fever,  which 
commences  suddenly  in  the  middle  of  the  night  with  a  sharp  rigor,  followed 
by  backache  {coup  de  harre),  headache,  lassitude,  and  epigastric  distress, 
with  or  without  pulsation  in  the  coeliac  region.  The  temperature  on  the 
first  day  may  exceed  105°  E.  (Naegele).  The  eyes  are  haggard  and  injected, 
the  face  is  red,  thirst  is  severe,  constipation  is  the  rule,  the  restlessness  and 
insomnia  are  sometimes  accompanied  by  delirium,  and  the  skin  is  erythe- 
matous. On  the  second  day  the  patient  is  seized  with  nausea  and  vomiting — 
first  of  food-stuffs,  later  of  mucus  and  of  bile.  The  urine  is  scanty  and 
usually  contains  albumin. 


INFECTIOUS  DISEASES  PROPER  TO  MAN  177.» 

Tills  first  stage,  which  is  very  sevorc,  hists  about  thro.c  days.  The 
Byniptoras  then  improve,  the  temperature  falls,  and  jaundice  appears. 
Jaundice,  which  is  the  most  constant  8yni])tom  of  the  disease,  and  has 
gained  for  the  disease  the  name  of  yellow  fever,  coincides  with  tlie  remission 
which  ends  the  initial  period.  In  benign  cases  the  disease  does  not  pass 
beyond  this  inflammatory  stage,  and  the  fever  does  not  reappear.  In 
severe  oases,  however,  the  remission  lasts  only  a  few  hours,  and  the  fever 
reappears,  though  it  may  not  be  as  high  as  in  the  first  stage. 

The  jaundice  varies  in  intensity  from  the  palest  to  the  deepest  greenish- 
yellow.  The  urine  contains  bile,  but  the  stools  are  not  colourless,  because 
the  flow  of  bile  is  free.  Jaccoud  thinks  that  the  pathogenesis  of  this  symp- 
tom is  not  always  the  same ;  he  is  of  opinion  that  the  jaundice  is  some- 
tunes  catarrhal  and  at  other  times  associated  with  hypercholia.  Vomiting 
of  dark  blood  {vomito  negro)  is  practically  contemporaneous  with  the 
jaundice,  though  it  is  much  less  constant,  being  present  in  about  50  per 
cent,  of  cases.  The  haemorrhage  from  the  stomach  is  often  accompanied 
by  bleeding  from  the  intestines,  from  the  pharynx,  or  from  the  mouth,  by 
metrorrhagia,  and  by  purpura. 

The  general  condition  of  the  patient  varies,  and  adynamic,  typhoid, 
and  delirious  forms  are  seen.  In  some  cases  the  anuria  is  complete,  and 
we  may  well  ask  if  the  symptoms  of  dyspnoea  and  ataxo-adynamia  should 
not  be  set  down  to  uraemia. 

Duration. — In  the  slight  forms  the  remission,  which  usually  occurs  about 
the  third  day,  is  accompanied  by  profuse  sweating,  and  recovery  speedily 
follows.  In  the  grave  forms  the  disease  lasts  from  six  to  ten  days,  or  even 
longer.     The  fulminant  form  is  fatal  in  three  or  four  days. 

Diagnosis. — We  are  not  likely  to  confound  yellow  fever  with  icterus 
gravis,  for  in  the  latter  disease  the  sudden  onset  of  the  fever,  the  backache,  the 
epigastric  distress,  and  the  injection  of  the  face  and  eyes  are  wanting.  We 
can  distinguish  yellow  fever  from  the  bilious  forms  of  malaria,  which  are 
accompanied  by  more  or  less  marked  swelling  of  the  spleen,  and  characterized 
by  the  presence  of  the  parasite  and  of  melanotic  pigment  in  the  blood.  The 
bilious  form  of  typhoid  fever  somewhat  resembles  the  typhoid  form  of 
yellow  fever,  but  in  the  former  the  temperature  rises  slowly  and  the  spleen 
is  enlarged.  The  mortality  varies  in  different  epidemics  of  yellow  fever 
from  14  to  50  per  cent.  (Dutroulau). 

Pathological  Anatomy. — The  chief  lesions  are  of  a  steatogenous  nature. 
The  liver  resembles  the  fatty  liver  of  phthisis  (Louis).  It  is  of  a  light 
yellow  colour,  bloodless  and  friable.  The  cells  rapidly  become  fatty,  but 
are  only  in  part  necrosed.  The  heart  and  the  kidneys  are  also  affected  by 
fatty  degeneration.  The  muscles,  especially  those  of  the  abdomen  and 
thighs,  are  sometimes  the  seat  of  ecchymoses.    Ecchymotic  patches,  which 


1780  TEXT-BOOK  OF  MEDICmE 

are  sometimes  ulcerated,  may  be  seen  in  the  stomach,  pharynx,  and  intestine. 
The  blood  is  of  abnormal  fluidity — a  condition  found  in  most  of  the  infectious 
diseases.     The  spleen  is  normal. 

Treatment. — In  countries  where  yellow  fever  reigns,  prophylaxis,  accord- 
ing to  the  latest  data,  consists  in  destroying  the  mosquitoes,  isolating  the 
patients,  and  protecting  them  against  the  Stegomya.  For  this  purpose  the 
beds  are  covered  by  mosquito  curtains,  the  doors  and  the  windows  are 
covered  with  fine  wire-netting.  The  mosquitoes  are  destroyed  by  fumiga- 
tion with  sulphurous  acid  or  by  the  fumes  of  pjTethrum.  Dr.  Diaz  Albertini, 
who  has  taken  great  interest  in  the  sanitation  of  Havana,  has  given  much 
interesting  information.  Each  room  in  the  house  is  subjected  to  the  fumes 
of  pyrethrum  after  every  aperture  has  been  hermetidally  sealed.  When  the 
rooms  are  opened  it  is  surprising  to  see  the  number  of  dead  mosquitoes  on 
the  floor  and  elsewhere.  Excellent  results  follow  this  method  of  disinfection 
where  mosquitoes  are  found. 

In  order  to  destroy  the  larvae,  petroleum  is  poured  into  the  drains, 
closets,  and  puddles  where  the  mosquito  lays  its  eggs.  The  Americans  have 
obtained  marvellous  results  in  Cuba  by  these  measures.  The  fight  against 
mosquitoes  commenced  at  Havana  on  February  16,  1901,  and  during  the 
half-year  from  April  to  October,  in  which  the  majority  of  cases  occur,  only 
eighteen  deaths  from  yeUow  fever  occurred,  while  the  mean  death-rate  in 
previous  years  had  been  483.  For  150  years  no  one  had  ever  seen  such  an 
excellent  state  of  sanitation  as  during  this  season. 

The  usual  treatment  consists  in  giving  gentle  purgatives,  such  as  castor- 
oil,  mixed  with  lemon-juice  (Fuzier),  and  in  treating  hyperthermia  by  means 
of  cold  aromatic  applications.  Acidulated  drinks,  quinine,  and  brandy  are 
prescribed. 

Prophylaxis  on  Board  Vessels.— I  quote  from  the  commumcation  of 
Chantemesse  and  Borel  (1905)  :  Let  us  take  the  case  of  a  vessel  leaving  a 
country  in  which  yellow  fever  is  prevalent.  After  sailing,  an  antimosquito 
crusade  must  be  carried  on  by  fumigation  of  their  local  habitats,  especially 
those  in  which  the  temperature  is  high  (gaUey,  engine-room,  etc.).  If  a 
case  of  yellow  fever  breaks  out  on  board,  the  cabin  occupied  by  the  patient 
must  be  evacuated  if  possible,  fumigated,  and  then  ventilated.  Search 
must  be  made  for  receptacles  likely  to  contain  stagnant  water,  and  the 
patient  must  sleep  under  a  net.  If  the  disease  breaks  out  on  a  sailing-ship, 
the  captain  should  steer  a  northerly  course. 

Prophylaxis  against  Yellow  Fever  in  Ships  on  their  Arrival  in  France. 
— Three  hypotheses  may  present  themselves  on  the  arrival  of  a  ship  from 
an  infected  part.  First  hypothesis  :  Nothing  has  happened  during  the 
voyage.  Free  pratique  should  be  given.  Second  hypothesis  :  One  or  two 
cases,  obviously  contracted  in  the  infected  country,  have  occurred  on  board, 


INFECTIOUS  DISEASES  i'liOl'iai  TO  MAN  1781 

witliout  giving  rise  to  any  furtlicr  trou])le.  Pratique  should  be  given  with- 
out restrictions  as  to  the  crew  and  the  cargo.  Tliird  hypothesis  :  A  scries 
of  cases  has  appeared  during  the  voyage.  Precautions  are  then  necessary. 
The  vessel  must  be  emptied,  and  the  most  thorougli  disinfection  of  all  local 
habitats  be  carried  out  with  sulphurous  acid.  If  the  cargo  is  of  a  nature 
liable  to  harbour  mosquitoes  (bananas,  fruit,  sugar,  or  damp  timber),  the 
holds  must  be  fumigated  with  sulphurous  acid. 

Lastly,  persons  suffering  from  yellow  fever,  on  arrival  in  ports  where  no 
quarantine  hospital  exists,  should  be  placed  in  the  local  hospital.  Yellow 
fever  is  not  considered  to  be  a  contagious  disease  in  France. 

The  most  rigorous  measures  are,  of  course,  necessary  in  countries 
inhabited  by  the  Stegomya. 


VIII.  PLAGUE. 

Plague  is  a  disease  which,  after  ravaging  the  greater  part  of  the  Old  World,  remained 
for  some  years  localized  to  certain  provinces  of  Turkey  in  Asia,  to  Persia,  and  f  o  the 
adjacent  States.  It  was  endemic  there,  but  at  intervals  epidemics  broke  out,  and 
spread  by  means  of  importation  from  their  original  centres,  causing  secondary  centres 
on  the  borders  of  the  Red  Sea,  of  the  Persian  Gulf,  and  of  the  Caspian  Sea. 

Plague  has  lately  resumed  its  widespread  course,  and  after  the  epidemic  at  Hong- 
Kong  has  made  constant  progress.  The  disease  appeared  at  Bombay  in  1896,  spread 
over  India,  passed  through  the  Suez  Canal,  and  invaded  Alexandria.  In  July,  1899, 
it  broke  out  at  Oporto,  and  later  showed  itself  at  Glasgow.  I  need  not  speak  of  the 
epidemic  at  Vierma  in  1898,  which  only  occurred  in  the  laboratory  and  was  stamped 
out  there. 

Let  us  remember  the  epidemic  on  the  s.s.  Senegal,  chartered  for  a  cruise  by 
La  Revue  des  Sciences,  which  ended  in  a  quarantine  at  Frioul,  so  weU  known  throughout 
the  scientific  world. 

Epidemiology. — Plague  is  due  to  a  microbe  discovered  by  Yersin  in 
1884.  The  conditions  necessary  for  the  development  of  plague  are  well 
known,  and  the  history  of  recent  epidemics  at  Oporto  and  Bombay  have 
yielded  abundant  data  as  to  its  epidemiology. 

In  the  Oporto  epidemic  the  breach  remained  unknown;  plague  was 
already  present  in  Portugal  in  the  early  spring  of  1899,  when  the  first  case 
was  oflB.ciaUy  notified  on  June  5.  Calmette  and  Salimbeni  think  that  the 
disease  was  brought  to  Oporto  by  rats  from  some  ship  coming  from  the 
Island  of  Mauritius,  the  Persian  G-ulf ,  or  from  Alexandria.  For  a  long  while 
dead  rats  were  found  in  the  narrow  streets  of  Fonte-Taurina  and  in  the 
neighbourhood.  The  disease,  disseminated  by  these  rodents,  quickly  spread 
among  the  rats  and  mice  which  swarm  in  the  vessels  and  in  the  docks  of  the 
port.  The  first  cases  of  human  plague  did  not  appear  until  several  weeks 
later,  the  first  victims  being  the  limapers  and  poor  people,  who  are  herded 
together  in  the  most  insanitary  houses  of  the  town, 
^  113 


1782  TEXT-BOOK  OF  MEDICINE 

It  appears  certain  that  the  disease  was  imported  into  Bombay  by  sea. 
The  onset  of  the  epidemic  in  the  Mandvi  quarter,  which  is  close  to  the 
port  and  includes  numerous  warehouses,  and  the  ease  with  which  rats 
from  ships  moored  in  the  docks  could  reach  the  land  and  overrun  this 
quarter,  are  strong  arguments  in  favour  of  this  opinion.  There  seems  to 
be  no  doubt  that  the  infection  came  from  Hong-Kong. 

Plague  is  chiefly  carried  by  the  rat  (Simond),  and  human  agency  is 
insufficient  to  explain  the  spread  of  the  disease.  The  epidemic  appears 
among  rats  before  it  does  among  the  inhabitants  in  plague-infected  towns. 
This  fact  also  obtains  in  the  case  of  ships,  and  Simond  quotes  a  striking 
example  : 

"  In  February,  1898,  the  s.a.  Shannon  went  from  Bombay  to  Aden  and  baok.  Plague 
was  raging  at  Bombay  at  this  time,  and  the  boat  was  submitted  before  its  departure 
to  the  rigorous  prophylactic  measures  laid  down  at  the  Venice  Conference.  Nothing 
special  happened  during  the  outward  voyage,  nor  during  the  stop  at  Aden,  but  during 
the  retiim  voyage  dead  rats  were  fotmd  in  the  mail  office,  where  the  mail-bags  were 
stored.  Shortly  after  the  postal  official  who  worked  in  this  room  was  attacked  by 
plague.  The  man  could  not  have  brought  the  plague  on  board  among  his  effects,  nor 
could  he  have  been  in  the  incubation  stage,  for  he  had  been  taken  on  board  at  Aden,  and 
did  not  come  from  a  plague-infected  area.  There  is  no  doubt,  therefore,  that  he  con- 
tracted the  disease  in  the  rat-infected  cabin.  It  is  also  certain  that  an  epidemic  among 
rats  had  broken  out  on  the  boat  long  after  its  departure  from  Bombay,  either  because 
sick  rats  had  come  on  board  the  ship  at  that  port,  or  because  the  rats  on  board  had 
contracted  plague  carried  in  the  cajgo." 

The  transmission  of  plague  from  the  rat  to  man  appears  in  most  cases 
to  be  efiected  by  means  of  parasites,  and  most  writers  have  incriminated 
fleas  (Simond),  which  live  on  corpses,  and  only  leave  them  when  they 
become  cold.  These  facts  explain  why  dead  rats  are  at  different  times  very 
dangerous  or  harmless  (Simond). 

Plague  respects  neither  age,  sex,  nor  race,  but  overcrowding,  want, 
famine,  and  dirt  are  very  favourable  to  its  development.  Its  incubation 
period  hardly  ever  exceeds  ten  days,  and  as  a  rule  it  is  under  five. 

Description. — Plague  usually  runs  the  course  of  a  malignant  infection, 
with  painful  sweUing  of  the  lymphatic  glands,  high  fever,  and  marked 
prostration.  This  is  the  classical  or  bubonic  form  of  plague.  In  some 
cases  it  chiefly  affects  the  lung  or  the  intestine,  bnt  in  other  cases  it  runs 
the  course  of  a  true  septicaemia. 

1.  Classical  Bubonic  Plague. — The  onset  is  usually  sudden,  and  accom- 
panied by  a  sharp  chill,  fever,  vomiting,  headache,  photophobia,  and  pains 
in  the  epigastrium,  kidneys,  and  limbs.  The  gait  becomes  uncertain  and 
reeling,  and  the  patient  is  quickly  compelled  to  lie  down.  At  this  period 
the  chief  symptoms  are  helplessness  and  prostration ;  the  power  of  speech 
is  embarrassed  or  abolished ;  the  look  is  dull  and  resigned,  and  the  patient 
is  sometimes  seized  with  vomiting  and  diarrhoea. 


INFECTIOUS  DISEASES  rKOPKit  T<J  MAN  178.". 

The  temperature  by  the  evening  of  the  second  day  may  reach  100''  F.  ; 
the  morning  remission  is  slight.  A  momentary  fall  of  2°  is  often  noticed 
on  the  second  or  third  day.  The  pulse  rises  to  120  or  140 ;  the  breathing 
becomes  quick ;  the  tongue  is  black,  dry,  and  cracked,  and  the  lips  are 
covered  with  sordes.  Delirium  may  appear  at  this  stage,  being  quiet  or 
violent,  with  convulsions,  carphologia,  chilling  of  the  extremities,  and 
cyanosis  of  the  lips.  The  vomiting  and  diarrhoea  become  more  severe. 
The  appearance  of  the  tongue  is  characteristic.  It  is  at  first  swollen,  covered 
by  a  whitish  coat,  except  at  the  edges  and  tip,  which  are  clean.  Later,  the 
dorsum  becomes  dry  and  covered  with  a  yellow  or  brownish  coat,  while 
the  edges  and  the  tip  remain  red.  Cough  and  other  signs  of  bronchial  con- 
gestion are  present,  and,  finally,  various  haemorrhages  help  to  complete 
the  clinical  picture  of  the  stationary  stage,  which  may  last  from  one  to 
three  days. 

The  third  period,  or  period  of  termination,  presents  two  characteristic 
symptoms,  which  may,  however,  appear  earlier — namely,  buboes  and 
carbuncles. 

The  buboes  may  affect  any  of  the  lymphatic  glands,  but  they  chiefly 
attack  the  glands  in  the  groin,  the  axillae,  the  popliteal  spaces,  and  the 
neck.  They  do  not  always  produce  discoloration  of  the  skin,  unless  sup- 
puration occur.  The  deep  glands  (mediastinal  and  mesenteric)  are  often 
affected  at  the  same  time,  giving  rise  to  a  train  of  symptoms  which  vary 
according  to  the  situation  of  the  enlarged  glands.  Their  size  varies  from  a 
hazel-nut  to  a  walnut.  They  are  sensitive  to  the  touch.  When  the  bubo 
is  situated  in  the  groin,  the  patient  flexes  the  thigh  upon  the  abdomen,  in 
order  to  avoid  stretching  of  the  painful  region.  When  the  axilla  is  affected, 
the  patient  lies  on  his  back,  with  the  arm  motionless  and  abducted  from  the 
trunk. 

The  situation  of  the  initial  bubo  is  of  some  importance  as  regards  prog- 
nosis. Buboes  in  the  neck  are  more  serious  than  those  in  the  groin.  Each 
fresh  invasion  of  glands  is  accompanied  by  a  return  of  the  fever.  In  rapidly 
fatal  cases  the  glands  remain  hard  and  very  painful.  If  the  disease  is  pro- 
longed, we  find  a  brownish  swelling  of  the  gland  and  of  the  neighbouring 
region.  This  condition  may  end  in  resolution,  or  more  often  in  suppura- 
tion, about  the  seventh  or  eighth  day.  When  the  bubo  is  opened,  yellowish 
or  sanious  pus  exudes.  The  sloughing  of  the  skdn  is  followed  by  an  indolent 
ulcer,  with  prominent  jagged  edges  and  a  greyish  floor,  in  which  the 
necrosed  glands  are  exposed.  These  ulcers  usually  take  several  weeks  to 
heal,  and  leave  large  and  deep  scars.  Any  gland  which  does  not  suppurate 
remains  indurated  for  a  lengthy  period  (Netter). 

The  appearance  of  buboes  coincides  in  some  patients  with  fall  of  tem- 
perature, moisture  of  the  skin,  and  general  feeling  of  comfort,  which  is  of 

113—2 


1784  TEXT-BOOK  OF  MEDICINE 

good  omen.  Events  do  not  always  run  this  course,  and  death  may  occur 
before  the  enlargement  of  the  glands. 

Let  us  now  study  the  characteristic  carbuncle  of  plague.  These  car- 
buncles are  comparable  to  the  first,  second,  and  third  degrees  of  burns 
(superficial  lesions,  eschars  of  the  dermis,  and  deep  gangrene  affecting  the 
muscles  and  even  the  bones).  They  vary  in  number  from  one  to  twelve, 
and  may  be  found  on  any  part  of  the  body,  except  on  the  palms  of  the  hands 
and  soles  of  the  feet.  They  are  of  evil  omen,  but  less  so  than  petechiae, 
and  the  body  is  sometimes  covered  with  black  ecchymoses  or  pustules 
resembling  hsemorrhagic  variola.  The  cutaneous  manifestations  almost 
always  accompany  the  very  severe  forms  of  plague.  They  are  charac- 
teristic of  the  type  called  black  plague  by  old  writers  (Calmette  and 
Salimbeni). 

Death  usually  appears  with  symptoms  of  ataxo-adynamia.  Eecovery, 
which  is  seen  in  half  of  the  cases,  may  be  interrupted  or  retarded  by  sup- 
puration in  the  glands  and  by  suppurative  inflammations  of  the  viscera 
and  serous  membranes. 

2.  Septicwmic,  Pneumonic,  and  Intestinal  Forms. — In  the  septicaemie 
form  the  buboes  are  absent.  The  onset  is  very  severe,  and  the  temperature 
rapidly  rises  to  105°  or  106°  F.  The  nervous  phenomena  are  very  marked. 
The  prostration  is  extreme,  even  on  the  first  day.  Coma  follows  delirium, 
when  it  is  present.  Diarrhoea,  tympanites,  retention  of  urine,  epistaxis, 
subconjunctival  hsemorrhages,  enterorrhagia,  and  hsematuria  have  been 
noted.     Death  may  occur  in  twenty-four  hours. 

Pneumonic  plague,  found  in  Bombay  (Childe),  was  the  only  form  seen 
in  Vienna  in  October,  1898,  in  the  laboratory  epidemic,  when  Miiller  and 
Barish  died.  This  terrible  form  of  the  disease  is  almost  always  fatal.  It 
may  be  secondary,  but  it  is  usually  primary.  "  The  glandular  enlargements 
are  wanting,  or  only  appear  late,  as  a  secondary  result.  The  lesion  in  the 
lung  replaces,  as  it  were,  the  initial  bubo,  and  forms  the  essential  expression 
of  the  disease  "  (Cheinisse).  The  symptoms  are  those  of  pneumonia.  Cal- 
mette and  Salimbeni  saw  patients  at  Oporto  with  a  temperature  of  106°  F., 
who  had  been  taken  iU  with  an  initial  rigor,  as  in  pneumonia.  The  breathing 
was  very  laboured  ;  the  rusty  sputum  became  viscid,  and  in  two  or  three 
days  took  on  the  appearance  of  prune- juice,  as  in  a  case  of  pneumonia  which 
is  passing  into  the  stage  of  grey  hepatization.  Auscultation  revealed  the. 
same  signs  as  in  pneumonia — fine  crepitant  rales  and  tubular  breathing. 

The  diagnosis  can  be  made  only  by  bacteriological  examination  of  the 
sputum.  The  prognosis  is  extremely  grave,  and  recovery  is  exceptional. 
In  the  epidemic  of  pneumonic  plague  at  Kolobovka  there  were  twenty-three 
deaths  out  of  twenty-four  cases  (Tchistowitch). 

The  intestinal  form  of  plague  is  characterized  by  chills,  fever,  pain,  and 


INFECTIOUS  DTSEASKS   I'lJUL'Kli  TO  MAX  Hftn 

vomiting,  with  diarrh(Tea,  distension  of  the  abdomen,  and  backache.  The 
glands  become  enlarged  in  a  few  days  (Hogel). 

Diagnosis. — The  diagnosis  of  classical  plague  is  very  easy,  especially 
during  an  epidemic.  The  sudden  onset,  the  appearance  of  the  tongue,  the 
tenderness  and  swelling  of  the  glands,  attract  attention.  This  does  not 
obtain  in  the  other  forms,  especially  in  the  pneumonic  form.  Miiller  took 
the  disease  while  nursing  and  examining  his  laboratory  assistant,  who  was 
stricken  with  plague  pneumonia,  which  remained  undiscovered  for  thirty-six 
hours.  He  had  not  at  that  time  the  slightest  suspicion  as  to  the  nature  of 
the  infection.  The  only  means  of  diagnosis  is  by  bacteriological  examina- 
tion of  the  sputum.  The  search  for  the  plague  bacillus  is  best  made  in  the 
brawny  area  around  the  buboes.  It  will  give  the  more  valuable  results  the 
sooner  it  is  made  after  the  onset  of  the  disease.  When  the  bubo  com- 
mences to  suppurate,  the  B.  festis  has  given  way  to  the  agents  of  secondary 
infection. 

Pathological  Anatomy  and  Bacteriology. — The  glands  in  plague  are 
swollen,  indurated,  or  softened,  of  a  reddish,  brownish,  or  yellowish  colour, 
and  filled  with  pus.  They  unite  with  the  neighbouring  glands,  so  as  to 
form  a  large  mass,  enclosing  nerves  and  vessels.  The  visceral  lesions  consist 
in  congestion  and  haemorrhages.  The  right  heart  is  dilated ;  its  walls  may 
be  softened  to  the  point  of  rupture  ;  and  the  venous  system  is  distended  and 
engorged  with  dark  blood,  both  in  the  sinuses  of  the  dura  mater  as  well  as 
in  the  veins  of  the  limbs  and  trunk.  The  liver  and  spleen  are  enlarged  and 
softened,  whUe  the  lung  is  hard  and  hypertrophied.  All  the  organs,  and 
in  particular  the  kidnej-s  and  the  walls  of  the  alimentary  canal,  show  infil- 
tration of  blood. 

Bacteriology. — Yersin  has  been  able  to  isolate  from  the  pulp  of  the 
buboes  a  short  truncated  bacillus,  with  rounded  ends,  staining  with  aniline 
dyes,  but  not  with  Gram. 

The  centre  of  the  bacillus  does  not  stain  as  deeply  as  its  extremities. 

The  bacillus  is  found  in  large  numbers  in  the  buboes,  glands,  and  also  in 

the  blood.     Cultures  on  broth  somewhat  resemble  those  of  erysipelas.    They 

show  chains  of  short  bacilli,  which  in  places  present  nodular  swellings. 

Cultures  on  agar  yield  transparent,  whitish  colonies,  with  radiating  edges. 

Rats  or  guinea-pigs  inoculated  with  cultures  or  with  the  pulp  of  the  buboes 

die  in  a  few  days.     Moreover,  in  plague  epidemics  rats  are  affected  by  the 

disease  in  plague-houses.     Yersin  found  the  same  bacillus  in  the  organs  of 

rats  which  have  died  from  plague  as  in  man.     He  is  of  opinion  that  plague 

is  inoculable  and  contagious,  because  he  was  able  to  cause  plague  by  placing 

healthy  mice  in  the  same  cage  as  inoculated  ones. 

"  La  peate,  puisqu'il  faut  I'appeler  par  son  nom. 
Capable  d'enrichir  en  rni  jour  rAcheron," 


1786  •  TEXT-BOOK  OF  MEDICINE 

has  decimated  a  part  of  the  globe  for  centuries,  but  is  becoming  more  and 
more  limited,  on  account  of  the  energy  of  sanitary  measures,  though  we 
cannot  keep  too  close  a  watch,  since  it  is  at  our  doors. 

Treatment. — Yersin  has  successfully  treated  patients  with  his  anti- 
plague  serum.  On  August  25,  1896,  Brouardel  announced  that  he  had 
just  received  a  despatch,  saying  that  Yersin  had  treated  and  cured  twenty- 
seven  cases  of  plague  with  the  serum.  I  give  the  result  of  the  first  case, 
which  is  destined  to  take  its  place  among  the  marvellous  methods  of  treat- 
ment which  are  the  outcome  of  Pasteur's  teaching  : 

"  On  June  26,  1896,"  says  Yersin,  "  at  the  Catholic  Mission  School  a  young  China- 
man called  Tise,  eighteen  years  of  age,  complained,  about  ten  o'clock  in  the  morning, 
of  pain  in  the  right  groin.  At  midday  he  felt  very  tired,  fever  appeared,  and  he  was 
obliged  to  go  to  bed.  I  saw  the  patient  at  three  o'clock  in  the  afternoon,  and  his  general 
condition  was  bad :  extreme  lassitude,  vertigo,  and  fever.  The  characteristic  bubo 
was  present  in  the  right  groin,  and  this  region  was  brawny,  and  formed  a  well-marked 
projection.  The  mass  was  exceedingly  painful  to  the  touch.  About  five  o'clock  I 
made  preparations  for  a  first  injection  of  serum.  The  patient's  condition  was  now 
worse.  The  weakness  was  extreme,  the  fever  was  higher,  and  delirium  was  setting  in. 
In  the  opiaion  of  all  those  accustomed  to  see  patients  with  plague  the  patient  was 
doomed  to  die  within  twelve  hours. 

"  I  gave  the  first  injection  of  serum  at  five  o'clock  (10  c.c.  under  the  skia  of  the 
flank),  using  serum  prepared  at  Nha-Tsang,  and  successfully  employed  in  the  case  of 
mice.  It  vaccinates  mice  with  ^  c.c.  Immediately  after  the  injection  the  patient 
vomited  food  and  bihary  matter  (a  frequent  symptom  in  cases  of  pestis  gravis).  At 
six  o'clock  in  the  evening  the  general  condition  appeared  a  httle  better ;  the  eye  was 
brighter,  and  the  patient  said  that  he  felt  stronger.  I  therefore  gave  a  second  injection 
of  serum  (10  c.c.  under  the  skin  of  the  flank). 

"  At  half -past  seven  the  fever  had  increased,  and  the  patient  was  restless  and 
wandering.  He  had  coUc  and  sUght  diarrhoea.  At  nine  o'clock  in  the  evening  I  gave 
the  third  and  final  injection  of  serum  (10  c.c.  imder  the  skin  of  the  flank).  The  fever 
was  now  very  marked,  and  the  patient  continued  to  wander,  but  he  slept  in  a  restless 
manner  from  nine  o'clock  tiU  midnight.  The  injection  wounds  were  painful.  At 
midnight  notable  improvement.  The  fever  diminished,  the  patient  regained  conscious- 
ness, said  that  he  felt  better,  and  slept  more  quietly  till  three  o'clock  in  the  morning. 
By  this  time  the  improvement  in  his  condition  was  manifest,  the  weakness  and  fever 
being  less  marked.  The  patient  passed  a  motion  (sKght  diarrhoea),  and  slept  quietly 
from  three  o'clock  till  six  in  the  morning,  when  he  awoke  quite  conscious.  The  weakness 
had  disappeared,  the  bubo  was  no  longer  painful  and  had  decreased  in  size,  and  the 
fever  had  vanished. 

"  At  eleven  o'clock  in  the  morning  the  patient  said  that  he  was  cured.  The  skin 
was  moist,  and  the  temperature  normal ;  no  trace  of  the  lassitude  and  prostration  of 
the  previous  evening  remained.  The  brawny  swelling  in  the  right  groin  had  completely 
disappeared.  This  region  was  now  painless  to  the  touch,  and  the  only  trace  of  the 
disease  remaining  was  one  or  two  glands  of  the  size  of  a  haricot-bean.  The  injection 
woimds  were  still  painful. 

"  June  28  :  The  patient  passed  an  excellent  day  and  night.  The  injection  wounds 
were  no  longer  painful,  and  the  resulting  induration  had  disappeared.  The  patient's 
strength  and  appetite  were  returning.  Jime  29 :  I  saw  the  patient  for  the  last  time 
to-day.  His  strength  continues  to  return,  and  he  is  able  to  take  a  short  walk  in  the 
garden  without  excessive  fatigue.     The  glands  of  the  groin  are  diminishing  in  size." 


1XKP:CTI01TS  diseases  PliOPKU  TU  .MAN  1787 

Yersin's  acruin  has  been  em))loyed  at  Tiombay  and  Oporto.  Calmette 
and  Salimbeni  who  have  obtained  (excellent  n'.sulta,  advise  as  early  as  possible 
an  intravenous  injection  of  20  c.c.  of  antiplague  serum,  followed  by  two 
subcutaneous  injections  of  40  c.c.  each,  repeated  during  the  first  twenty-four 
hours.  The  mortality  at  Oporto  reached  63'72  per  cent,  before  sero- 
therapy, but  fell  to  1478  per  cent,  after  the  use  of  the  serum.  The  differ- 
ence between  those  two  figures  indicates  the  efficiency  of  the  serum. 

This  method  of  treatment  forms  one  of  the  greatest  triumphs  of  sero- 
therapy. 

Antiplague  serum  has  a  preventive  action,  conferring  an  immunity  which 
lasts  about  a  fortnight.  It  is  necessary,  therefore,  during  epidemics,  to 
give  an  injection  every  two  weeks.  A  dose  of  5  c.c.  is  sufficient.  The 
death  of  Dr.  Pestana,  who  was  vaccinated  on  September  18,  and  contracted 
plague  on  October  13,  through  omitting  re  vaccination  in  the  interval,  is  the 
best  example  of  the  necessity  for  revaccination  every  fortnight. 

Injection  of  cultures  of  plague  bacilli  killed  by  heat  at  70°  C.  (Haffkine) 
has  also  given  good  prophylactic  results,  but  it  is  not  free  from  danger 
during  an  epidemic,  as  it  may  hasten  and  aggravate  the  course  of  plague 
in  patients  already  infected  with  the  disease  (Calmette  and  Salimbeni). 

IX.  TETANUS. 

Tetanus  {malvoa),  I  stretch)  is  characterized  by  paroxysmal  contrac- 
tures affecting  a  large  number  of  muscles.  This  condition  is  due  to  the 
exaggeration  of  the  excito-motor  force  of  the  spinal  cord  and  bulb,  and, 
consequently,  to  the  abnormal  excitation  of  their  grey  matter.  Certain 
poisons,  such  as  strychnine  and  brucine,  cause  tetaniform  conditions,  but 
true  tetanus  is  a  microbic  disease. 

Bacteriology. — The  bacillus  of  tetanus  was  foimd  in  1885  by  Nicolaier 
in  the  pus  of  wounds  in  mice  and  guinea-pigs  which  had  been  infected  with 
tetanus  by  placing  earth  under  their  skin,  Rosenbach  found  it  later  in  the 
wound  of  a  man  suffering  from  spontaneous  tetanus.  Kitasato  isolated  it 
and  obtained  pure  cultures  in  1889. 

The  bacillus  of  tetanus  is  very  thin  and  straight.  It  stains  deeply  with 
all  the  basic  anOine  dyes  in  hydro-alcoholic  solution.  In  some  cases  it  may 
be  elongated  into  a  thread  which  somewhat  resembles  the  Vibrio  septicus. 

The  bacillus  may  also  occur  in  another  form,  which  is  much  more  charac- 
teristic. The  bacillus,  either  in  cultures  or  in  wounds,  passes  into  the 
sporula  (Rosenbach)  stage.  It  assumes  the  shape  of  a  pin,  a  drumstick, 
or  a  racquet.  This  form  is  due  to  the  spore  which  develops  at  one  end  of 
the  bacillus,  and  often  at  both  ends,  in  which  case  the  bacillus  assumes  the 
form  of  a  dumb-bell.     In  somewhat  older  cultures  the  spores  detached  from 


1788  TEXT-BOOK  OF  MEDICINE 

the  rods  resemble  cocci,  and  do  not  stain  as  tlie  bacillus  does.  The  methods 
used  for  the  tubercle  bacillus  or  for  the  B.  h'prcB  must  be  employed  to  stain 
them.  The  spores  are  very  virulent  and  resistant.  They  may  remain  alive 
for  six  months  in  cultures,  in  the  tissues,  or  in  the  earth  (Nicolaier,  Bonane, 
Sanchez  Toledo  and  Veillon). 

A  stab  culture  on  gelatine  at  22°  C.  or  on  agar  at  37°  C.  gives  rise  to 
colonies  of  the  tetanus  bacillus,  developing  in  the  form  of  small  cloudy 
points,  from  which  small  rays  extend  perpendicularly,  presenting  the  flaky 
appearance  of  a  thistle.  The  bacillus  of  Nicolaier  is  anaerobic ;  when 
cultivated  in  hydrogen  or  in  vacuo  in  the  ovum  at  37°  C,  it  yields  abundant 
spores  after  twenty-four  hours. 

The  tetanus  bacillus  exists  in  the  superficial  layers  of  the  soU.  It  is, 
therefore,  a  telluric  microbe  (Nicolaier).  It  has  been  met  with  in  the  soils 
of  fields,  in.  streets  (Socin),  in  the  dust  from  houses  and  gardens,  in  hay 
(Sanchez  Toledo  and  Veillon),  iu  manure  (Sormani),  and  in  animal  excreta. 
It  gains  entrance  by  a  wound  or  by  a  break  in  the  continuity  of  the  skin  or 
of  the  mucous  membrane.  Animals  (especially  the  guinea-pig,  the  mouse, 
and  the  rat)  can  be  infected  with  experimental  tetanus  by  inoculation,  and 
death  almost  always  occurs  after  a  period  varying  from  one  to  five  days. 
The  bacillus  is  found  at  the  point  of  inoculation,  but  is  not  met  with  else- 
where. Like  the  diphtheria  bacillus,  it  does  not  become  general.  It  is  only 
diffused  through  the  organs  and  the  blood  after  death  (Nicolaier,  Kitasato, 
Sanchez  Toledo  and  Veillon). 

The  virulence  of  the  tetanus  bacillus  is  increased  by  successive  passages 
through  anitnals  (Nicolaier,  Nocard,  Dor),  and  by  the  association  of  the 
B.  prodigiosus  (Baillard).  It  is  diminished  by  the  action  of  high  temperatures 
(Dor,  VaHlard),  antiseptics,  and  lactic  acid  (Tizzoni  and  Cattani,  Vaillard). 

The  tetanus  toxine  secreted  by  the  bacillus  is  very  active,  but  its  chemical 
composition  is  not  yet  decided.  It  would  appear  to  be  composed  of  several 
ptomaines,  albuminoid  substances,  a  diastasis,  and  a  soluble  ferment.  The 
poison  is  exceedingly  active,  and  a  hundredth  part  of  a  c.c.  is  sufficient  to 
kill  a  guinea-pig.  In  this  case,  too,  as  in  diphtheria,  the  bacillus  is  confined 
to  the  wound,  and  secretes  continuously  a  poison  which  has  upon  the  nerve 
centres  an  action  siuular  to  that  of  strychnine  or  of  brucine  (VaiUard  and 
Vincent).  Courmont  and  Dujon  attribute  this  toxic  power  to  a  soluble 
ferment,  harmless  in  itself,  which  elaborates  a  tetanizing  substance  at  the 
expense  of  the  organism. 

A  previous  mild  attack  of  tetanus  does  not  confer  immunity.  Immunity 
may  be  produced  in  animals  by  injecting  tetanus  toxine  with  trichloride  of 
iodine  (Behring  and  Eatasato).  The  blood  of  animals  treated  in  this  manner 
is  antitoxic.  Their  serum,  when  inoculated  in  other  animals,  vaccinates 
them  against  tetanus  (Behring  and  Kitasato,  Tizzoni  and  Cattani),  and 


INFECTIOUS  DLSKASKS  i'LiOi'Klt  TO  MAX  1789 

cures  animals  suffering  from  tetanus  (Tizzoni  and  Cattani).  This  vaccina- 
tion by  antitoxic  serum  is  transmitted  from  the  mother  to  the  foetus  (Tizzoni 
and  Cattani),  and  is  also  carried  by  the  milk  (Ehrlich).  The  duration  of 
the  immunity  produced  by  antitoxic  serum  is  not  very  long  (Roux  and 
Vaillard).     In  one  case  Vaillard  noticed  its  disappearance  after  a  fortnight. 

Recent  researches  on  the  tetanus  toxine  have  allowed  us  to  settle  certain 
interesting  points  in  its  action,  and  to  open  up  new  vistas  in  therapeutics. 
Marie  has  shown  that  the  toxine  does  not  spread  through  the  blood-stream. 
The  intravenous  injection  of  tetanus  toxine  must  be  eight  to  ten  times  as 
strong  as  the  subcutaneous  injection  in  order  to  produce  death,  because 
the  poison  travels  almost  exclusively  along  the  nerves  to  fix  itself  in  the 
cells  of  the  spinal  cord  or  of  the  bulb. 

The  nerve  cells  show  considerable  ajQ&nity  for  the  tetanus  toxine.  If  the 
toxine  is  directly  applied  to  the  nervous  substance  (Roux  and  Borrel),  it  is 
immediately  fixed  and  produces  in  rabbits  and  guinea-pigs  a  special  form 
of  tetanus,  called  cerebral  tetanus,  characterized  by  restlessness,  epileptiform 
attacks,  polyuria  and  motor  troubles. 

Roux  and  Borrel  have  formed  the  idea  of  injecting  the  antitoxine  into 
the  brain.  "  The  antitoxine  is  injected  at  this  spot  in  order  to  hinder  the 
progress  of  the  toxine,  and  to  preserve  the  vital  portions  of  the  spinal  cord 
before  they  are  attacked."  These  injections  have  been  successful  in  arrest- 
ing tetanus  in  guinea-pigs  twenty-four,  twenty-eight,  and  even  thirty-two 
hours  after  the  appearance  of  the  convulsions. 

If  the  tetanus  toxine  is  injected  into  the  viscera  of  the  gidnea-pig — i.e., 
testis,  peritoneal  cavity,  liver,  kidney,  bladder,  stomach,  uterus,  trachea, 
lung,  or  Ijrmphatic  glands — splanchnic  tetanus  results.  It  is  never  followed 
by  permanent  contractures  and  antitoxine  inoculated  by  the  subcutaneous 
or  by  the  intracerebral  method  has  no  effect  on  it. 

vEtiology. — Tetanus  is  always  consecutive  to  a  wound  or  to  a  scratch. 
The  worst  cases  are  seen  in  the  wounds  of  the  extremities  (feet  and  hands), 
or  in  gun-shot  injuries  and  jagged  wounds.  Tetanus  may  foUow  a  physio- 
logical injury,  as  of  the  uterus  after  delivery,  or  of  the  umbilicus  in  the 
new-bom  infant.  The  disease  is  more  frequent  in  men  than  in  women,  and 
is  endemic  in  certain  tropical  countries  (India,  Madagascar,  and  Guiana), 
It  is  epidemic  and  contagious. 

The  inquiry  pursued  by  Vememl  aims  at  ascertaining  whether  the  horse 
has  not  something  to  do  with  the  development  of  tetanus.  The  disease  is 
common  in  warm  countries  where  horses  are  numerous.  It  has  developed 
following  a  wound  from  the  lash  of  a  whip,  and  Nicolaier's  bacUlus  was 
found  on  the  lash  itself  (Poisson)  ;  but  the  horse  is  not  an  agent  of  immediate 
contagion  between  the  soil  and  man  and  the  telluric  origin  of  tetanus  is  the 
only  one  at  present  admitted. 


1790  TEXT-BOOK  OF  MEDICmE 

Pathological  Anatomy. — The  anatomical  study  of  tetanus  is  as  yet 
incomplete,  for  the  lesions  which  have  been  seen,  including  ascending 
neuritis,  granular  degeneration  of  the  cells  of  the  spinal  cord,  and  prolifera- 
tion of  the  neuroglia,  are  applicable  to  but  few  cases  and  appear  to  be 
secondary  changes.  Hunter  has,  however,  found  in  the  spinal  cord  of  man 
similar  cellular  lesions  to  those  of  experimental  tetanus  in  animals — globular 
swelling  of  the  cell,  rarefaction  of  the  chromatic  elements,  slight  swelling  of 
the  protoplasmic  processes,  granular  condition  of  the  axis-cylinder,  etc. 
Lastly,  Joukowsky  found  in  a  fatal  case  of  cephalic  tetanus  in  man  that 
the  cells  of  the  motor  area  of  the  cerebral  cortex  were  impregnated  with 
clear  yellow  pigment  in  great  abundance.  It  was  also  present  in  the  bulb 
and  cord,  but  it  does  not  appear  to  be  a  characteristic  lesion.  The  accumu- 
lation of  migratory  rounded  cells  around  the  nerve  cells,  with  penetration 
into  their  protoplasm,  may  be  of  more  importance. 

Description. — Tetanus  usually  commences  with  painful  stiffness  ia  the 
cervico-dorsal  region,  and,  when  it  is  of  traumatic  origin,  the  appearance  of 
the  wound  changes,  the  suppuration  diminishes  and  the  cicatrization  is 
arrested.  As  a  rule,  trismus  (contracture  of  the  jaw)  is  the  first  symptom. 
It  is  often  associated  with  contracture  of  the  nuchal  and  facial  muscles 
(risus  sardonicus).  The  cramp  then  reaches  the  muscles  of  the  trunk  and 
limbs.  The  trunk  is  bent  backwards  (opisthotonos),  though  in  rare  cases 
it  may  be  bent  forwards  or  to  one  side.  The  abdomen  is  retracted  by  the 
spasm  of  the  abdominal  muscles  and  the  lower  limbs  are  rigidly  extended. 
The  arms  are  less  affected. 

This  tetanic  contraction  is  not  continuous.  We  find  alternate  relaxation 
and  spasms,  which  are  very  painful.  Trifling  causes,  such  as  touching  the 
skin,  contact  of  the  bed-clothes,  or  any  reflex  excitation,  are  sufficient  to 
bring  on  an  attack.  During  the  attack  the  trismus  is  more  severe.  The 
opisthotonos  is  so  marked  that  the  patient  is  bent  in  the  form  of  a  bow, 
and  only  touches  the  bed  at  the  head  and  the  toes ;  and  the  constriction  of 
the  pharynx  and  glottis,  associated  with  a  tetanic  contraction  of  the  iaspira- 
tory  muscles,  causes  dyspnoea  borderiug  on  asphyxia.  The  patient  13 
cyanosed,  bathed  in  sweat,  and  tortured  by  the  pains  of  the  contractions. 
He  is  unable  to  speak  or  to  make  any  sign,  although  he  retains  full  con- 
sciousness. The  attacks,  which  are  at  first  short,  with  intervals  between 
them,  in  favourable  cases  become  gradually  less  frequent ;  but  iu  unfavour- 
able cases  they  occur  at  shorter  intervals,  and  end  in  death. 

The  temperature  in  tetanus  rises  above  106°  F.  during  the  attack.  This 
rise  is  not  the  result  of  fever  and,  in  spite  of  some  contradictory  facts,  it 
must  be  attributed  to  the  heat  given  off  by  the  muscles  during  the  condi- 
tion of  tonic  contraction.  The  pulse-rate  and  the  breathing  show  the  same 
variations  as  the  temperature. 


INTKCTIOUS  DISEASES  PROPER  TO  MAX  1791 

Whon  tetanus  is  rapid  in  its  course,  the  ])atient  is  ojirried  of!  jftter  a  few 
days  hj  asphyxia  (tetanization  of  the  respiratory  niusoles).  It  may  be 
prolonged  for  several  weeks  as  the  result  of  remissions,  but  recovery  is 
exceptional  in  this  disease. 

Cephalic  Tetanus. — In  some  cases  tetanus  is  limited  to  the  head,  several 
forms  being  seen  :  (1)  The  contraction  is  bilateral,  the  stiffness  of  the  neck 
is  sometimes  associated  with  rigidity  of  the  jaws,  and  the  cervical  opistho- 
tonos mechanically  causes  dyspnoea  and  dysphagia  (Verneuil)  ;  (2)  the  con- 
tracture is  unilateral,  and  at  first  sight  resembles  facial  paralysis  ;  (3)  cephalic 
tetanus  is  accompanied  by  symptoms  of  dysphagia  ;  (4)  it  is  accompanied  by 
symptoms  of  hydrophobia  (Rose's  hydrophobic  tetanus) ;  (5)  cephalic  tetanus 
is  accompanied  by  facial  paralysis. 

Tetanus  in  the  Puerperal  Condition  and  in  the  New-Born. — Epidemics 
of  tetanus  in  lying-in  women  and  new-born  infants  may  be  seen  in  maternity 
hospitals.  The  infection  enters  through  the  placental  site  and  through  the 
umbilical  sore.  The  symptoms  are  identical  with  those  described  above. 
The  gravity  of  the  condition  is  extreme,  and  of  twenty-one  women  suffering 
from  puerperal  tetanus,  only  one  recovered  (Rubeska).  Among  forty-four 
children  only  two  recoveries  were  noted. 

Tetanus  by  Injection  of  Gelatinized  Serum. — The  stir  naturally  caused 
by  Chauffard's  report  and  by  my  communication  to  the  Academic  de  Mede- 
cine*  leads  me  to  give  details  of  this  question.  The  following  case  was  under 
my  care  at  the  Hotel-Dieu  ; 

A  woman  in  the  Sainte-Jeanne  ward  was  taken  iU  with  symptoms  of  tetanus.  The 
trismus  had  commenced  suddenly  about  three  o'clock  in  the  morning.  When  we  exam- 
ined the  patient  at  nine  o'clock,  she  presented  the  characteristic  picture  of  tetanic 
trismus.  The  teeth  were  shut  so  tightly  that  we  could  not  separate  the  jaws  ;  the  neck 
was  stiff  and  painful ;  the  risus  sardonicus  was  present  and  speech  was  almost  im- 
possible. It  was  evident  that  she  was  suffering  from  tetanus,  but  it  remained  to  find 
the  cause  thereof. 

The  patient,  who  was  thirty-eight  years  of  age,  had  been  imder  my  care  for  some  six 
weeks  for  advanced  pulmonary  tuberculosis,  when  haemoptysis  supervened.  The 
treatment  employed  was  chloride  of  calcium  and  preparations  of  rhatany.  Some  days 
later  a  fresh  attack  of  haemoptysis  occurred,  and  my  house  physician  prescribed  an 
injection  of  gelatinized  serum,  a  method  of  treatment  much  in  vogue  for  haemorrhage. 
The  solution  was  carefully  prepared  in  the  dispensary,  and  the  sterilization  exceeded 
half  an  hour.  The  injection  was  given  in  the  upper  part  of  the  left  thigh  with  every 
aseptic  precaution.  The  tetanus  appeared  eleven  days  after  the  injection  of  gelatine. 
As  we  were  unable  to  find  any  other  cause,  it  was  reasonable  to  attribute  the  tetanus 
to  the  injection  of  gelatine. 

I  examined  the  spot  where  the  injection  had  been  made,  but  only  an  insignificant 
trace  of  the  puncture  was  seen ;  the  skin  was  normal ;  redness,  pain,  oedema,  and 
swelling  were  absent ;  there  was  no  contraction  of  the  thigh. 

I  gave  a  very  bad  prognosis.  Treatment  was  at  once  commenced.  Although 
injections  of  antitetanic  serum  after  the  onset  of  symptoms  are  not  of  much  use,  we 

*  Dieulafoy,  Acadimie  de  Medecine,  stance  du  12  Mai,  190:3. 


1792  TEXT-BOOK  OF  MEDICmE 

gave,  as  a'lorlom  hope,  an  injection  of  20  c.c.  of  antitetanic  serum,  and  repeated  the 
dose  two  hours  later  in  the  region  where  the  injection  of  gelatine  had  been  given.  An 
enema  containing  15  grains  of  chloral  was  given  every  hour  and  in  the  evening  injec- 
tions of  carbolic  acid  were  ordered.  In  spite  of  the  treatment,  the  symptoms  became 
worse.  At  four  o'clock  in  the  afternoon  the  head  was  stiff  and  retracted,  opisthotonos 
was  present,  and  the  pains  were  continuous.  The  patient  was  much  distressed,  and 
could  not  spit  out  the  mucus  which  accumulated  in  her  throat.  In  the  evening  the 
symptoms  became  worse,  although  the  temperature  did  not  rise  above  98°  P.,  the 
dyspnoea  increased  in  severity,  and  the  poor  woman  died  at  half- past  one  in  the  morning, 
in  a  fit  of  suffocation. 

Griffon  made  experiments  in  order  to  clear  up  this  case  ;  on  the  one  hand  he  exam- 
ined the  pus  from  a  small  abscess  found  at  the  spot  where  the  injection  of  gelatine  had 
been  made,  and  on  the  other  hand  the  gelatine  furnished  by  the  dispensary.  The 
results  of  these  experiments  were  : 

Although  a  post-mortem  was  refused  by  the  family,  we  were  able,  with  every  aseptic 
precaution,  to  incise  the  spot  where  the  injection  of  gelatine  had  been  given,  and  found 
under  the  skin  a  small  abscess  of  the  size  of  a  hazel-nut.  The  pus  was  creamy,  very 
thick,  of  a  greyish-white  colour,  but  without  odour.  The  pus  was  collected  in  two 
sterile  Pasteur  pipettes,  which  were  sealed  by  heat  and  taken  to  the  laboratory.  The 
pus,  after  staining,  was  examined  under  the  microscope.  Several  shdes  were  treated 
with  different  stains,  and  we  found  polynuclear  leucocytes  with  clearly  stained  nuclei, 
but  no  sign  of  any  organisms.  After  staining  by  Gram's  method,  the  examination  for 
micro-organisms  was  also  negative  ;  neither  Nicolaier's  bacilli  nor  other  microbes  were 
present. 

Aerobic  Cultures. — The  pus  from  the  pipettes  was  sown  on  agar  and  on  broth,  and 
cultivated  in  the  presence  of  air.  The  culture  taken  from  one  of  the  pipettes  remained 
sterile,  but  that  from  the  other  pipette  showed  colonies  of  a  bulky  rod,  which  hquefied 
gelatine  and  gave  off  a  fcetid  odour.  This  condition  was  evidently  due  to  a  bacterium 
of  putrefaction,  probably  derived  from  the  skin  of  the  corpse  ;  this  hypothesis  was  con- 
firmed by  the  fact  that  the  removal  of  pus  had  been  delayed,  and,  further,  that  only  one 
of  the  pipettes  was  found  to  be  contaminated. 

Anaerobic  Cultures. — The  pus  from  the  pipette  found  to  be  sterile  as  regards  aerobic 
cultures  was  then  sown  deeply  in  long  tubes  of  agar,  which  was  not  set  out  at  an  angle, 
following  the  procedure  of  Liborius.  We  obtained  pure  cultures  of  Nicolaier's  bacillus 
after  twenty-four  hours'  incubation  in  the  oven  at  37°  C  The  colonies  were  puncti- 
form,  spherical,  and  opaque,  and  scattered  throughout  the  whole  culture  medium, 
except  in  the  upper  layer  next  to  the  air.  After  three  or  four  days  some  of  these  colonies 
took  on  the  flaky  appearance  of  a  tuft,  and  at  length  a  few  bubbles  of  gas  burst  through 
the  agar  in  certain  places.  Under  the  microscope,  after  drying  upon  a  slide  in  a 
drop  of  water,  these  colonies  appeared  to  be  formed  of  rods,  which  retained  Gram's 
stain,  and  which  showed  a  single  spore  (drumstick  form),  and,  more  rarely,  a  spore  at 
each  end  (dumb-beU  form). 

Inoculation  of  Guinea-Pigs. — The  pus  was  found  to  be  very  virulent.  Several 
animals  died  in  less  than  twenty-four  hours,  even  after  inoculation  with  a  minute  dose 
of  pus  taken  from  either  pipette.  A  guinea-pig,  inoculated  with  4  or  6  drops  of  pus 
made  into  an  emulsion  with  1  centimetre  of  sterile  broth,  died  in  less  than  twenty  hours 
with  typical  tetanic  contractions. 

The  animal's  body  was  bent  to  the  left  in  emprosthotonos,  the  head  was  retracted 
to  the  side,  and  the  four  limbs  were  in  a  position  of  extension.  Locally,  the  autopsy 
revealed  in  the  thigh  of  these  animals  only  a  Httle  serous  fluid  without  microbes.  The 
organs  were  congested,  and  the  blood  from  the  heart,  upon  microscopical  examination 
and  upon  culture,  contained  no  microbes. 

After  these  results  obtained  by  inoculation  of  the  pus,  we  moculated,  for  compara- 


IXFKUTlUUS  J)LSEA.Sl<:S  PUUi'Eli  TU  MAX  1793 

tive  purposos,  a  giiinoa-pig,  a  mouso  and  a  rabbit,  with  culture  of  broth  in  vacuo, 
imprognated  with  a  portion  of  a  colony  grown  in  a  Liborius  tube.  All  the  animals 
died  of  tetanus. 

Inoculation  of  Pure  Spores. — Tho  pxjiorimcnts  of  Vaillard  and  Vincent 
have  resulted  in  the  eonchision  that  sporular  cultures,  from  which  the  living 
bacilli  and  the  tetanus  toxine  have  been  removed  by  heating  for  three  hours 
at  80°  C,  are  harmless  in  the  guinea-pig  as  long  as  they  are  not  associated 
with  a  culture  of  the  so-called  assisting  microbes  or  with  a  mechanical 
agent,  such  as  lactic  acid,  producing  negative  chemiotaxis  as  regards  the 
phagocytes. 

"  It  is  possible  to  inoculate  guinea-pigs  with  doses  of  i  to  §  c.c.  of  these 
cultures,  which  contain  only  spores,  without  the  animal  presenting  any 
symptom  of  tetanus.  The  pure  spores  do  not  germinate  in  the  healthy 
tissue,  and  therefore  cannot  produce  the  toxine  which  is  indispensable  to 
the  development  of  tetanus  "  (Besson). 

Since  in  my  patient  bacteriological  analysis  of  the  abscess  from  the  thigh 
proved  that  the  bacillus  must  have  acted  on  its  own  account,  it  was  inter- 
esting to  place  guinea-pigs  experimentally  under  the  same  conditions  as  the 
patient — ^that  is  to  say,  to  include  the  spores  in  a  solution  of  gelatine. 

Two  guinea-pigs  were,  therefore,  inoculated  with  ^  c.c.  of  a  sporular 
culture,  to  which  a  10  per  cent,  solution  of  gelatine  had  been  added.  Only 
one  animal  showed  symptoms  of  tetanus  at  the  end  of  twelve  days. 

Two  other  control  guinea-pigs  were  given  injections  of  pure  spores  in 
the  thigh  (^  c.c,  of  a  sporular  culture,  without  the  addition  of  gelatine). 
They  also  suffered  from  tetanus  after  an  incubation  of  twelve  days,  just  as 
did  the  guinea-pig  inoculated  with  the  first  solution.  The  contractions  were 
limited  to  the  inoculated  Hmb. 

The  experiments  made  in  the  laboratory  justified  the  conclusions  formu- 
lated in  regard  to  my  patient,  and  proved  that  the  abscess  was  due  to  the 
development  of  Nicolaier's  bacillus  in  a  pure  state. 

Search  for  the  Tetanus  Bacillus  in  Gelatine  from  the  Laboratory. — 
Experiments  upon  guinea-pigs  in  order  to  find  in  the  gelatine  from  the 
laboratory  the  bacillus  or  the  spores  yielded  only  negative  results.  Guinea- 
pigs,  whether  inoculated  with  a  weak  or  with  a  concentrated  solution  (1  per 
cent,  or  10  per  cent.)  of  gelatine  heated  in  a  water-bath  to  boiling-point, 
remained  healthy. 

Cultures  on  anaerobic  agar,  however,  gave  positive  results.  A  10  pei 
cent,  solution  of  gelatine  was  kept  boiling  at  100°  C.  for  several  minutes, 
and  a  few  drops  were  placed  in  a  Liborius  tube.  After  incubation  for  forty- 
eight  hours  in  the  oven  at  37°  C,  numerous  colonies  of  the  tetanus  bacillus 
were  found.  One  of  these  colonies  caused  tetanus  in  an  inoculated  guinea- 
pig,  which  died  in  less  than  twenty-four  hours.     The  experiment  is,  therefore, 


1794  TEXT-BOOK  OP  MEDICINE 

absolutely  conclusive.  Spores  of  a  very  virulent  tetanus  bacillus  were 
found  by  culture  in  the  pieces  of  gelatine  taken  from  tlie  hospital  dispensary. 
These  results  confirmed  the  researches  of  Levy  and  Brus,  Anderson,  etc., 
as  regards  commercial  gelatine. 

This  case  proves — (1)  the  presence  of  the  tetanus  miicrobe  in  commercial 
gelatine  ;  (2)  the  development  of  tetanus  in  men  and  animals  by  the  patho- 
genic agent  in  a  pure  state  ■without  other  microbes.  This  case  of  tetanus 
due  to  the  injection  of  gelatine  is  not  exceptional.  On  the  contrary,  several 
cases  of  fatal  tetanus  following  injection  of  gelatinized  serum  have  been 
published  during  the  last  two  years.  I  give  a  summary  of  some  of  these 
cases : 

On  October  20,  1901,  Mereati  was  called  to  see  a  patient  siifferiiig  from  severe 
hEematemesis,  due  to  an  ulcer  of  tiie  stomach.  As  several  methods  of  treatment  pro- 
duced no  effect,  an  injection  of  f  htre  of  serum  with  10  per  cent,  of  gelatine,  previously- 
boiled  for  five  minutes,  was  injected  into  the  left  flank,  with  every  aseptic  precaution. 
Eight  days  later  the  subjacent  muscles  became  the  seat  of  very  painful  contractions, 
although  the  injected  region  appeared  free.  During  the  day  the  patient  was  very  rest- 
less, and  complained  of  great  discomfort  in  the  muscles  of  the  neck ;  she  could  not 
open  the  jaw,  because  the  masseters  were  contracted.  On  the  following  morning  the 
patient  had  attacks  of  unbearable  pain,  opisthotonos  was  marked,  and  the  lower  limbs 
were  contracted  in  the  extended  position.  The  constriction  of  the  larynx  and  pharynx 
during  the  attacks  brought  on  acute  dyspnoea,  and  she  passed  away. 

On  January  6,  1902,  a  physician,  called  to  see  a  woman  suffering  from  severe  metror- 
rhagia, which  had  resisted  all  treatment,  gave  an  injection  of  30  c.c.  of  gelatinized  serum 
in  the  right  gluteal  region.  On  January  7  a  fresh  injection  of  50  c.c.  was  made  in  the 
left  buttock.  Both  these  regions  became  painful,  fever  appeared,  and  the  temperature 
during  the  next  few  days  stood  at  105°  F.  Brachet  was  called  in  consultation,  and 
found  that  the  left  buttock  was  inflamed.  On  the  evening  of  January  10  tetanus 
appeared,  stiffness  at  the  back  of  the  neck,  and  retention  of  urine,  requiring  catheteriza- 
tion. On  the  11th  convulsions  appeared,  followed  by  trismus,  which  resisted  every 
remedy.  The  back  of  the  neck  was  contracted.  On  the  12th  the  gluteal  abscess  was 
incised.  Soon  afterwards  a  terrible  attack  came  on,  with  spasm  of  the  respiratory 
muscles,  hvidity  of  the  face,  and  projection  of  the  tongue  between  the  teeth,  which 
were  tightly  shut.  After  lasting  a  few  seconds,  the  crisis  appeared  at  an  end,  but  the 
attacks  increased  in  number,  and  death  supervened  at  eleven  o'clock  the  same  night. 

The  cases  of  fatal  tetanus  following  injections  of  gelatinized  serum  are 
so  numerous  that  Chaufiard  succeeded  in  collecting  eighteen  in  a  report 
which  he  presented  to  the  Academie.  I  can  add  five  others  to  these  eighteen, 
including  those  of  Mereau  and  Krug,  two  cases  reported  by  Doerfler  (Berlin, 
1903),  and  one  case  which  I  saw  myself.  We  have,  therefore,  the  large 
total  of  twenty-three  cases  in  two  years,  without  counting  those  which  have 
escaped  my  notice,  or  which  have  not  been  published. 

All  these  cases  are  very  similar.  Without  entering  into  useless  discus- 
sions, we  know  that  tetanus  may  occur  in  patients  because  the  gelatine 
employed  in  the  preparation  of  the  serum  contains  the  germ  of  tetanus. 
In  order  to  avoid  such  accidents,  it  is  necessary  either  to  abolish  once  for 


i^i^'l!:UTiUU.S  DISEASES  TROPEIl  T<J  .MAN  1705 

all  injections  of  goliitinizcd  serum  or  to  employ  serum  from  an  abBolutely 
reliable  source.  The  difficulty,  however,  is  to  find  such  a  source,  and  every 
care  must  be  taken  in  the  preparation  of  gelatinized  serum,  and  also  in  the 
manufacture  of  the  gelatine  itself. 

In  Germany,  at  Merck's  laboratory,  fresh  calves'  feet  are  used,  and 
boiled  for  an  hour  at  120°  C.  The  gelatine  is,  therefore,  absolutely  pure. 
It  is  filtered  and  placed  in  tubes,  which  are  sterilized  on  two  successive  days 
at  120°  C.  for  a  period  of  one  hour.  A  large  amount  of  the  gelatine  prepara- 
tion is  then  injected  into  mice  and  guinea-pigs,  and  if  the  animals  remain 
healthy  for  twenty  days  after  the  operation,  the  solution  of  1  per  cent, 
gelatine  is  placed  on  the  market. 

In  order  to  obtain  preparations  absolutely  free  from  danger,  I  agree 
with  Chaufiard  that  the  preparation  of  gelatinized  serum  "  should  not  be 
free,  but  should  be  restricted  by  the  laws  and  rules  which  regulate  the 
preparation  of  therapeutic  serums."  And  even  then,  in  spite  of  every  pre- 
caution, we  shall  always  feel  anxious  when  we  prescribe  this  treatment. 
For  my  part,  I  have  never  made  use  of  gelatinized  serum,  and  in  the  future 
I  shall  hold  to  the  same  principle. 

Moreover,  the  haemostatic  properties  of  gelatinized  serum  are  nil,  as  the 
observations  and  experiments  of  Labbe  and  Froin  conclusively  prove. 

We  may,  therefore,  abandon  without  regret  this  useless  and  harmful 
remedy. 

Diagnosis. — The  diagnosis  of  tetanus  is  easy  when  the  characteristic 
symptoms  are  present.  Tetanus  can  scarcely  be  confounded  with  acute  or 
chronic  strychnine-poisoning,  as  there  are  certain  differences.  We  usually 
find  in  strychnine-poisoning  that  trismus  appears  later,  delirium  is  frequent, 
blue  vision  may  be  present  (Tardieu),  and  the  pupils  are  dilated  (Brouardel). 
Treatment. — In  order  to  avoid  the  contagion  of  tetanus,  it  is  necessary 
to  disinfect  localities  contaminated  by  individuals  or  by  animals  with  tetanus, 
to  isolate  the  clearly  defined  cases  and  to  cleanse  suspected  wounds  with 
the  greatest  care.  When  tetanus  is  present,  isolation  of  the  patient  in  the 
most  quiet  surroundings,  chloral,  morphia  and  Calabar  bean  have  been 
advised.  If  the  infected  focus  is  accessible  and  if  amputation  does  not 
entaU  too  serious  a  mutilation,  it  should  be  performed  without  delay,  in 
order  to  avoid  the  formation  of  fresh  toxines  (Berger).  Lastly,  the  patient 
must  be  given  injections  of  antitoxic  serum,  which  is  the  only  rational 
method  of  treatment.  The  failures  resulting  from  Behring  and  Eatasato's 
method  are  explained  by  the  extreme  fixity  of  the  tetanus  toxine  in  the 
nerve  cells,  and  by  the  impossibility  of  the  antitoxine  reaching  them  in 
time  if  it  is  given  by  subcutaneous  or  by  intravenous  injection.  Accord- 
ingly, the  experimental  treatment  proposed  by  Roux  and  Borrel  in  the  case 
of  the  guinea-pig  (intracerebral  injection  of  antitoxine)  has  been  used  in 


1796  TEXT-BOOK  OF  MEDICINE 

man.  In  twenty-six  cases  collected  last  year  Lereboullet  found  eighteen 
deaths  and  eight  recoveries.  Early  intracerebral  injection,  as  soon  as  trismus 
occurs,  appears  to  be  one  of  the  conditions  for  success  and  there  is  then 
some  chance  of  arresting  the  disease. 

Sicard  has  related  the  cases  of  three  patients  suffering  from  tetanus  who 
were  treated  and  cured  by  subarachnoid  injections  of  tetanus  antitoxine. 
In  one  of  these  cases  several  injections  of  antitetanic  serum  were  also  made 
into  the  large  peripheral  nerve  trunks. 

Preventive  injections  of  antitoxins  are  very  efficacious  in  any  patient 
sufiering  from  a  suspected  wound  which  has  been  soiled  by  earth  (Vaillard 
and  Roux).  The  injection  of  10  c.c.  of  antitetanic  serum,  repeated  a  fort- 
night after  the  first  injection,  is  an  excellent  safeguard  against  tetanus,  and 
I  cannot  recommend  its  use  too  strongly. 

X.  MALAEIA. 

The  researches  of  recent  years  have  enriched  the  history  of  raalaria  with  fresh  and 
exact  knowledge,  which  has  cleared  up  many  previously  obscure  questions.  The 
infectious  agent  of  paludism — the  hsematuzoon — is  well  known  (Laveran).  We  know 
that  certain  mosquitoes  are  extremely  act;»«  agents  of  propagation  and  contagion,  and 
this  knowledge  has  furnished  prophylactic  measures  which  give  excellent  results.  The 
discovery  of  the  pathogenic  agents  and  the  use  of  sero-diagnosis  helps  to  elucidate  the 
obsciu-e  points  ia  complex  cases  of  typho-malarial  fever.  It  is,  indeed,  evident  that 
the  views  held  twenty  years  ago  are  very  different  from  those  we  hold  to-day. 

Malaria  may  assume  many  forms,  including  intermittent,  remittent,  continuous, 
pernicious,  or  larval  fever,  chronic  lesions,  and  cachexia ;  and  certainly,  of  aU.  the 
infectious  diseases,  it  occupies  the  largest  surface  of  the  globe.  Few  countries  escape  ; 
it  holds  sway  either  in  an  endemic  or  in  an  endemo-epidemic  form  in  the  five  divisions 
of  the  world,  increasing  in  virulence  in  tropical  chmates. 

When  the  infection  has  entered  the  economy,  it  remains  there  with  such  pertinacity 
that  it  may  reappear  for  years  in  different  forms,  either  febrile  or  afebrile,  even  after 
the  patient  has  long  since  left  the  original  centre  of  infection. 

Tn  tropical  climates  malaria  is  often  associated  with  other  infections,  such  as  typhoid 
fever  or  dysentery,  and  these  comphcations  play  a  large  part  in  the  severity  of  epidemics. 

At  every  moment  in  large  imdertakings  and  great  enterprises  mankind  encounters 
malaria,  which  is  his  most  terrible  enemy.  Many  examples  of  this  may  be  quoted. 
At  Bordeaux,  in  1805,  the  swamp  of  Chartreuse,  which  is  close  to  the  town,  was  drained 
in  the  summer ;  12,000  inhabitants  were  taken  ill  with  malarial  fever,  and 
3,000  died.  The  Saint-Martin  canal  was  dug  at  Paris  in  1811,  and  the  Temple, 
Vniette,  and  Pantin  quarters  of  the  city  paid  a  heavy  tribute  to  malarial  fever. 
Epidemics  of  malarial  fever  broke  out  during  the  work  upon  the  Suez  Canal  and  the 
Panama  Canal. 

When  it  was  found  advisable  to  replant  the  vine  in  the  Department  of  Herault  some 
years  ago,  the  pick  and  plough  opened  up  old  swampy  areas  in  the  sand  on  the  sea- 
shore, and  malarial  fever  appeared  in  an  epidemic  form  (Jeannel). 

Our  troops  were  decimated  by  the  terrible  scourge  in  Algeria,  the  Crimea,  Italy, 
China,  Cochin-China,  Mexico,  and  Tonkin.  In  the  United  States,  during  the  famous 
War  of  Secession,  tens  of  thousands  were  attacked  by  malarial  and  typho-malarial 
infection . 


INFKCTIOUS  inSEASKS   I'lM  U'KR  T«  •   MAX  17*J7 

Towns  wliich  were  formerly  flourishing  have  been  ruinod  by  thoir  proximity  to  salt 
niarshtw. 

Tlio  greatest  disaster  recorded  in  history  is  certainly  the  blotting  out  of  the  British 
army  in  Walchoren.  This  took  placo  in  1H09.  "  Kngland,"  says  Thiers,  the  liistorian, 
"sent  to  the  Scheldt  a  formidable  expedition,  composed  of  470  vessels,  with  44, WJ 
men,  in  order  to  capture  ilntwerp  and  the  French  fleet.  Some  anxiety  was  felt  in 
Paris  as  to  the  issue  of  this  expedition,  but  Napoleon,  who  was  at  Schoenbrunn,  re- 
tissured  everyone  ;  for  ho  saw,  by  a  flash  of  genius,  that  the  British  army  would  perish 
in  the  malarial  regions  of  the  Scheldt.  Ho  therefore  ordered  his  Generals  to  hold  the 
army  in  check  in  this  region,  and  not  to  give  battle.  His  prognosis  was  verified  : 
malaria  caused  terrible  ravages  among  the  EngUsh,  and  27,000  of  their  soldiers  perished 
or  were  sent  to  hospital." 

Parasitology. — Until  recent  years  the  pathogenesis  and  the  nature  of 
malaria  was  a  matter  of  supposition,  because  micro-biology  had  not  as  yet 
revealed  the  intimate  cause  of  the  infectious  diseases.  The  honour  of  dis- 
covering the  pathogenic  agent  of  malaria  was  reserved  for  a  French  physician, 
Laveran,  who,  on  November  6,  1880,  saw  for  the  first  time  the  flagella  of 
the  hsematozoon,  and  his  first  publication,  which  dates  from  1881,  is  several 
years  prior  to  the  works  of  Marchiafava  and  Celli,  "  who  in  1889  simply 
verified  the  facts  announced  by  Laveran  between  1880  and  1882." 

The  parasite  of  malaria  is  a  haematOZOOn.  It  shows  two  forms  {parva 
et  magna),  so  called  from  the  size  of  the  parasitic  elements.  "WTien  a  patient 
returns  to  France  after  the  small  variety  has  been  found  in  his  blood  in  a 
malarial  country,  we  find  the  large  variety  in  the  blood  if  he  has  a  return 
of  the  fever.  Accordingly,  they  aie  7iot  two  different  species,  but  only 
varieties  of  the  same  species.  Its  torms  may  be  classified  in  the  following 
four  types  : 

1.  Spherical  Bodies. — These  represent  the  most  common  form  of  the 
parasite,  and  are  composed  of  transparent  hyaline  substance.  The 
largest  ones  may  exceed  the  size  of  the  red  corpuscles.  The  spherical 
bodies  show  amoeboid  movements.  They  may  be  free  in  the  serum,  or  may 
be  incorporated  in  the  red  blood-corpuscles,  which  may  show  two  or  three 
in  each  corpuscle. 

These  parasites  live  at  the  expense  of  the  red  corpuscles.  As  the  spherical 
body  grows,  it  becomes  filled  with  pigment,  and  the  red  corpuscle  becomes 
pale,  until  it  is  as  transparent  as  the  parasite.  The  granules  of  pigment  are 
often  absent  in  the  smallest  spherical  bodies,  but  they  may  form  a  regular 
crown  of  black  granules  in  the  large  ones.  After  half  an  hour  the  amoeboid 
movements  cease,  the  pigment  collects  at  certain  points  and  the  spherical 
bodies  take  on  their  cadaveric  form.  They  differ  from  melaniferous  leuco- 
cytes in  the  absence  of  a  nucleus. 

2.  Flagella. — In  preparations  from  fresh  blood,  where  the  spherical 
bodies  are  free  in  the  serum,  we  may  see  excapsulation  of  the  flagella.  The 
flagella  are  mobile  threads  moving  actively  and  varying   in  length  from 

11.  "  114 


1798 


TEXT-BOOK  OF  MEDICINE 


m        I? 


Fig.  81. — Evolution- Cycle  op  the  Pahasite  oe  Malakia  (Bokdas). 

Complete  cycle  of  the  Plasmodium  malarise,  after  Laveran,  Grassi,  Bignami,  Bastia- 
nelli,  Ross,  Sdiamdiim,  etc.  The  portion  above  the  dotted  line  represents  the 
asexual  cycle  (Grolgi's  febrile  cycle).  This  cycle  (AS.H.)  occui-s  in  the  patient's 
blood ;  I  to  V,  growth  of  the  parasite,  p ;  6  to  9,  stages  in  the  division  of  the 
parasite,  and  production  of  mezoites,  m ;  9,  rosette ;  iu  10,  the  mezoites,  m,  are 
free,  and  one  of  them,  p,  has  entered  the  red  corpuscle  I. 

The  portion  below  the  dotted  line  shows  the  sexual  cycle  of  the  haematozoon  in  the 
body  of  the  Anopheles ;  YII,  crescent-bodies  which  enter,  at  the  time  of  biting, 
the  body  of  the  mosquito,  mi ;  YII  to  XII,  sexual  generation,  GS ;  VIII  9 
to  X  9 ,  evolution  of  the  macrogamete ;  YIII  6  to  X  d ,  evolution  of  the 
microgametocyte ;  X  <J ,  formation  of  flagella,  fl.  or  microgametes ;  XI,  fecun- 
dation or  penetration  of  the  microgamete  into  the  macrogamete :  XII,  zygote 
with  two  nuclei  (male  or  female) ;  XIII,  mobile  zygote  (ookinete)  ;  ookinete 
passes  through  stomach- waU  (ei)  of  the  Anopheles ;  XYI  to  XYIII,  sporogonia, 
S  ;  XIY,  cyst  or  zygote  in  the  stomach-wall ;  XY,  nucleus  of  the  cyst  divides ; 
XYI,  formation  of  sporoblasts,  spo ;  XYII,  the  sporoblasts  produce  sporozoites ; 
XYIII,  cyst  after  rupture  of  its  walls ;  pr,  residual  protoplasmic  mass ;  the 
sporozoites,  sp,  fall  into  the  general  cavity,  and  reach  the  salivary  glands,  01, 
of  the  Anopheles,  mi ;  they  then  pass,  at  the  moment  of  biting,  into  the  blood  of 
the  healthy  human  being,  and  communicate  malaria  to  him ;  XIX,  numerous 
sporozoites,  sp,  with  nuclei,  n,  in  the  blood ;  they  next  enter  the  red  corpuscles,  I,  p. 


TXFFXTIOUS  DISEASES  PROPER  I'O  MAN  IT'.'O 

20  to  28  fi.  Two,  three,  or  four  flagella  are  sometimes  attached  to  one 
spherical  body,  which  then  resembles  a  pseudopod.  The  free  end  of  the 
flagella  always  presents  a  pyriform  swelling.  These  filaments  become 
detached  from  the  spherical  body  at  a  given  moment.  According  to 
Laveran,  the  flagella  are  the  most  characteristic  elements  of  the  parasite, 
as  he  found  them  92  times  in  432  cases.  The  flagella  are  the  male  elements, 
destined  to  fertilize  the  female  elements  (MacCallum,  Koch,  Marchaix). 

3.  The  crescent  bodies  have  a  length  equal  to  that  of  the  diameter  of 
the  red  blood-corpuscles.  The  horns  of  the  crescent  are  tapered  and  curved. 
Grains  of  black  pigment  accumulate  at  the  central  part, 

4.  The  rosettes  closely  resemble  the  shape  of  a  rose.  They  are  pig- 
mented at  the  centre  and  segmented  at  the  periphery.  Laveran  was  at 
first  of  opinion  that  they  were  retrogressive  forms  of  the  spherical  bodies. 
Golgi  studied  them  carefully  in  1886,  and  again  in  1889.  The  peripheral 
segments  break  up,  becoming  free,  and  are  converted  into  small  amoeboid 
spherical  bodies.  According  to  some  authorities,  the  rosettes  are  more 
numerous  in  tertian  than  in  quartan  fever. 

5.  Cadaveric  Forms. — We  find  in  the  blood  of  malarial  patients  immo- 
bile, irregular  and  pigmented  hyaline  bodies,  which  are  the  remnants  of  the 
haematozoon. 

Phagocytosis. — The  leucocytes  are  recognized  by  their  regular  form, 
and  by  their  nuclei,  which  stains  readily  with  carmine.  These  melaniferous 
leucocytes  absorb  the  pigment  from  the  dead  parasite.  They  may  even 
absorb  it  from  the  li\^g  organism. 

Evolution  of  the  Parasite. — The  first  act  of  this  polymorphous  parasitism 
is  its  appearance  in  the  form  of  a  transparent  vacuole  in  the  red  corpuscle. 
The  vacuole  becomes  a  spherical  body  and  is  filled  with  pigment  granules 
at  the  expense  of  the  red  corpuscles.  Aiter  this,  the  spherical  bodies  push 
out  the  flagella.  The  haematozoon  sometimes  assumes  the  form  of  a  crescent 
incorporated  in  a  red  corpuscle  which  has  been  digested,  but  at  other  times 
it  breaks  up  and  forms  a  rosette  body.  Segments  or  spores  numbering  ten 
to  twenty  become  free  and  pass  into  the  plasma,  where  the  cycle  starts  afresh. 

Frequency  of  the  Types. — In  the  cases  observed  by  Laveran  the  types 

of  the  hsematozoon  alone  or  combined  were  divided  as  follows  : 

Spherical  body    . .  . .  . .  . .     389  times. 

Crescent  . .  . .  • .  . .     107      „ 

FlageUa..  ..  ..  ..  . .       92      „ 

It  has  recently  been  stated  that  the  t^-pe  of  the  parasite  varies  with  that 
of  the  fever.  According  to  Golgi,  there  is  a  special  parasite  for  tertian  fever, 
quartan  fever,  etc.  This  is  an  error.  The  flagella  and  the  spherical  bodies 
are  more  frequent  in  acute  malaria,  the  crescent  bodies  are  more  often 
found  in  chronic  cases,  but  the  parasite  is  always  the  same. 

114—2 


1800  TEXT-BOOK  OF  MEDICINE 

Technique. — In  order  to  find  the  haematozoon,  we  must  look  for  it  at 
the  onset  of  an  attack  before  the  paroxysm,  and  before  the  administration 
of  quinine.  A  drop  of  blood  is  withdrawn  and  spread  upon  a  slide,  and 
the  cover-glass  should  be  ringed  in  order  to  prevent  currents.  Laveran 
usually  employs  methylene  blue  as  the  staining  reagent. 

Giemsa's  method  shows  better  the  intimate  structure  of  the  hsemato- 
zoon.  A  dried  and  fixed  blood-film  is  placed  for  twenty  minutes  in  cold 
Giemsa's  mixture,  diluted  eleven  times.  The  preparation  is  dried  in  the 
air.  The  corpuscles,  stained  rosy  or  pale  green,  form  a  clear  ground  on 
which  we  can  readily  see  the  ruby  nucleolus  of  the  Schizonte,  the  colourless 
vesicle  formed  by  the  nucleus,  and  the  blue  edge  which  represents  the 
j)rotoplasmic  body  of  the  haematozoon,  studded  with  pigment  granules  in 
organisms  advanced  in  their  evolution. 

Discussion. — According  to  some  authors,  Lavefan's  haematozoon  is  not 
the  specific  agent  of  malaria,  because  it  is  present  in  the  lizard,  tortoise, 
jackdaw,  etc.  The  haematozoon  is  no  doubt  found  among  the  animal 
species  (Danilewsky),  but  in  man  it  is  pathogenic.  The  proofs  furnished 
by  Laveran  are  :  haematozoa  are  found  in  malaria  wherever  it  occurs.  They 
have  never  been  met  with  iu  persons  who  were  not  sufferiag  from  malaria. 
The  development  of  the  haematozoa  is  intimately  related  to  the  production 
of  melanaemia,  which  is  characteristic  of  malaria.  The  salts  of  quinine 
cause  the  parasite  to  disappear  from  the  blood  and  at  the  same  time  cure 
malaria.  Malaria  has  been  successfully  transmitted  from  animal  to  man 
by  injecting  into'  the  veins  of  a  healthy  individual  a  small  quantity  of 
blood  containing  the  parasites  from  a  malarial  patient  (Mariotti  and 
Ciarrochi) 

etiology. — The  hypotheses  put  forward  by  Laveran  and  Patrick 
Manson  concerning  the  propagation  of  malaria  by  some  sucking  insect, 
such  as  the  mosquito,  have  received  definite  acknowledgment.  Ronald 
Ross  has  found  that  the  haematozoon  of  birds  develops  in  the  mosquito  in 
the  form  of  pigmented  bodies  and  germ  filaments  which  have  recently 
developed  in  the  venomo-salivary  gland  of  the  mosquito.  These  bodies  pass 
with  the  secretion  of  the  gland  into  the  wound  made  by  the  insect  upon  the 
skin  of  a  healthy  subject,  mix  with  the  blood,  and  produce  infection. 
Ronald  Ross  was  able  in  this  way  to  infect  healthy  birds,  which  succumbed. 
The  liver  and  the  spleen  were  filled  with  black  pigment  characteristic  of  the 
disease  in  birds.  AH  mosquitoes  are  not  capable  of  propagating  malaria. 
The  Anopheles  must  be  held  guilty.  The  coexistence  of  the  Anopheles 
and  of  endemic  malarial  fever  have  been  recognized  in  several  parts  of 
the  world.  On  the  other  hand,  the  Oulex  is  only  found  in  healthy 
localities  (Laveran), 

In  London,  where  this  disease  does  not  exist  normally,  Manson  succeeded 


INFECTIOUS  DISEASES  IMfOI'KR  TO  MAN  1801 

in  ciiisiiig  ni;ilari;i  in  llio  fuUowiug  manner:  Tbo  huvuu  of  Lite  Anopheles 
wi>ro  collected  in  Rome,  and  were  kept  in  close  confinement.  When  they 
bocanio  adult,  they  were  placed  in  mosquito-proof  cylinders  and  were  ho 
far  harmless.  In  order  to  make  them  poisonous,  the  cylinder  was  placed 
upon  a  ])atient  suffering  from  malaria,  and  the  mosquitoes,  hiting  the  patient 
through  the  meshes  of  the  gauze,  absorbed  both  the  blood  and  the  hsema- 
tozoa.  The  cylinders  containing  the  infected  mosquitoes  were  sent  from 
Rome  to  London.  Manson's  son,  who  was  studying  medicine  at  Guy's 
Hospital,  allowed  these  mosquitoes  to  bite  him  and  was  attacked  by 
malaria.     The  hasmatozoa  were  found  in  his  blood. 

Another  experiment,  the  inverse  of  the  preceding,  clearly  shows  the  part 
played  by  the  mosquito  in  the  spread  of  malaria.  Sambon,  Low,  and  three 
other  persons  lived  near  the  mouth  of  the  Tiber,  in  a  locality  where  malaria 
attacks  both  the  inhabitants  and  travellers.  They  were  careful,  however, 
to  live  in  a  wooden  hut  specially  constructed  in  London,  with  windows 
fitted  with  such  fine  wire  blinds  that  the  Anopheles  could  not  pass  through 
them.  The  beds  were  protected  by  mosquito- curtains.  The  experimenters 
remained  a  month  in  their  hut  without  going  out  between  bedtime  and 
sunrise.     They  were  not  attacked  by  malaria. 

The  Anopheles  is  distinguished  from  the  Culex  by  the  position  of  its 
head.  In  the  former,  the  trunk  and  the  palps  are  of  the  same  length, 
instead  of  the  palps  being  shorter  than  the  trunk.  The  Anopheles  does 
not  rise  above  the  ground,  as  it  is  a  poor  flier,  and  does  not  travel  far  from 
the  pool  where  it  is  bom.  During  the  day  the  Anopheles  hides  on  plants 
or  in  dark  places,  but  at  night  it  comes  out  on  the  pools.  The  female  alone 
bites  man  at  dusk.  The  larvae  of  the  Anopheles  live  in  the  water,  like 
those  of  the  Culex,  but  their  shape  is  very  different.  In  the  Culex  a  respira- 
tory tube  which  projects  out  of  the  water  is  found  at  the  tail  end  ;  the 
Anopheles  breathes  by  means  of  the  whole  surface  of  the  body,  which 
remains  in  a  horizontal  position  just  under  the  water.  It  is  possible  to 
deprive  them  of  air  and  kill  them  by  pouring  on  the  water  petroleum  oil 
or  some  fatty  material. 

The  development  of  the  hsBmatozoon  in  the  Anopheles  is  exogenous  and 
sexual.  The  female  bites  a  malarial  patient  during  the  night,  and  injects 
into  him  some  of  the  poison  which  is  secreted  by  the  salivary  glands,  and 
which  has  the  property  of  preventing  the  coagulation  of  the  blood.  In  this 
manner  it  absorbs  human  blood,  which  contains  the  haematozoon  in  the 
form  of  spherical  bodies  or  of  crescents.  The  spherical  bodies  are  destroyed 
by  the  digestive  juices  of  the  mosquito,  and  the  crescents  alone  survive. 
In  the  digestive  tube  of  the  Anopheles  the  latter  form  ovoid  bodies  of  two 
kinds — one  is  the  male  (microgametocyte),  and  the  other  is  the  female 
(macrogametocyte).     The  male  sends  out  several  flagella,  which  become 


1802  TEXT-BOOK  OF  MEDICINE 

detached,  and  unite,  like  spermatozoa,  with  the  female.  Fertilization  is 
followed  by  the  expulsion  of  a  fertile  egg,  the  zygote,  which  lengthens 
and  becomes  encysted  in  the  muscular  wall  of  the  stomach.  It 
grows,  forming  a  hernia  upon  the  external  wall  of  the  stomach  of  the 
Anopheles  and  becomes  filled  with  numerous  fusiform  bodies,  the 
sporozoites.  These  become  free,  pass  into  the  blood  of  the  mosquito 
and  are  found  in  the  salivary  glands  and  in  their  excretory  ducts.  Ten 
thousand  sporozoites  have  been  counted  in  a  single  Anopheles.  In  human 
blood  they  are  converted  into  spherical  bodies  and  destroy  the  blood- 
corpuscles. 

The  sporozoites  develop  only  at  a  temperature  of  80*^  to  85°  F.,  which 
explains  the  absence  of  malaria  in  northern  countries  and  in  France  during 
the  winter. 

Badly  drained  marshes,  the  mixing  of  sweet  and  salt  waters  (Dutroulau), 
the  great  disturbance  of  soil  in  the  cutting  of  canals  and  in  the  reclamation 
of  ground,  are  favourable  media  for  the  development  of  the  pathogenic 
agent.  The  marshy  soils  formed  by  thin  sheets  of  water  and  mud,  rich  in 
vegetable  matter  and  exposed  to  the  rays  of  the  sun,  are  most  favour- 
able to  the  hatching  of  malaria.  It  also  appears  in  localities  which  are 
not  marshy,  but  on  closer  inspection  we  see  that,  under  the  dry  crust 
of  these  localities,  damp  earth,  which  is  the  origin  of  miasma,  is  found; 
and  we  can  thus  explain  the  appearance  of  malaria  which  broke  out 
in  Paris  during  the  great  disturbance  of  the  soil  in  1811  in  order 
to  cut  the  Saint-Martin  Canal  and  in  1840  for  the  construction  of 
fortifications. 

The  conditions  which  I  have  just  enumerated  are  not,  however,  abso- 
lutely indispensable  to  the  production  of  malaria,  for  it  is  endemic  in 
countries  which  are  composed  of  sandy,  granitic,  or  volcanic  soils. 

Thus,  in  Algeria  malaria  appeared  during  the  reclamation  of  our  colony 
in  a  very  "  dry  and  sterile  country,  where  neither  damp  nor  decomposition 
in  marshes  is  seen."  The  term  palustral  infection,  paludism,  or  palustral 
fever,  which  comes  from  fdus,  a  marsh,  is,  therefore,  not  exact  f  although 
we  preserve  it  from  custom,  it  does  not  apply  to  all  cases. 

Malaria  may  be  caused  by  drinking  marshy  water,  and  the  report  by 
Boudin  on  the  small  epidemic  which  broke  out  on  a  Sardinian  vessel,  the 
Arago,  leaves  no  doubt  on  this  point.  A  first  attack,  instead  of  conferring 
immunity,  is  generally  the  origin  of  later  troubles.  In  a  coimtry  where 
malaria  is  endemic  the  inhabitants,  by  reason  of  their  acclimatization,  are 
little  subject  to  acute  attacks,  though  they  often  suffer  from  malarial 
cachexia,  and  their  children  are  sometimes  cachectic  from  birth.  The 
black  races  enjoy  marked  immunity. 

Malaria,  whUe  very  rare  in  cold  countries,  is  endemic  in  many  warm  and 


INFECTIOUS  DISEASES  PROrER  TO  MAN  1803 

temperate  climates,  and  among  such  I  may  mentiou  Erance  (Uresse  and 
Sologiie),  Italy  (the  Pontino  Marshes  and  the  Roman  Campagna),  Greece, 
the  mouths  of  the  Danube,  Lower  Hungary,  Algeria,  Lower  Egypt,  Senegal, 
Madagascar,  India,  Persia,  ('mliin-CliitiH,  tlu;  fJulf  of  Mexico,  the  Antilles, 
Central  America,  etc. 

In  countries  where  malaria  is  eudeniic,  the  fever  is  most  frequent  and 
most  severe  during  the  summer,  and  the  disease  is  most  severe  in  very  hot 
climates  and  in  tropical  regions.  Malaria  sometimes  assumes  an  epidemic 
form  in  countries  where  it  is  endemic,  and  may  then  extend  to  countries 
which  apparently  offer  conditions  unfavourable  to  its  development.  These 
epidemics  have  often  preceded  those  of  cholera. 

Manifestations  of  Malarial  Fever. — The  manifestations  of  malarial  fever 
are  febrile  and  afebrile.  The  former  have  long  been  included  under  the 
name  of  intermittent  fevers,  and  at  the  present  day  we  are  still  too  prone  to 
employ  this  vicious  sjmonym,  as  though  the  parasite  could  only  cause  inter- 
mittent fever.  In  our  climate,  it  is  true,  intermittent  fever  is  the  most 
general  manifestation  of  malaria ;  but  in  tropical  climates  the  intermittent 
form  becomes  more  rare  and  the  poison  shows  itself  by  remittent  and  con- 
tinuous fevers.  If  we  make  intermittence  the  essential  character  of  malaria, 
we  return  to  the  erroneous  classification  of  Pinel.  In  1828  Annesley  made 
it  known  that  the  same  miasmatic  cause  produces  the  intermittent,  remittent, 
and  continuous  fevers  of  India;  in  1836  Maillot,  in  Algeria,  definitely 
established  the  remittent  and  continuous  types  of  malaria,  and  noted  their 
relation  to  the  intermittent  ones.  "  In  Algeria  we  have  been  able  to 
extricate  the  tertian  and  the  quartan  forms,  to  free  ourselves  from  the 
nosological  prejudice  of  the  type,  and  thus  to  include  them  under  a  wider 
pathology,  which  for  medical  purposes  is  more  correct  and  more  practical. 
In  Algeria  we  have  been  able  to  recognise  defaced  and  mixed  types,  so  that 
our  classical  intermittent  fevers  have  changed  into  continuous  ones,  as  well 
as  to  note  the  error  of  a  pyretology  exclusively  foimded  on  the  consideration 
of  the  type  "  (Trousseau  and  Pidoux). 

Malaria  also  shows  afebrile  forms,  which  we  shall  study  later.  We  shall 
see  that  these  manifestations  are  usually  chronic  and  follow  the  primary 
febrile  attacks. 

The  febrile  and  afebrile  forms  of  malaria  may  appear  alone  or  in  associa- 
tion. They  may  succeed  one  another,  or  may  be  combined  in  different 
cases.  For  purposes  of  description,  I  shaU  divide  them  into  the  following 
groups : 

1.  Intermittent  fevers  of  variable  type. 

2.  Remittent  and  continuous  fevers, 

3.  Pernicious  fevers. 

4.  Malarial  cachexia. 

5.  Larval  fevers. 


1804  TEXT-BOOK  OF  MEDICIXE 


Intermittent  Fevers. 

Description. — Intermittent  fever  is  the  commonest  form  of  malaria.  It 
occurs  in  attacks.  It  is  quite  sufficient  to  liave  stayed  for  a  short  time,  or 
even  to  have  passed  through  a  country,  where  malaria  is  prevalent,  to  sufier 
from  intermittent  fever.  The  period  of  incubation  lasts  six,  eight,  or  ten 
days,  and  rarely  more  than  three  weeks.  In  some  cases  the  attack  of  fever 
appears  suddenly,  but  in  other  cases  it  is  preceded  for  a  few  hours  or  for  a 
day  by  malaise,  chills,  and  gastric  troubles,  which  simulate  febrile  gastritis, 
although  they  are  really  due  to  malaria.  In  some  persons  unusual  lassitude, 
pains  in  the  muscles  or  in  the  joints,  turbid  urine,  and  chills  with  headache, 
which  cannot  be  mistaken,  indicate  that  an  attack  is  about  to  appear. 
Then  the  rigor  occurs. 

In  the  regular  attack  we  ffiid  three  stages — cold,  hot,  and  sweating. 

The  cold  stage— or,  rather,  the  stage  of  the  rigor — ^is  characterised  by 
a  rigor,  accompanied  by  shaking,  which  at  first  affects  the  muscles  of  the 
jaw  (chattering  of  the  teeth),  and  then  the  whole  body,  so  as  to  shake  the 
patient's  bed.  The  sldn  is  dry  and  the  prominent  papillae  give  to  it  the 
appearance  of  goose-flesh.  The  face  and  extremities  are  cold  and  bluish, 
the  restlessness  is  acute,  the  oppression  is  marked,  the  voice  is  weak,  the 
pulse  is  small  and  rapid  and  the  urine  is  scanty  and  watery.  Although 
the  patient  feels  extremely  cold,  the  temperature  in  the  axilla  may  exceed 
104°  F.  during  this  cold  stage. 

The  rigor  is,  however,  only  the  apparent  starting  of  the  attack.  Rise 
of  temperature,  changes  in  the  urine,  and  increase  in  the -quantity  of 
urea  (Jaccoud),  as  well  as  of  the  carbonic  acid  excreted  by  respiration 
— in  short,  an  excess  of  organic  combustion — appear  several  hours 
before  the  rigor.  Chills  alternate  with  hot  flushes  after  a  duration  which 
varies  from  one  to  two  hours.  This  forms  the  commencement  of  the  hot 
stage. 

During  the  hot  stage  the  feeling  of  heat  becomes  gradually  more  severe, 
and  may  be  extremely  painful.  Patients  throw  off  the  bed-clothes,  and 
frequently  change  their  position  in  bed  to  obtain  a  cool  spot.  The  pulse 
becomes  full,  but  remains  rapid.  The  skin  is  dry  and  burning,  and  the 
face  is  injected.  The  respiration  is  quickened ;  delirium  is  sometimes  present ; 
the  thirst  is  acute  ;  and  the  urine  is  high-coloured.  This  stage  usually 
lasts  one  to  two  hours. 

The  sweating  stage  commences  with  moisture  and  a  general  feeling  of 
well-being.  The  sweating  is  abundant ;  the  temperature  falls  rapidly ;  the 
skin  becomes  cool ;  the  pulse  improves,  but  is  stiU  somewhat  full ;  the  urine 
is  thick,  high-coloured,   and   sometimes  contains   albumin.      This  stage, 


INFECTIOUS   DISF.ASKS   ri.'ol'Kr.  TO  MAN"  1805 

which  is  the  lungcsL  ol'  Lho  three,  usually  hists  IVdiu  two  to  four  hours. 
Refreshing  sleep  comos  on  as  soon  as  the  calm  has  reappearj'd.  An  eruption 
of  lierpes  is  sometimes  seen  on  tlie  face. 

Tlie  above  description  represents  a  typical  attack,  hut  the  malady  does 
not  always  show  the  classical  course  above  described.  The  series  is  not 
always  complete.  Some  persons  may  not  shiver,  while  others  perspire  but 
little.  The  attack'  almost  always  commences  between  midnight  and  midday, 
in  contradistinction  to  the  attacks  of  symptomatic  intermittent  fever,  which 
commence  in  the  evening.  The  pains  in  the  left  h3rpochondrium  of  which 
patients  sometimes  complain  arc  due  to  the  swelling  of  the  spleen  which 
accompanies  the  attack.  This  swelling  is  at  first  transient,  but  becomes 
permanent  after  repeated  attacks.  At  the  end  of  the  attack  the  patient, 
except  for  a  certain  lassitude,  feels  well ;  but  if  the  period  of  apyrexia  is 
short,  and  the  attack  is  repeated,  the  patient  feels  ill,  even  during  the 
periods  of  apyrexia,  and  suffers  from  weakness,  which  is  often  accompanied 
by  digestive  troubles. 

I  have  just  described  an  attack  of  intermittent  fever,  such  as  we  see  in 
France,  but  in  different  countries  it  presents  certain  variations  deserving 
of  notice.  Thus,  in  Persia  the  fever  is  often  accompanied  by  vomiting  or 
by  delirium,  and  sometimes  simulates  meningitis,  although  the  prognosis  is 
not  of  much  gravity. 

Types. — The  period  of  apyrexia  determines,  according  to  its  duration, 
a  type  of  the  intermittent  fever. 

Quotidian  fever  is  characterized  by  daUy  attacks. 
Tertian  fever  is  characterized  by  attacks  which  return  every  two  days, 
and  show  a  period  of  apyrexia  for  twenty-four  hours. 

Quartan  fever  is  characterized  by  attacks  which  return  every  third 
day. 

We  also  see  very  rare  types  in  which  the  fever  is  quintan,  sextan, 
septan,  or  oetan. 

The  tertian  and  quotidian  fevers  present  varieties  which  have  been 
called  doubled  and  redoubled  fever. 

The  former  are  more  rare  than  the  latter ;  they  are  characterized  by  two 
attacks  occurring  in  the  same  day.  Both  attacks  come  on  dady  in  double 
quotidian  fever,  every  two  days  in  double  tertian  fever,  and  every  three 
days  in  double  quartan  fever. 

The  latter  forms,  also  called  double  tertian  and  double  quartan,  are 
characterized  by  attacks  which  occur  in  the  following  manner  :  In  the 
double  tertian  form  there  is  an  attack  every  day,  but  the  attack  of  the  next 
day  does  not  resemble  that  of  the  previous  one,  as  in  quotidian  fever,  the 
resemblance  being  confined  to  the  attack  of  two  days  previously — that  is 
to  say,  the  attack  on  the  third  day  resembles  in  its  severity,  duration,  and 


1806  TEXT-BOOK  OF  MEDICINE 

time  of  appearance  the  attack  of  the  first  day,  tlie  attack  of  the  fourth 
day  resembles  that  of  the  second,  and  so  on.  In  doable  quartan  fever 
attacks  occur  every  two  days,  the  attack  on  the  fourth  day  resembling 
that  of  the  first,  and  the  attack  of  the  fifth  day  resembling  that  of  the 
second. 

The  tertian  and  quotidian  fevers  are  the  most  frequent  of  all  these 
types.  In  our  country  we  have  the  tertian  or  the  quotidian  type,  but  the 
fever  is  rarely  quartan  at  its  onset.  The  doubled  and  redoubled  types  are 
never  primary.  The  type  appears  to  depend  upon  the  nature  of  the  miasma 
which  infects  the  particular  locahty. 

In  a  patient  who  is  not  under  treatment  the  attack  of  true  intermittent 
fever  returns  on  a  fixed  day,  and  practically  at  the  same  hour.  If  it  occur 
later,  it  is  said  to  postpone  ;  if  it  occur  earlier,  it  is  said  to  anticipate  ;  and 
if  a  fresh  attack  appear  before  the  end  of  the  preceding  one,  the  fever  is 
subintrant. 

One  type  may  be  converted  into  another.  Thus,  quotidian  fever  becomes 
double  tertian,  then  genuine  tertian,  and,  inversely,  tertian  fever  may  be 
converted  into  quotidian  fever.  The  tertian  type  changes  into  the  quartan, 
especially  in  autumn  (Van  Swieten),  and  the  quartan  fever  may  assume 
the  tertian  type.  The  more  the  fever  differs  from  the  quotidian  type,  the 
more  obstinate  it  is ;  the  quartan  fever  is  specially  rebelHous,  as  the  Latin 
curse  shows  :  Quartana  te  teneat  / 

Course — Diagnosis. — Intermittent  fever  may  recover  without  treatment 
after  a  duration  of  some  weeks,  but  the  first  attack,  whether  treated  or  not, 
is  generally  followed  by  a  series  of  fresh  attacks,  which  come  on  weeks, 
months,  or  even  years  apart,  sometimes  without  appreciable  cause,  and  at 
other  times  as  the  result  of  a  chill,  fatigue,  or  injury  (Vemeuil),  or  as  the 
sequela  of  an  acute  disease.  This  return  of  malaria,  following  some  external 
or  internal  disturbance,  is  highly  important. 

When  the  recurrences  foUow  in  close  succession,  they  usually  appear 
with  such  regularity  that  the  paroxysm,  according  as  the  fever  was  tertian 
or  quartan,  returns  on  the  day  upon  which  it  would  have  been  due  if  the 
succession  of  attacks  had  not  been  interrupted.  After  several  recurrences, 
the  short  rhythms  become  more  frequent,  the  attacks  at  length  lose 
their  regularity,  the  stages  are  less  clear  and  complete,  the  periodicity 
is  less  precise,  and  the  type  loses  its  clearness,  so  that  the  fever  is  said  to 
be  irregular. 

In  some  cases  the  patient,  who  is  wasted  and  ansemic,  is  liable  to  head- 
ache, to  cold  shivers  followed  by  sweating,  and  to  dyspepsia,  and  the  febrUe 
attacks  appear  at  times.  The  spleen  sometimes  becomes  very  large.  The 
liver  is  also  bulky,  the  nutrition  is  faulty,  and  i£  remedial  measures  are 
not  employed,  the  patient  passes  into  the  cachectic  stage. 


,  INFECTIOUS  FUSE  A  RES  PIIOPER  TO  MAN  1807 

Tlie  diagnosis  of  interinitteiit  fever  is  sometiiiie.s  difficult,  and  we  may 
be  unable  to  give  a  correct  opinion  without  having  seen  several  attacks 
unless  the  heomatozoon  has  been  found.  In  countries  where  malaria  is 
endemic,  cases  of  pyrexia  which  are  naturally  continuous — as,  for  example, 
typhoid  fever — sometimes  conmience  with  intermittent  attacks  before 
assiuning  their  proper  type.  We  cannot  say  in  any  case  that  malaria  has 
been  converted  into  typhoid  fever,  but  we  shall  see  later  that  typhoid  fever 
and  malaria  may  run  a  couicident  course,  forming  a  mi.xcd  type — typho- 
malarial  fever. 

We  see  in  marshy  countries  continuous  fevers  which  at  first  simulate 
typhoid  fever,  but  the  fever  soon  becomes  interrupted,  rigors  mark 
the  onset  of  true  attacks,  and  genuine  intermittence  appears.  In  every 
case  in  which  the  diagnosis  between  the  continuous  forms  of  malaria 
and  typhoid  fever  is  difficult  sero-diagnosis  (Widal)  will  remove  all 
doubts. 

The  diagnosis  has  also  to  be  made  from  Kala-Azar,  which  was,  till  1904, 
confused  with  malaria.  Clinically,  the  two  affections  offer  many  points  of 
similarity,  and  the  diagnosis  must  rest  on  the  blood-examination.  The 
parasite  (Piroplasm  of  Leishman-Dono /an)  is  rarely  met  with  in  the 
peripheral  blood,  and  in  blood  taken  from  the  liver  and  from  the  spleen 
the  piroplasm  shows  a  predilection  for  the  polynuclear  leucocytes ;  this 
feature  is  of  much  importance  in  diagnosis.  The  piroplasm  differs  from 
the  haematozoon  in  its  stick-like  centrosome.  In  case  of  doubt,  some  drops 
of  blood  should  be  collected  with  aseptic  precautions  in  a  sterilized  tube, 
and  citrate  of  soda  added ;  after  a  few  days  special  forms  of  piroplasms 
appear  which  resemble  a  trypanosome  without  an  undulating  membrane. 

We  shall  not  confound  symptomatic  intermittent  fevers  (tuberculosis, 
suppuration,  cachexia)  with  malaria.  They  are  associated  with  different 
morbid  states.  Hypertrophy  of  the  spleen  is  absent  and  the  attack  comes 
on  in  the  evening. 

Remittent  and  Continuous  Fevers. 

Remittent  fever  is  a  continuous  fever  in  which  the  paroxysms  are  more 
or  less  marked,  while  the  remissions  never  show  the  complete  apyrexia 
characteristic  of  intermittence.  The  terms  remittent  fever  and  continuous 
fever  might,  therefore,  be  blended.  In  the  remittent  forms,  however,  the 
paroxysms  are  fairly  well  marked,  and  are  sometimes  preceded  by  a  cold 
stage,  while  in  the  continuous  fever  no  periodicity  is  seen. 

The  remittent  forms  may  be  converted  into  intermittent  ones.  The 
fever  is  generally  remittent  from  the  first.  In  some  cases,  however,  the 
remittence  or  the  continuity  is  established  after  the  intermittent  attacks 
have  become  subintrant. 


1808  TEXT-BOOK  OF  MEDICINE  ^ 

Eemittent  fever  has  little  tendency  to  recur  in  its  initial  form.  When 
it  does  so,  it  takes  the  intermittent  type  (CoHn). 

Remittent  fever  is  endemic  in  some  countries  of  Europe  (South  of  France, 
Greece,  Italy,  countries  of  the  Lower  Danube),  but  it  is  chiefly  found  in  hot 
climates  (Algeria,  Senegal,  India,  Cochia-China,  the  Antilles,  centre  of 
America,  etc.).  It  often  appears  in.  an  epidemic  form,  and  may  then  dis- 
appear for  some  years.  In  some  tropical  countries  the  remittent  form  is 
found  at  the  coast,  while  the  intermittent  form  is  present  in  the  interior  or 
upon  the  plateaux.  The  native  or  the  acclimatized  individual  usually  con- 
tracts intermittent  fever,  but  the  new-comer  is  stricken  down  with  the 
remittent  form  (Griesinger).  These  facts  have  been  discovered  in  Rome 
and  Algeria  by  French  physicians,  and  by  English  doctors  in  India,  where 
the  great  epidemics  of  remittent  and  continuous  fever  chiefly  appear  in 
newly-arrived  troops,  while  the  acclimatized  soldiers  suffer  for  the  most  part 
from  the  intermittent  forms. 

The  remittent  and  continuous  fevers  show  several  varieties,  which  are 
briefly  as  follows  : 

Solitary  Remittent  Fever. — An  individual  living  in  a  marshy  country 
is  seized  with  violent  headache ;  fever,  lassitude,  lumbar  pains  like  those  of 
variola,  epistaxis,  prostration,  vertigo,  and  insomnia,  similar  to  that  of 
typhoid  fever,  are  present.  Anorexia,  nausea,  vomiting,  acute  thirst,  and 
dry  tongue  occur,  as  in  gastric  disorders.  The  spleen  is  large  and  painful, 
and  slight  jaundice  is  seen.  The  fever  is  pseudo-continuous,  presenting 
exacerbations,  which  are  sometimes  preceded  by  a  rigor,  and  reaching  as 
high  as  104°  F.  The  disease  lasts  from  eight  to  ten  days.  It  may  then 
terminate  quickly,  with  abundant  sweating,  or  it  may  drag  on  for  a  long 
while  if  quinine  be  not  exhibited.  It  may  also  be  converted  into  the  inter- 
mittent form.  The  above  type  is  that  of  simple  remittent  fever,  unaccom- 
panied by  comphcations. 

Bilious  Remittent  Fevers. — In  other  cases  the  remittent  fever  is  not 
"  solitary,"  but  is  accompanied  by  gastric  or  biliary  symptoms,  which  are 
of  sufficient  importance  to  create  the  gastric  or  the  biliary  types  of  remittent 
fever.  Here,  as  in  all  infectious  diseases,  we  find  every  intermediate 
grade  between  benign  and  fatal  cases.  These  variations  depend  largely 
upon  the  severity  of  the  epidemic  and  upon  the  country  in  which  the 
fever  occurs. 

Indeed,  the  nearer  we  come  to  the  equatorial  zones,  the  more  frequent 
are  bilious  fevers,  such  as  biliary  typhoid  fever,  yellow  fever,  and  biliary 
malarial  fever.  It  has  even  been  asked  if  there  may  not  be  a  climatic 
biliary  fever  independent  of  other  groups.  As  regards  bilious  remittent 
fever,  the  severe  forms  run  the  following  course  : 

An  individual  living  in  a  warm  country  where  malaria  is  prevalent  is  at 


INFECTIOUS  DISEASES  PROPKR  TO  MAX  1800 

first  taken  ill  with  rcmitteul  fever  or  with  intenuittent  attacks,  wliich 
quickly  become  remittent.  The  onset  is  characterized  by  headache,  lassi- 
tude, chills,  and  fever.  A  violent  attack  soon  sets  in,  with  gastric  pain, 
vomiting  of  food  and  of  bile,  vertigo,  nausea,  and  a  feeling  of  faintness. 
The  intolerance  of  the  stomach  may  be  so  great  that  nothing  can  1)0  retained. 
The  tongue  is  coated.  Diarrhoea  is  frequent.  In  some  cases  floods  of  bile 
are  vomited  or  passed  in  the  stools.  The  jaundice  may  be  of  every  degree. 
It  appears  on  the  third  or  fourth  day  of  the  disease,  and  is  bUipheic  and 
hsemapheic,  but  rarely  one  or  the  other.  The  liver  is  enlarged,  and  at  times 
so  painful  as  to  cause  suspicion  of  an  abscess.  The  spleen  is  hypertrophied 
and  very  painful.  The  symptom-complex  of  bilious  remittent  fever,  there- 
fore, comprises  pain  in  the  liver,  in  the  spleen,  in  the  lumbar  region,  in  the 
muscles,  in  the  joints,  and  in  the  stomach. 

The  fever  during  the  course  of  this  trouble  exceeds  104°  F.  The  usual 
remission  is  1°  F.,  and  may  occur  in  the  evening  or  in  the  morning,  while  the 
patient  remains  conscious  of  the  attack  during  the  paroxysms.  Haemor- 
rhages are  frequent  (epistaxis,  purpura,  melaena).  Nervous  troubles,  rest- 
lessness, delirium,  and  ataxo- adynamic  symptoms  are  common.  Coma  is 
somewhat  rare.  The  gastric,  intestinal,  biliary,  hsemorrhagic,  and  nervous 
phenomena  are  much  intermingled  in  difierent  cases. 

When  the  patient  does  not  succumb  in  these  severe  forms,  convalescence 
is  long  and  painful.  It  is  at  times  ushered  in  by  the  change  to  a  remittent 
or  to  an  intermittent  type,  by  the  complete  remission  of  the  fever  or  by 
abundant  sweating,  but  fresh  attacks  are  always  to  be  feared. 

In  other  cases  the  bilious  troubles  are  less  marked,  and  the  chief  symptom 
is  the  continuous  nature  of  the  fever,  with  only  slight  remissions,  with  pre- 
dominance of  ataxo-adynamic  symptoms,  such  as  weakness,  prostration, 
stupor,  delirium,  dryness  of  the  tongue,  distension  of  the  belly  and  foetid 
diarrhoea,  which  recall  the  clinical  picture  of  typhoid  fever. 

Lastly,  in  some  cases  the  typhoid  symptoms  and  the  bilious  symptoms 
may  be  intermixed. 

The  severe  forms  of  remittent  fever  present,  therefore,  the  most  different 
aspects.  Sometimes  the  typhoid  state  is  marked  from  the  first,  and  the 
remissions  are  irregular,  though  appreciable,  for  some  days.  If  at  a  later 
stage  they  are  no  longer  seen,  the  prognosis  is  grave,  and  in  this  case  adynamia 
sets  in  early.  In  other  cases  we  see  multiple  haemorrhages  from  the  nose  or 
from  the  kidneys,  and  in  the  skin,  forming  the  haematuric  type  common  in 
Senegal  and  the  Antilles.  In  some  instances  the  chief  feature  of  the  disease 
comprises  symptoms  of  jaundice,  dysentery,  or  of  cholera.  We  may  also 
see  purulent  collections  in  the  serous  membranes,  abscesses  of  the  liver, 
oedema  followed  by  coagulation  in  the  veins,  and  gangrene  of  the  extremities. 
These  terrible  forms  often  result  in  death. 


1810  TEXT-BOOK  OF  MEDICINE 

Typho-Malarial  Fever. — I  have  said  that  malaria  in  many  cases  resembles 
t5!^hoid  fever  by  reason  of  the  continuity  of  the  apyrexia  and  of  the  nature 
of  the  symptoms,  so  that  the  diagnosis  is  at  times  very  difficult.  In  other 
cases  there  is  genuine  association  of  tjrphoid  and  of  malarial  infection.  This 
form  develops  in  centres  where  malaria  and  typhoid  fever  are  endemic. 
It  is  rare  ia  France,  though  common  in  Algeria  and  in.  many  other  countries. 
Typhoid  fever  sometimes  appears  in  a  patient  who  already  has  malaria,  and 
the  two  diseases  run  a  parallel  course  without  afiecting  one  another ;  but 
at  other  times  the  two  diseases  appear  at  the  same  moment  in  the  same 
individual,  forming  the  typho -malarial  type.  In  the  latter  case  each  of  the 
diseases  runs  its  own  course,  and  a  special  symptomatology,  depending  on 
the  preponderance  of  one  of  these  two  maladies,  is  seen  in  the  course  of  the 
disease. 

Patients  suffering  from  typho-malarial  fever  present  during  life  or  post 
mortem  the  changes  special  to  the  two  diseases.  Accordingly,  in  typhoid 
fever  we  find  hypertrophy  and  ulceration  of  Peyer's  patches,  and  in 
malaria  we  find  melanic  pigment  in  the  blood  and  in  the  tissues,  but  I  should 
like  to  know  if  these  patients  show  at  the  same  time  E  berth's  baciUus  and 
Laveran's  haematozoon.  Sero-diagnosis  will  render  great  service  in  the 
case  of  so-called  typho-malarial  fever  (Widal)  by  defining  the  extent  of  the 
typhoid  infection. 

Hsemoglobinurie  Fever. — Malarial  fevers  are  often  accompanied  by 
multiple  haemorrhages.  Purpura,  ecchymoses,  and  nasal,  buccal,  or  intes- 
tinal haemorrhage  are  seen  both  in  the  bUious  and  non-bUious  forms  of 
remittent  fever.  The  biUous  condition  is  not  absolutely  associated  with 
haemorrhages.  Thus,  in  the  Antilles,  Carvajal  saw  cases  where  patients 
suffering  from  acute  malaria,  with  haemorrhages  from  the  mucous  mem- 
branes of  the  eyes,  mouth,  or  nose,  and  haemorrhages  into  the  sjkin  from 
the  intestines  or  from  the  kidneys,  showed  no  jaundice,  just  as  occurs  in 
some  cases  of  infectious  purpura. 

Side  by  side  with  these  cases,  however,  in  which  multiple  haemorrhages  are 
or  are  not  associated  with  bilious  fevers,  there  are  others  in  which  haematuria 
alone  is  seen.  This  form,  formerly  called  haematuric  fever,  should  be  called 
hsemoglobinurie  bilious  fever,  because  we  find  haemoglobin,  and  not  blood, 
in  the  urine.  This  disease  (Corre)  is  especially  frequent  in  tropical  countries, 
but  it  has  also  been  seen  in  the  Mediterranean  regions,  in  Greece  and  Algeria, 
as  the  following  example  shows  : 

A  man  suffers  from  quotidian  or  tertian  attacks,  or  from  remittent  fever, 
which  implies  a  gravity  usually  absent  in  the  intermittent  form.  In  the 
case  of  intermittent  attacks  the  cold  stage  is  accompanied  by  lumbar  pains, 
gastric  distress,  vomiting  of  bile,  and  dyspnoea,  which  becomes  still  more 
marked  during  the  hot  stage.     The  haemoglobinuria  appears  before  or  with 


INFECTIOUS  DISEASES  PROPER  TO  MAN  1811 

the  chill,  increases  gradually  during  the  attack,  and  ends  with  the 
stage  of  apyrexia.  The  urine,  which  during'  the  attack  assumes  in 
succession  the  tint  of  claret,  sherry,  and  brown  beer,  beoonuis  ck;ur 
after  the  attack. 

The  bilious  symptoms  commence  with  the  attack,  and  the  vomiting  of 
bile  is  often  accompanied  by  bilious  stools.  The  jaundice  appears  so  rapidly 
that  the  skin  is  of  a  saffron  colour  in  the  hot  stage.  The  bilious  attack, 
which  is  very  marked  in  the  first  attack  of  haemoglobinuria,  often  becomes 
less  severe  during  the  following  attacks.  Haemoglobinuria  may  appear 
daily  or  every  two  days.  The  jaundice  does  not  disappear  between  the 
attacks.  The  spleen  is  enlarged,  and  the  patient  is  very  anaemic  ;  but  in 
spite  of  its  apparent  gravity,  the  form  just  described  usually  results  in 
recovery. 

Haemoglobinuric  bilious  fever  is  more  severe  if  the  hot  stage  is  prolonged, 
if  the  attacks  are  subintrant — in  short,  if  the  fever  is  remittent  or  continuous. 
The  vomiting  is  then  more  frequent,  the  jaundice  is  more  severe,  the  urine 
is  black,  the  tongue  becomes  dry,  the  eyes  sink  in,  hiccough  appears,  and 
the  patient  dies,  sometimes  from  weakness ;  at  other  times  from  anuria 
and  uraemia.  Fulminant  forms  are  also  seen ;  they  carry  the  patient  ofi  in 
three  or  four  days  (Leroy  de  Mericourt). 

In  these  bilious  forms  the  urine  presents  the  following  characters  :  Very 
abundant  sediment,  with  epithelial  cells,  hyaline  casts,  white  corpuscles, 
few  or  no  red  corpuscles,  and  abundant  haemoglobin,  which  can  be  recog- 
nized with  the  spectroscope.  The  colour  of  the  urine  is  due  to  urobilin, 
to  the  chromogenes,  to  the  bile-pigments,  and  to  the  haemoglobin.  As 
regards  the  pathogenesis  of  haemoglobinuria,  the  reader  will  find  it  discussed 
under  Paroxysmal  Haemoglobinuria. 


Pernicious  Fevers. 

The  malarial  fevers  are  called  pernicious  when  they  cause  such  dis- 
turbance of  the  economy  as  to  endanger  in  a  few  days  or  in  a  few  hours 
the  patient's  life.  In  some  cases  the  pernicious  forms  show  themselves  by 
exaggeration  of  an  ordinary  symptom  (algid  or  sweating  fever),  but  at 
other  times  they  are  associated  with  complications  which  affect  certain 
systems  or  organs.  In  this  case  the  fevers  are  called  "  accompanied,"  or 
comitatcB. 

The  imminence  of  the  danger,  however,  does  not  depend  so  much  on 
the  importance  of  the  organ  infected  as  on  the  nature  and  the  viru- 
lence of  the  infective  element,  which  causes  a  '•  true,  primary,  protopathic. 


1812  TEXT-BOOK  OF  MEDICINE 

malignant  cliaracter,  wMch  in  most  cases  is  apparent  from  the  first " 
(Trousseau). 

The  pernicious  forms  are  more  frequent  in  tropical  regions.  We  may- 
see  them  in  some  departments  of  France,  but  hardly  ever  in  Paris.  Their 
development  is  notably  influenced  by  seasons.  In  Rome  they  are  more 
frequent  between  July  and  October  (BacceHi),  and  at  Senegal  they  chiefly 
appear  at  the  end  of  the  rainy  season,  from  August  to  November.  They 
nearly  always  appear  in  an  epidemic  form.  If  an  individual  leaves  a 
country  in  which  malaria  is  prevalent,  he  does  not  avoid  thereby  the  return 
of  symptoms  of  malaria  contracted  in  the  country,  but  he  does  avoid  per- 
nicious attacks.  Negroes  are  less  susceptible  than  white  men.  Youth 
confers  no  immunity,  and  children  are  more  liable  than  adults  to  the  per- 
nicious forms. 

Cerebro-Spinal  Pevers. — Coma,  delirium,  convulsions,  and  paralyses 
are  the  troubles  seen  in  this  group.  The  comatose  form  is  the  most  frequent 
and  the  best  known  of  these  varieties. 

The  coma  comes  on  during  an  attack  of  intermittent  or  of  remittent 
fever,  though  in  some  cases  it  seems  to  be  established  at  once,  and  com- 
prises the  whole  attack.  In  the  slight  form  it  is  said  that  the  attack  is 
accompanied  by  somnolence,  so  that  the  patient  appears  to  be  under  the 
influence  of  opium.  In  severe  cases  the  attack  is  said  to  be  apoplectiform. 
The  attack  of  coma  is  characterized  by  loss  of  consciousness  and  of  sensa- 
tion, with  involuntary  evacuations,  immobility  of  the  pupil,  and  relaxation 
of  limbs.  The  attack  lasts  about  a  day.  It  sometimes  disappears  rapidly, 
without  leaving  traces ;  in  other  cases  it  is  accompanied  by  hemiplegia, 
monoplegia,  and  amaurosis,  and  we  find  post  mortem  congestion  and 
haemorrhage  in  the  cerebro-spiaal  meninges. 

The  convulsive  form  simulates  at  times  epilepsy,  and  at  other  times 
tetanus. 

These  different  cerebro-spinal  forms  may  be  combiaed.  The  diagnosis 
is  simple  when  the  symptoms  appear  in  a  patient  who  is  known  to  be  malarial, 
but  when  a  man  suflering  from  contractions  simulating  tetanus,  from  con- 
vulsions like  those  of  epilepsy,  from  delirium  simulating  delirium  tremens, 
or  from  coma  which  resembles  apoplexy,  insolation,  or  sunstroke,  is  admitted 
to  hospital,  the  diagnosis  is  sometimes  difficult,  the  more  so  as  the  attack 
may  be  larval,  while  fever  is  absent,  or  appears  only  later.  A  prompt 
diagnosis  can  alone  be  made  by  the  discovery  of  the  parasite  in  the  blood. 

Algid  Fevers. — Under  this  term  Kelsch  includes  pernicious  forms 
characterized  by  cyanotic  colour  and  icy  coldness  of  the  body,  and  we  may 
note  the  following  forms :  choleraic,  cardialgic,  dysenteric,  diaphoretic, 
algid,  and  syncopal. 

The  algid  form,  which  is  the  gravest  of  all,  does  not  consist  in  exaggera- 


INFECTIOUS   DISEASES  PROl'MR  TO  MAN  1813 

tidu  uf  the  cold  stage,  as  might  be  supposed,  fur  tln'  cliilliug  ol'  Ihe  body 
takes  j)l;U'C  and  becomes  accontuated  diiriu<;  the  hot  stage,  or  even  during 
the  sweating  stage.  The  patient  does  not  shiver,  but  the  skin  becomes 
livid  and  ice-cold,  the  voice  sinks  to  a  whisper,  cold  clammy  sweat  breaks 
out,  the  distress  is  terrible,  the  dysjmoea  is  extreme,  the  expired  air  is  cold, 
the  pulse  is  small  and  frequent,  and  the  face  assumes  a  death-like  expres- 
sion—carfavem  imaginem  refert  (Borstieri).  This  chilling  of  the  body 
may  end  in  death,  or  may  be  followed  by  healthy  reaction.  Tn  this  form 
we  also  see  cholera-like  symptoms,  which  may  give  rise  to  the  choleraic  form 
of  the  disease.  The  s}Tnptoms  comprise  vomiting  and  imcontrolialjle 
diarrh(ca,  with  cramps  and  suppression  of  urine,  as  in  the  algid  stage  of 
cholera. 

In  the  diaphoretic  form,  which  is  not  so  serious  as  the  algid  form,  the 
sweating  stage  brings  the  patient  no  relief,  as  it  does  in  true  intermittent 
fever.  On  the  contrary,  the  distress  increases,  the  body  and  face  arc 
bathed  in  cold  sweat,  the  algid  condition  makes  rapid  progress,  and  the 
patient  falls  into  a  state  of  collapse. 

These  various  forms  are  not  always  isolated,  and  we  may  see  them  in 
association  in  the  same  subject,  with  predominance  of  algid,  sudoral,  or  of 
choleraic  phenomena. 

In  dysenteriform  fever  the  troubles  become  so  intense  as  to  end  in 
collapse  and  the  algid  condition. 

In  the  syncopal  form  the  patient  remains  for  a  long  while  in  a  state  ol 
apparent  death. 

The  cardialgic  form  is  characterized  by  acute  pains  in  the  epigastrium 
(cardiac  region),  with  a  sensation  of  burning  or  of  tearing,  and  with  vomiting 
of  bile  or  of  blood.  This  form  is  often  an  exaggeration  of  the  gastric  re- 
mittent form.  In  very  grave  cases  it  ends  in  syncope  or  in  the  algid  con- 
dition. 

Pernicious  fever  may  also  assume  other  forms.  The  peripneumonic 
form  is  characterized  by  pulmonary  symptoms,  the  breathing  is  laboured 
and  difficult  as  in  sufiocative  catarrh,  the  expectoration  is  mucous  and 
blood-stained,  and  subcrepitant  rales  are  audible  over  the  whole  chest. 

The  pleuritic  form  is  characterized  by  sharp  pain  in  the  side,  with 
painful  and  jerky  breathing  and  more  or  less  considerable  effusion,  which 
is  usually  absorbed  after  the  attack. 

The  pernicious  fevers  show  some  differences,  according  to  their  type. 

Torti  and  Morton,  who  saw,  on  the  one  hand,  a  case  in  the  North  of 
Italy,  and,  on  the  other,  a  case  in  England,  said  that  the  pernicious  attack 
assumes  the  tertian  type,  and  their  assertion  remains  in  part  true  as  regards 
temperate  climates,  but  not  as  regards  hot  countries  (Algeria),  and  especially 
as  regards  tropical  regions  (India,  Senegal),  where  the  pernicious  fevers 
U.  115 


1814  TEXT-BOOK  OF  MEDICINE 

chiefly  assume  the  remittent  and  the  continuous  type.  We  may  even  see 
in  some  European  climates  (Roman  Campagna,  Greece,  Corsica,  etc.)  that 
the  pernicious  form  changes  from  the  periodic  type  to  the  continuous  type 
(Colin). 

As  a  general  rule,  in  the  Mediterranean  pernicious  symptoms  do  not 
appear,  except  after  a  certain  number  of  previous  intermittent  or  remittent 
attacks ;  but  in  some  countries  where  malaria  occurs  in  a  severe  epidemic 
form,  such  as  India,  Senegal,  Tonkin,  etc.,  the  symptoms  may  be  pernicious 
from  the  first.  It  is  very  rare  that  pernicious  fever  is  fatal  during  its 
invasion.  As  the  pernicious  fevers  are  anomalous  ia  nature  and  do  not 
show  the  regularity  of  the  intermittent  fevers,  as  the  paroxysms  often 
anticipate  or  are  subintrant,  and  as  the  pernicious  form  often  changes  from 
the  periodic  to  the  continuous  type,  the  delirium,  algidity,  and  coma  some- 
times last  more  than  a  day  without  any  possibility  of  noting  either  a  remis- 
sion or  a  periodic  type.  The  fever  sometimes  remains  in  abeyance.  We 
should  be  quite  wrong  if  we  took  the  periodicity  as  a  guide  in  cases  which 
demand  special  attention  and  prompt  intervention. 

In  some  instances,  the  pernicious  fever  runs  a  quasi-fulminant  course. 
When  Dr.  Poncy  directed  the  health-service  among  the  railroad  employes 
in  the  Amazon  region,  he  saw  appalling  forms  of  malarial  infection.  A 
workman  would  be  suddenly  taken  ill  with  shivering,  hot-stage,  delirium 
and  a  kind  of  ambulatory  mania.  He  would  rush  into  the  forest  near  the 
construction-track,  and,  when  found  two  or  three  hours  later,  he  had  either 
fallen  to  the  ground  or  was  clutching  the  trunk  of  a  tree  in  a  state  of 
tetanus.  Death  from  coma  followed  in  a  few  hours,  unless  intra-muscu- 
lar  injections  of  15  to  30  grains  of  hydrochlorate  of  quinine  were  at  once 
given,  without  counting  whether  the  temperature  were  96°  or  106°  E. 

It  is  often  difl&cult  to  appreciate  the  shades  which  indicate  that  a  re- 
mittent or  intermittent  fever  wUl  become  pernicious.  During  an  epidemic 
we  must  be  warned  by  the  abnormal  symptoms  and  the  nervous  troubles 
which  appear  during  the  period  of  remission. 

The  diagnosis  of  malarial  fever  is  often  very  difficult,  especially  in  warm 
climates,  where  malaria,  by  reason  of  its  multiple  aspects,  so  closely  simu- 
lates other  diseases  (bUiary  typhoid  fever,  yellow  fever,  cholera,  dysentery, 
and  sunstroke).  In  cases  of  doubt,  we  always  commence  with  the  ad- 
ministration of  quiuuie,  but  this  means  is  often  iasufficient  to  clear  up  the 
diagnosis.  The  only  real  control  measure  is  the  examination  of  the  blood, 
and  the  discovery  of  the  parasite  wiU,  save  in  very  exceptional  cases,  remove 
all  doubts. 


INFI-X'TIOUS   I>[S5KASKS  PROrER  To  MAN  181.'. 

Chronic  Malaria— Anaemia  and  Cachexia. 

Patients  who  have  had  intermittent  or  remittent  fever  often  suffer  from 
organic  troubles,  which  are  more  marked  in  proportion  as  the  attacks  have 
been  severe  or  often  repeated.  The  anaemia  is  early,  and  this  is  not  sut 
prising  when  we  remember  that  a  single  attack  causes  a  loss  of  several 
hundreds  of  thousands  of  red  blood-corpuscles  per  cubic  millimetre  (Kelsch). 
The  skin  assumes  an  earthy  tint,  and  the  patient  wastes  and  complains  of 
prostration,  headache  and  palpitation. 

The  spleen  is  enlarged.  When  the  hypertrophy  is  slight,  the  organ  is 
not  palpable,  and  does  not  extend  beyond  the  edge  of  the  ribs.  On  per- 
cussion, we  find  that  its  vertical  diameter  remains  parallel  with  the  edge 
of  the  false  ribs.  WTien  the  hypertrophy  is  considerable,  the  spleen  forms 
an  enormous  tumour  parallel  with  the  middle  line,  invades  the  left  hypo- 
chondrium  and  the  neighbouring  regions,  and  becomes  movable  if  the 
phrenico-splenic  ligament  is  elongated  or  torn.  The  hypertrophied  spleen 
often  gives  rise  to  a  feeling  of  weight.  An  old-standing  tumour  of  the 
spleen  is,  however,  by  no  means  incompatible  with  satisfactory  health. 

The  liver  shows  similar  swelling  to  that  of  the  spleen,  but  the  hepatic 
lesions  are  more  rare,  and  appear  less  slowly.  I  am  speaking  of  what 
occurs  in  France,  for  the  first  attack  in  hot  climates  often  causes  acute 
swelling  of  the  liver.  The  hj-pertrophy  of  the  liver,  though  genenil,  chiefly 
affects  the  surface  of  the  organ  (ague-cake).  In  some  cases  the  hepatic  and 
splenic  tumours  unite,  and  invade  a  part  of  the  abdominal  cavity. 

Chronic  malaria  may  cause  lesions  in  the  lungs  and  bronchi.  The  cases 
published  on  this  point  are  conclusive  (Frerichs,  Lancereaux,  Grasset). 
Chronic  bronchitis  and  pulmonary  fibrosis  of  malarial  origin  may  either 
commence  with  acute  attacks  or  may  be  chronic  from  the  first. 

Among  the  pulmonary  manifestations,  says  De  Brun,  we  see  a  form  of 
chronic  congestion,  localized  to  one  or  both  apices  of  the  lung,  and  showing 
itself  by  dullness,  increase  of  tactile  vocal  fremitus,  tubular  breathing,  and 
exaggerated  voice-sounds.  This  congestion  is  rarely  accompanied  by  rales. 
It  generally  yields  to  prolonged  treatment  with  sulphate  of  quinine.  As  it 
most  often  coexists  with  febrile  cachexia,  we  may  readily  confound  it  with 
tubercular  induration  of  the  lung  (De  Bnm). 

Retinal  haemorrhages  have  been  seen  in  chronic  malaria,  as  well  as 
after  acute  attacks.  They  lead  to  ocular  troubles,  which  may  recur  and 
persist  for  several  months. 

The  symptoms  of  malarial  anaemia  end  in  confirmed  cachexia  in  persons 
who  have  been  hard  hit  by  the  infection  and  in  those  who  live  under  bad 
hygienic  conditions.  The  colour  is  dark,  the  skin  is  dry,  and  the  wasting 
contrasts  with  the  size  of  the  abdomen,  due  to  the  enlargement  of  the  liver 

115—2 


1816  TEXT-BOOK  OF  MEDICINE 

and  of  the  spleen.  (Edema,  ascites,  albuminuria,  diarrhoea,  epistaxis, 
ulcers  on  the  legs,  and  amenorrhosa  are  often  noticed.  This  cachectic 
stage,  sometimes  interrupted  by  irregular  paroxysms,  may  end  in  recovery, 
but  more  often  terminates  fataUy  (hectic  fever,  tuberculosis,  chronic  hepa- 
titis, chronic  nephritis,  pneumonia). 

In  some  malarial  countries  a  large  number  of  the  inhabitants  bear  the 
stamp  of  anaemia  and  cachexia  due  to  malarial  infection,  although  they 
have  never  had  intermittent  or  remittent  attacks.  The  cachexia  is  estab- 
lished from  the  first,  like  a  chronic  intoxication.  W?  may  even  see  new- 
bom  children  with  enlargement  of  the  spleen  and  the  liver,  and  with  a 
cachectic  colour  of  the  skin.  Fractures  unite  badly,  and  the  formation  of 
callus  is  often  retarded  (Verneuil)  in  persons  who  have  sufiered  from  malaria. 

The  prognosis  in  malarial  cachexia  is  very  grave,  because  the  cachexia 
is  the  result  of  all  the  manifestations  of  malarial  infection,  and  survives  the 
endemo -epidemic  recrudescences  of  malaria. 

Larval  Malaria. 

A  larval  disease  is  one  which  assumes  the  appearance  {induit  larvam) 
of  another  disease  with  which  it  has  little  or  no  analogy.  Malarial  infection 
is  larval  when  it  assumes  the  form  of  neuralgia,  of  a  flux  or  of  a  neurosis. 
In  these  larval  forms  fever  is  completely  absent,  or  is  confined  to  slight 
symptoms.  The  febrile  element  is  secondary  and  accessory,  and  the 
neuralgic  or  digestive  element  predominates. 

These  larval  fevers,  as  a  rule,  aflect*  the  fifth  pair  of  nerves.  The 
neuralgia  is  usually  ap}rretic.  It  may  appear  at  indefinite  times,  and  affect 
a  pseudo-continuous  type.  The  pains  sometimes  return  at  the  fixed  time, 
just  as  the  symptoms  which  comprise  the  complex  of  facial  neuralgia : 
injection  of  the  conjunctivae,  abundant  secretion  of  tears,  etc.  The 
paroxysms  generally  occur  in  the  morning,  and  the  attacks  may  assume 
the  quotidian,  tertian,  or  quartan  type. 

We  also  see  neuralgia  affecting  the  occipital,  intercostal,  and  sciatic 
nerves,  and  certain  neuralgias  of  the  breast,  stomach,  intestines  and  heart 
are  really  larval  fevers. 

The  larval  fever  is  represented  in  some  cases  by  congestion  or  by  haemor- 
rhages. In  this  class  we  may  place  coryza,  tonsillitis,  cutaneous  hyperaemia, 
urticaria,  partial  or  extensive  oedema,  intermittent  diarrhoea,  arthralgic 
pains,  epistaxis,  purpura,  and  perhaps  the  reawakening  of  the  rheumatic 
diathesis. 

Among  the  neuroses  seen  in  these  forms  of  larval  fevers  I  may  quote 
spasmodic  cough,  pseudo-asthmatic  dyspnoea,  migraine,  and  hiccough. 

All  these  larval  manifestations  have  certain  characters  ui  common. 
They  may  present  a  certain  periodicity.     The  individuals  whom  they  attack 


INFECTIOUS  DISKASKS  rUOPKR  TO  MAX  1817 

have  dwelt  in  a  malarial  country,  and  present  more  or  less  considerable 
enlarf];ement  of  the  spleen,  and  have  very  often  sulTcred  from  attacks  of 
malaria.  These  various  considerations  assist  in  the  diagnosis  of  the  larval 
fevers. 

Many  pernicious  fevers  might  be  considered  as  larval,  but  the  febrile 
element  usually  accpiires  a  severity  not  found  in  the  forms  just  examined. 
They  are  really  pseudo-larval. 

Pathological  Anatomy. — Let  us  first  study  the  lesions  of  acute  malaria, 
and  the  changes  present  in  the  blood  during  life.  The  number  of  red  cor- 
puscles diminishes  by  from  100,000  to  1,000,000  per  cubic  millimetre  in 
twenty-four  hours  as  the  result  of  the  attacks  of  fever.  This  diminution  is 
proportionate  to  the  severity  of  the  attack,  and  explains  the  rapid  anaemia. 
And  yet,  when  speaking  of  the  intensity  of  the  attack,  I  do  not  allude 
merely  to  the  severity  of  the  fever,  but  to  the  morbid  process  as  a  whole, 
for  some  pernicious  attacks  destroy  an  enormous  quantity  of  red  blood- 
corpuscles,  although  the  fever  is  not  high. 

The  red  corpuscles  are  deformed,  and  during  the  period  of  apyrexia 
many  hsematoblasts  (Hayem)  are  found.  The  white  corpuscles  increase  in 
number,  and  become  three  or  four  times  as  numerous  as  in  the  normal 
condition. 

The  quantity  of  pigment  found  in  the  blood  (melanaemia)  is  in  direct 
proportion  to  the  severity  of  the  disease.  The  melansemia  is  not  continuous. 
Kelsch  has  shown  that  it  is  intermittent,  and  intimately  associated  with 
the  attacks.  The  melansemia  appears  during  the  attack,  especially  at  the 
time  of  the  paroxysm.  The  pigment  is  very  abundant  in  the  case  of  severe 
or  of  pernicious  fever.  If  the  attacks  are  trifling,  and  occur  at  sufficiently 
long  intervals,  the  pigment  may  entirely  disappear  between  two  attacks, 
and  even  when  the  attacks  are  severe  and  repeated  the  melanaemia  does  not 
persist  for  more  than  five  or  six  days  after  the  last  attack.  Melanaemia  is 
absent  when  the  malarial  cachexia  is  not  interrupted  by  acute  attacks. 

The  melanic  pigment  is  present  in  the  form  of  grains  or  irregular  masses, 
measuring  at  most  1  /z  in  diameter,  and  collected  into  small  blackish  masses, 
which  may  be  free  or  enclosed  in  the  white  corpuscles.  The  pigment  arises 
from  the  destruction  of  the  red  corpuscles,  due  to  the  parasite  which  lives 
upon  them.  The  black  pigment  which  accumulates  in  the  haematozoon 
results  from  the  digestion  of  the  haemoglobin.  This  melanaemia  is  charac- 
teristic of  malaria,  and  is  reproduced  in  no  other  disease. 

Melanaemia  induces  melanosis.  The  melanic  pigment  blocks  the  capil- 
laries and  infiltrates  the  organs.  In  some  cases  the  pigment  is  not  solely 
intravascular,  but  penetrates  the  cells  of  the  organ,  giving  them  a  slaty  or 
a  brownish  colour.  This  phenomenon  is  seen  in  the  spleen,  in  the  bone- 
marrow,  and  later  in  the  liver.     In  other  organs  (brain,  kidneys,  lungs, 


1818  TEXT-BOOK  OF  MEDICINE 

muscles)  the  pigment  remains  intravascular,  and  does  not  enter  tlie  cells 
(KelscK). 

Kelsch  and  Kiener  have  been  very  careful  not  to  confound  the  melanic 
pigment  with  an  ochre  pigment,  which  is  not  found  in  the  blood,  but  infil- 
trates the  cells  of  the  liver,  the  kidney,  the  spleen,  the  spinal  cord,  and  the 
bones,  where  it  may  cause  trophic  troubles. 

If  the  patient  has  died  from  acute  malaria  or  from  pernicious  fever,  the 
spleen  is  enlarged,  and  its  weight  may  reach  30  to  40  ounces.  It  is  pig- 
mented, and  softened  to  the  point  of  diffluence.  Rupture  of  the  organ  is 
extremely  rare.  The  liver  shows  inflammatory  hypersemia.  The  capUlary 
networks  are  blocked  by  melaniferous  cells  and  pigment,  and  the  hepatic 
cells  are  cloudy.  The  biliary  vessels  are  intact,  but  the  bile  is  thick  and 
abundant.  The  meninges  are  congested,  and  the  convolutions  of  the  brain 
are  of  a  characteristic  slate  colour.  It  might  be  said  that  the  capillaries 
have  been  injected  with  black  material.  The  kidneys,  even  in  the  absence 
of  haemoglobinuria,  show  constant  lesions.  The  tubules  are  blocked  with 
casts,  mixed  with  pigmented  granules.  In  the  lungs  pigmented  granu- 
lations are  found  in  the  interior  of  the  vessels  and  in  the  blood  of  the 
alveoli. 

In  short,  the  lesions  of  acute  malaria  are  characterized  by  the  presence 
of  a  melanic  pigment  in  the  blood,  in  the  capillary  network,  where  it  forms 
emboli,  in  the  parenchyma  of  the  spleen  and  of  the  bones,  where  the  altered 
red  corpuscles  are  destroyed. 

The  lesions  of  chronic  malaria  must  next  occupy  our  attention.  The 
presence  of  the  parasites  causes  a  congestive  and  irritative  process,  which 
shows  itself  by  inflammatory  lesions,  especially  well  marked  in  the  organs 
where  the  parasite  dwells  (Laveran). 

The  spleen  is  enlarged,  and  at  times  enormous,  hard,  and  cirrhosed. 
On  section,  it  is  pigmented,  slaty- coloured,  and  blackish,  and  presents 
fibrous  bands  of  connective  tissue.  It  is  sometimes  affected  by  amyloid 
degeneration. 

The  changes  in  the  liver  occur  later  than  those  in  the  spleen.  The  organ 
is  enlarged,  pigmented,  and  indurated.  The  hypertrophy  chiefly  affects  the 
surface,  and  gives  the  organ  a  flattened  form..  The  melanic  pigment  ob- 
structs the  capillaries  of  the  portal  vein,  and  finally  enters  the  hepatic  cells, 
especially  at  the  periphery  of  the  acinus.  Amyloid  degeneration  is  rare. 
On  section,  the  parenchyma  is  sometimes  mammillated,  as  the  result  of 
parenchymatous  hepatitis,  with  hypertrophy  and  hyperplasia  of  the  hepatic 
cells.  The  nodular  form  of  parenchymatous  hepatitis,  with  large  adeno- 
matous areas,  has  been  carefully  studied  by  Kelsch  and  Kiener.  These 
lesions  are  associated  with  cirrhotic  changes. 

The  kidneys  show  multiple  lesions — ^fibrous  changes  in  the  glomeruli. 


INFF.CTIOUS  DISEASES  PROPER  TO  MAN  1819 

fatty  condition  of  the  epitheliiuu,  colloid  degeneration,  and  pigmentation 
of  the  organ. 

The  lungs  })resent  the  lesions  of  chronic  interstitial  pneumonia,  with  or 
without  dilatation  of  the  bronchi. 

Treatment. — The  organism  may  struggle  against  the  parasites  by  reason 
of  phagocytosis,  and  recovery  may  occur  in  mild  cases  without  any  treat- 
ment, but  thoy  arc  the  exception.  In  most  cases  it  is  necessary  to  prescribe 
quinine,  which  is  the  specific  drug  for  malaria. 

"  It  is  possible  to  prove  directly  the  action  of  quinine  salts  upon  the 
parasites  by  mixing  a  drop  of  blood  which  contains  them  with  a  drop  of  a 
weak  solution  of  sulphate  of  quinine.  The  movements  of  the  pigmented 
granules,  and  also  those  of  the  mobile  threads,  rapidly  disappear,  and  we 
see  only  the  dead  parasites  "  (Laveran). 

Cinchona  and  quinine  are  the  drugs  in  malaria.  An  individual  is  suffer- 
ing from  tertian  or  from  quotidian  fever.  Upon  what  lines  are  we  to 
proceed  ?  A  purgative  is  ordered,  and  then  sulphate  of  quinine  is  adminis- 
tered in  a  dose  of  10  to  15  grains.  The  quinine  shoidd  be  divided  into  two 
doses,  one  being  given  as  far  as  possible  from  the  coming  attack,  and  the 
other  being  given  four  or  five  hours  before  the  supposed  return  of  the  attack. 
The  quinine  should  be  continued  for  a  week,  when  it  may  be  suspended,  to 
be  again  given  if  the  attacks  of  fever  reappear. 

The  same  treatment  is  applicable  in  remittent  fever.  Since  the  remittent 
form  is  nearly  always  accompanied  by  gastric  or  bilious  symptoms,  an 
emetic  is  prescribed,  and  quinine  is  then  given  in  doses  of  10  to  15  grains 
daily,  choosing  as  far  as  possible  the  moment  of  remission. 

In  severe  and  pernicious  fever,  as  there  is  no  time  to  be  lost,  and  as  the 
attacks  are  often  subintiant,  large  doses  of  quinine  (30  to  40  grains)  are 
given  during  the  attack,  either  by  the  mouth  or  by  subcutaneous  injections 
of  the  following  solution  : 

Distilled  water        . .  . .  . .  . .  . .     18  parts. 

Alcohol     . .  . .  . .  . .  . .  . .       4     „ 

Hydrobromate  of  quinine      . .  . .  . .  . .       2     „ 

Care  must  be  taken  to  make  the  injection  deeply  into  a  region  rich  in 
cellular  tissue,  and  strict  asepsis  must  be  observed. 

By  this  means  it  does  not  matter  if  the  patient  is  comatose  or  delirious. 
We  have  not  to  consider  whether  he  can  swallow  the  drug  or  to  think  of  the 
tolerance  of  the  stomach,  as  the  medicine  quickly  reaches  its  destination 
by  means  of  cutaneous  absorption.  We  may  also  administer  quinine  in  an 
enema.  In  acute  malaria  of  the  pernicious  type,  however,  it  is  well  to 
administer  quinine  by  every  possible  means  at  once — by  the  mouth,  by 
subcutaneous  injections,  by  enemata,  and  by  inunction.  The  above  com- 
prises the  treatment  of  acute  malaria  with  quinine.     In  persons  who  cannot 


1820  TEXT-BOOK  OP  MEDICINE 

take  the  stilphate  weU  vre  may  give  tlie  lactate  or  the  hvdrobromate  of 
qumine. 

Quinine  has  not  the  same  efhcacy  in  all  cases,  especially  when  the 
disease  is  of  long  standing  and  when  the  patient  has  already  sufiered  from 
several  attacks.  It  is  then  necessary  to  substitute  cinchona,  which  is, 
under  these  circumstances,  superior  to  quinine.  I  have  often  been  able 
to  help  soldiers  who  had  returned  from  Cochin-China  or  from  Tonkin  suSer- 
icLg  from  inveterate  and  irregular  fever  to  shake  it  ofi  by  means  of  cinchona 
when  quinine  had  no  action.  We  may  prescribe  every  morning  120  grains 
of  powdered  yellow  cinchona  in  black  coffee  or  in  lemonade,  care  being 
taken  to  stir  the  powder,  so  that  it  is  well  mixed  with  the  fluid.  Slight 
diarrhoea  sometimes  foUows  the  exhibition  of  cinchona,  and  in  such  cases  a 
pill  of  opium  may  be  given  in  conjunction  with  it.  We  mav  also  give 
cinchona  in  the  form  of  an  electuary  (powdered  cinchona  and  conserve  de 
rose),  or  mixed  with  orange  syrup. 

The  exhibition  of  quiuine  or  of  cinchona  must  be  repeated  for  eight  days 
in  succession.  After  this  period  we  may  spread  the  doses  out  according  to 
Trousseau's  method  by  giving  them  at  successive  intervals  of  two.  three, 
four,  and  up  to  eight  days. 

In  the  treatment  of  fever  which  resists  cinchona  or  quinine  I  have 
obtained  good  results  by  the  subcutaneous  injection  of  carbolic  acid.  I 
employ  a  2  per  cent,  solution,  so  that  each  Pravaz  syringe  contains  4  centi- 
grammes of  carbolic  acid.  vSeveral  injections  are  given  daily,  so  as  to  com- 
prise a  total  dose  of  from  10  to  20  centigrammes  of  carbolic  acid.* 

Arsenical  preparations  (Boudin)  give  good  results.  Cacodylate  of  soda  and 
arrhenal  have  been  advised  in  the  form  of  subcutaneous  injections,  repeated 
for  a  more  or  less  lengthy  period,  according  to  the  obstinacy  of  the  fever. 

Hydrotherapy  also  renders  the  greatest  service,  but  the  douches  should 
not  be  too  cold  at  first,  lest  they  should  cause  fresh  attacks. 

Prophylaxis. — Prophylaxis  comprises  the  following  measures  :  To  render 
marshy  lands  healthy,  but  not  to  undertake  drainage  works  during  the  hot 
season  and  during  epidemics.  Inhabitants  should  remove  from  the  plains, 
and  seek  high  levels,  or  leave  the  country  in  which  malaria  is  prevalent. 
In  cachexia  it  is  absolutely  necessary  for  the  patient  to  change  his  residence, 
and  to  leave  the  country  in  which  the  disease  is  endemic. 

Neveu-Lemaire  has  given  an  excellent  summary  of  the  method  of  general 
and  individual  prophylaxis.  It  is  necessary  to  do  away  with  pools,  weUs, 
cisterns,  and  water-butts  in  the  neighbourhood  of  dwelling-houses,  since  the 
larvae  of  the  Anopheles  swarm  in  the  water,  where  they  are  promptly 
hatched,  and  invade  the  neighbouring  house. 

The  direct  means  consist  in  the  destruction  of  the  larvae  in  the  water. 
*  Dieulafoy,  Gazette  Hebdom.,  Octobre  17,  188-4. 


INFECTT(~)US  J)ISKASES  TROrKU  To  MAN  1821 

In  large  ponds  rearing  of  fish  should  be  encouragt^d,  as  thev  eat  tho  larvae 
of  the  mosquitoes.  When  the  mass  of  stagnant  water  is  not  large  (reservoir, 
pool,  or  well),  rag  impregnated  with  petroleum  and  tar  is  placed  on  the 
surface  of  the  water  ;  10  c.c.  of  this  mixture  are  sufficient  per  square  metre 
of  surface.  This  operation  should  be  performed  in  the  springtime,  and 
repeated  every  fortnight. 

As  regards  individual  protection,  care  should  be  taken  to  protect  all  the 
openings  of  the  house,  such  as  windows  and  chimneys,  etc.,  with  a  wire 
network,  the  meshes  of  which  are  so  fine  that  the  mosquitoes  cannot  pass 
through  them.  Beds  should  always  be  covered  with  mosquito-curtains. 
When  the  individual  goes  out,  the  face  and  the  neck  should  be  protected 
with  a  veil,  tlie  hands  covered  with  gloves,  and  the  trousers  securely  fastened 
at  the  bottom.     The  Anopheles  are  most  formidable  at  nightfall. 

The  Italian  Railway  Companies  on  the  Mediterranean  and  Adriatic 
coasts  have  reduced  the  number  of  cases  of  malaria  among  their  employees 
by  fitting  all  windows  of  their  stations,  gate-keepers'  houses,  and  switch- 
point  cabins  with  wire  gauze,  and  insisting  on  their  employees  wearing  a 
special  mask  and  gloves,  in  order  to  avoid  mosquito-bites.  These  results 
are  the  more  interesting,  as  on  the  parts  of  the  railways  where  these  pre- 
cautions have  not  been  taken  malaria  has  not  diminished  in  severity. 

Quinine  and  cinchona  taken  daily  in  malarial  countries  may  act  as 
prophylactics.  It  is  necessary  to  avoid  going  out  in  the  morning  when  the 
dew  is  still  on  the  ground,  or  in  the  evening  after  sunset. 


XL  SLEEPING  SICKNESS. 

The  history  of  sleeping  sickness  dates  from  the  clinical  studies  of  Winter- 
bottom  (1803),  ^loreau,  Jonnes,  and  Guerin.  The  pathogenesis  has  been 
elucidated  by  the  researches  of  Forde,  Dutton,  CasteUani,  and  Brumpt. 
This  peculiar  affection  is  due  to  the  invasion  of  the  organism  by  a  flagellated 
parasite,  the  next  of  kin  to  the  trypanosomes,  which  in  animals  determines 
dourine,  nagana,  and  surra.  The  parasite  is  called  the  Tryfanosoma  Gam- 
biense.     Sleeping  sickness  is  transmitted  to  man  by  the  bite  of  the  tsetse-fly. 

Geographical  Distribution. — The  disease  is  endemic  in  a  region  extend- 
ing from  Gambia  to  the  Portuguese  Congo.  French  Guinea,  Benin,  the 
French  Congo,  and  the  Congo  Free  State  are  the  chief  seats  of  the  disease. 
It  has  extended  across  Africa  as  far  as  Uganda.  The  basins  of  the  Senegal, 
Niger,  Congo,  and  Upper  Nile  have  been  thus  infected.  The  disease  is 
becoming  more  frequent  in  the  European  colonies  of  the  Congo.  "  Sleeping 
sickness  is  as  terrible  in  its  results  as  the  most  severe  epidemics  of  plague 
reported  in  history  "  (Blanchard).  Men  and  women,  old  and  young,  may 
fall  victims.     Persons  of  every  station  are  liable  to  the  disease,  and  if  negroes 


1822  TEXT-BOOK  OF  MEDICINE 

are  more  afiected,  it  is  simply  because  they  work  aU  day  in  places  where  the 
flies  are  more  numerous. 

Parasitology. — In  1901  Forde,  an  English  physician  residing  in  Gambia, 
found  in  the  blood  of  one  of  his  patients  a  parasite  whose  nature  he  could 
not  determine.  It  was  recognized  by  Button  as  belonging  to  the  trypano- 
somes.  Other  cases  were  published,  and  the  existence  of  a  special  fever 
caused  by  the  T.  Gamhiense  was  established.  Two  years  later  Castellani 
found  a  trypanosome  in  the  cerebro -spinal  fluid  of  a  patient  with  sleeping 
sickness.  This  discovery  was  confirmed  by  Castellani,  Bruce,  Nabarro, 
Wiggins,  and  Brumpt.  Lumbar  puncture  in  cases  of  sleeping  sickness 
almost  always  yielded  trypanosomes.  The  results  were  always  negative 
in  other  persons.  Was  CasteUani's  parasite  identical  with  Forde's  trypano- 
some ?  The  answer  is  afl&rmative.  It  has  been  proved  that  sleeping  sick- 
ness is  the  terminal  stage  of  Gambia  fever,  that  both  diseases  have  the  same 
field  of  distribution,  and  that  their  parasites  are  identical.  Finally,  sleeping 
sickness  has  been  reproduced  in  monkeys  by  inoculating  them  with  blood 
from  persons  with  Gambia  fever. 

The  trypanosome  is  a  flagellated  organism.  Its  length  is  four  times 
that  of  a  red  blood-corpuscle,  while  its  breadth  is  less  than  a  third  of  the 
diameter  of  a  corpuscle.  Appropriate  methods  show  that  the  parasite  pos- 
sesses a  protoplasmic  body,  studded  with  granulations,  and  having  an  oval 
nucleus.  The  posterior  extremity  is  rounded  ;  the  anterior  extremity  ends 
in  a  fine  flageUum.  A  kind  of  crest  {membrana  undidans)  unites  the 
flageUum  to  a  centrosome,  situated  at  the  opposite  end  of  the  parasite.  In 
fresh  blood  the  parasite  is  mobile,  and  advances  rapidly  by  turning  on  its 
long  axis.     The  undulating  membrane  then  assumes  the  shape  of  a  spiral. 

The  trjrpanosomes  multiply  in  the  blood  by  longitudinal  division.  They 
may  be  cultivated  on  liquid  media  rich  in  hsemoglobin.  Inoculation  of  the 
trypanosome  produces  a  fatal  disease  in  the  dog,  the  rat,  and  the  guinea- 
pig.  If  the  parasites  are  inoculated  under  the  skin  of  a  monkey,  they 
appear  in  the  blood  a  fortnight  later,  and  the  animal  sufiers  from  febrile 
attacks,  anaemia  and  wasting ;  death  follows  within  two  months,  aU  the 
symptoms  of  sleeping  sickness  being  present. 

The  Tsetse-Fly. — Since  the  role  of  the  trypanosome  in  sleeping  sickness 
has  been  known,  it  has  been  suggested  that  the  contamination  might  result 
from  the  bites  of  the  tsetse-fly.  It  was  already  known  that  another  form  of 
trypanosomiasis — "  nagana  " — was  transmitted  by  this  dipteran.  Brumpt 
proved  that  sleeping  sickness  was  met  with  in  the  regions  where  a  special 
species  of  tsetse-fly — ^the  Glossina  fdfalis — was  found,  and  Bruce  and 
Nabarro  were  able  to  transmit  sleeping  sickness  to  monkeys  by  the  bites 
of  this  fly.  The  Glossina,  which  is  intermediate  in  size  between  a  house-fly 
and  a  bee,  is  readily  distinguished  by  its  wings — "  folded  over  its  back  like 


INFECTIOUS  DISEASES  TEOPEK  TO  MAN  182r5 

the  bliulos  of  a  pair  of  scissors."  It  lives  on  the  banks  of  rivers,  and  flies 
quickly,  producing  the  noise  which  has  given  to  it  its  name  (tsetse).  It 
bites  during  the  day,  and  the  bite  is  somewhat  painful.  In  about  twenty 
seconds  the  insect's  belly  is  filled  with  blood.  The  tr}'j)an()some8  which 
the  insect  has  thus  imbibed  from  the  patient's  circulation  multiply  in  its 
stomach,  and  enter  the  salivar}'-  gland.  They  are  then  injected  during  the 
bite,  and  thus  transmit  the  disease. 

Symptoms. — The  disease  comprises  two  successive  phases.  During  the 
former  the  infection  is  limited  to  the  blood  ;  during  the  latter  the  parasites 
invade  the  nerve  centres,  and  sleep  results. 

First  Period. — It  is  only  seen  in  white  people,  and  is  characterized  by 
a  syndrome  which  Forde,  Dutton,  Manson,  Daniels,  Laveran  and  Mesnil, 
and  Nattan-Larrier  have  studied.  The  fever  is  characterized  by  attacks 
lasting  about  two  days.  The  attacks  may  succeed  one  another  at  brief 
intervals,  or  may  be  separated  by  months  of  apyrexia.  "  The  rise  of  tem- 
perature is  rarely  preceded  by  chills,  and  when  a  chill  occurs  it  is  often  very 
slight.  The  temperature  begins  to  rise  about  midday,  and  reaches  its 
maximum  about  6  p.m.  Defervescence  takes  place  during  the  night ; 
sweating  is  absent,  and  slight  hypothermia  may  be  noticed."  The  fever 
does  not  yield  to  quinine.  In  the  intervals  between  the  attacks  the  pulse 
is  quick,  irregular,  and  compressible.  This  tachycardia  is  not  always  in 
direct  proportion  to  the  rise  of  temperature. 

The  epitrochlear  glands,  the  chain  along  the  stemo-mastoid,  and  the 
supraclavicular  glands  are  always  afEected.  The  glands  are  painless,  hard, 
mobile,  quite  isolated,  and  rarely  larger  than  a  hazel-nut.  Erythema  is  a 
very  characteristic  feature  of  the  disease,  but  it  is  not  seen  in  every  case. 
It  is  usually  of  the  circinate  variety,  and  comes  out  in  successive  crops. 
The  spots  vary  in  size,  and  are  seen  on  the  shoulder,  at  the  upper  part  of 
the  chest,  and  in  the  hypochondriac  regions.  Acceleration  of  the  respira- 
tion-rate and  hypertrophy  of  the  spleen  are  constant.  Pruriginous  ery- 
thema and  pseudo-phlegmonous  oedema  are  sometimes  met  with.  In  most 
cases  the  syndrome  is  incomplete,  and  the  disease  would  pass  unnoticed  if 
we  did  not  find  the  tachycardia  and  the  glandular  enlargements.  In  some 
instances,  on  the  other  hand,  the  patient  during  the  first  stage  is  apathetic 
and  asthenic,  severe  and  obstinate  headache  is  present,  the  upper  limbs  are 
affected  by  tremors,  and  the  eyelids  and  the  face  are  swollen. 

Second  Period — Sleeping  Sickness. — The  duration  of  the  first  period 
varies.  In  some  cases  it  does  not  exceed  ten  or  twelve  months  ;  in  other 
cases  it  lasts  for  years,  although  the  patient's  health  is  not  deeply  affected. 
The  second  period  is  characterized  by  the  appearance  of  nervous  symptoms, 
and  in  particular  of  lethargy.  "  At  first  it  is  a  question  of  drowsiness 
rather  than  of  sleepi    The  patient  sleeps  for  a  couple  of  hours  after  his 


1824  TEXT-BOOK  OF  MEDICINE 

midday  meal.  He  then  wakes  up,  and  perhaps  attends  to  his  business. 
The  drowsiness  is  not  very  deep,  and  the  patient  at  once  wakes  up  when 
spoken  to.  After  a  certain  time  a  second  spell  of  sleep  comes  on  in  the 
evening  before  dinner,  and  finally  the  patient  sleeps  nearly  all  day.  The 
sleep  is  very  profound,  and  it  is  possible  to  drag  the  bed  about  the  room 
without  awakening  the  patient.  In  order  to  awaken  the  sleeper  it  is  neces- 
sary to  shake  him.  He  raises  his  eyelids  with  difficulty,  and  answers  in 
monosyllables  to  the  questions  asked.  If  food  is  given  the  patient  forgets 
to  swaUow  it,  and  goes  to  sleep  with  it  in  his  mouth.  The  sleep  becomes 
more  prolonged  and  more  profound,  and  finally  ends  in  coma  "  (Le  Dentec). 

As  a  matter  of  fact,  the  patient  does  not  sleep  during  the  onset  of  the 
second  period.  He  suffers  from  extreme  asthenia,  with  headache,  pain  in 
the  back,  and  cutaneous  hyper sesthesia.  He  dreads  the  least  movement. 
The  eyelids,  too,  are  shut  as  the  result  of  ptosis,  which  he  may  attempt  to 
overcome  by  contracting  the  frontalis  muscle.  In  some  cases  mental 
troubles  take  the  place  of  the  lethargic  symptoms,  and  the  patient  commits 
lawless  acts,  and  suffers  from  attacks  of  mania  with  homicidal  impulses, 
followed  by  a  stage  of  coma. 

Tremor  is  never  absent.  It  affects  the  tongue  and  the  upper  limbs. 
In  the  tongue  it  simulates  the  tremor  of  general  paralysis,  and  causes  dis- 
turbance of  speech.  In  the  upper  limb  it. assumes  the  alcoholic  type.  It 
is  rapid,  persists  during  rest,  and  is  increased  by  movement. 

The  patellar  reflex  may  be  abolished.  The  loss  of  the  light  reflex  and 
the  existence  of  ArgyU-Robertson's  sign  at  times  cause  the  disease  to 
resemble  tabes.  Confusion  is,  however,  impossible,  on  account  of  the 
presence  of  lethargy  and  fever.  At  this  stage  the  fever  appears  daily,  the 
temperature  at  night  being  very  high,  but  falling  to  normal  in  the  morning. 
The  tachycardia,  the  enlargement  of  the  glands,  and  the  erythema  still 
persist ;  oedema  of  the  face  and  of  the  eyelids  is  often  present. 

The  terminal  period  generally  supervenes  at  the  end  of  ten  or  twelve 
months.  The  fever  gives  place  to  hypothermia,  the  tachycardia  disappears, 
the  breathing  becomes  slow  and  sighing,  micturition  is  involuntary,  alimen- 
tation becomes  impossible,  and  the  wasting  is  extreme.  The  patient  is 
plunged  in  coma,  interrupted  at  times  by  epileptiform  crises  or  by  contrac- 
tures of  the  face,  arms,  and  legs.  He  dies  in  a  state  of  cachexia.  "  It  is 
exceptional  for  the  disease  to  be  prolonged  for  a  year  after  the  onset  of  the 
nervous  symptoms  "  (Laveran  and  Mesnil). 

Pathological  Anatomy. — The  essential  lesion  is  a  chronic  meningitis. 
"  In  some  cases  the  meningitis  is  well  marked — meninges  injected,  thickened, 
and  adherent  to  the  brain — in  others  we  find  hypersemia,  which  is  but  little 
characteristic  if  we  are  content  with  a  macroscopic  examination  "  (Laveran 
and  Mesnil).     The  histological  lesions  are  characterized  by  lymphocytic 


IXFFX'TIOUS  DISEASES  TKOrKK  To  MAN  1825 

infiltration  of  the  perivascular  spaces,  in  which  we  may  see  stained  trypano- 
somes.  These  clianges  are  found  in  the  brain,  in  the  bull^  and  in  the  spinal 
cord.  The  cere])ro-8])inal  fluid  is  always  very  rich  in  albumin,  and  cyto- 
diagnosis  reveals  numerous  mononuclear  cells. 

Diagnosis. — We  may  suspect  trypanosomiasis  if  we  find  tachycardia, 
enlargemi'ut  of  glands,  and  circinate  erythema.  Moreover,  the  nature  of  the 
febrile  attacks  and  their  resistance  to  quinine  will  be  of  much  value.  The 
clinical  diagnosis  should  always  be  confirmed  by  the  examination  of  the 
blood.  This  examination  is  difficult  if  we  only  employ  smears,  because  the 
trypanosomes  are  always  very  few  in  dried  films  prepared  by  the  ordinary 
methods.  Other  methods  have,  therefore,  been  proposed.  We  take  from 
the  arm  5  c.c.  of  blood  rendered  incoagulable  by  the  addition  of  any  equal 
quantity  of  a  5  per  cent,  solution  of  sodium  citrate.  The  mixture  is  centri- 
fugalized,  and  dried  preparations  are  made  from  the  thin  layer  of  leucocytes 
which  settles  above  the  red  corpuscles.  Grieg  and  Gray  have  attemj^ted  to 
procure  the  parasite  from  lymph  obtained  by  puncture  of  the  enlarged 
glands.  Nattan-Larrier  has  found  the  parasite  in  blood  obtained  by  scari- 
fying the  er}i;hematous  areas. 

In  the  second  period,  the  tremor,  the  dysarthria,  the  mental  troubles, 
and  the  absence  of  the  reflexes  slightly  resemble  the  conditions  seen  in 
general  paralysis,  but  the  attacks  of  sleeping  prevent  any  confusion.  In 
any  case,  the  discovery  of  the  trypanosomes  in  the  cerebro-spinal  fluid  w^ill 
remove  all  doubt,  but  we  must  remember  that  the  parasite  is  only  found  in 
nine  out  of  every  ten  cases.  If  the  direct  examination  is  negative,  we  must 
employ  inoculation  of  a  monkey  or  of  a  rat. 

Prophylaxis  and  Treatment. — Proper  prophylaxis  can  only  be  realized 
by  an  international  agreement  between  the  colonies  concerned.  Early 
diagnosis  of  the  disease  is  essential,  and  the  administration  of  each  colony 
must  try  to  prevent  the  migration  of  infected  natives  into  healthy  regions. 
It  is  necessary,  whenever  possible,  to  isolate  the  sick  in  regions  where  the 
tsetse-fly  is  not  found.  The  bush  should  be  destroyed  on  the  banks  of 
rivers  where  the  Glossina  exists.  It  is,  unfortunately,  very  difficult  to 
apply  these  measures  in  vast  tracts  ^of  unexplored  country.  The  covering 
of  doors  and  windows  with  netting  is  more  useful  in  the  case  of  the  Anopheles 
than  in  that  of  the  tsetse -fly. 

Serotherapy  has  so  far  given  no  results.  Aisenious  acid  delays  the 
progress  of  the  disease,  but  does  not  cure  it.  Improvement  appears  to  have 
been  obtained  with  atoxyl.  The  adult  dose  is  50  centigrammes  by  hypo- 
dermic injection.  This  is  gradually  increased  to  a  gramme.  The  injections 
are  given  every  five  days,  then  every  eight  days,  and  continued  for  several 
months.  "  It  is  probable,"  says  Laveran,  "  that  success  will  be  obtained, 
provided  the  disease  is  not  in  an  advanced  stage." 


1826  TEXT-BOOK  OF  MEDICINE 


XII.  LEPEOSY. 

History  and  Geography. — Leprosy  is  by  common  accord  regarded  as  a  Biblical 
malady,  but  it  is  probable  that  the  leprosy  of  the  Hebrews  included  the  most  diverse 
affections  of  the  skin.  The  disease  is,  in  any  case,  of  great  antiquity,  and  was  imported 
into  Europe  from  India  and  from  Egypt  some  centuries  before  our  era.  It  became 
a  scourge  during  the  Crusades.  At  this  time  the  number  of  leper -houses  which  had 
existed  since  the  seventh  century  mtdtipHed  to  a  remarkable  extent ;  the  order  of 
Saint  Lazarus  was  formed,  in  order  to  take  care  of  lepers,  and  these  unfortunate  people 
were  subject  to  severe  measures  of  isolation,  which  saved  Europe  from  contagion. 

It  must  not  be  thought,  however,  that  leprosy  is  completely  extinct  in  our  country  ; 
it  is  always  ready  to  make  an  invasion  upon  the  least  defect  in  our  watchfulness.  The 
rare  cases  of  leprosy  seen  in  Paris  are  all  of  exotic  origin,  but  some  discrete  centres  exist 
along  the  Comiche  and  the  Riviera.  It  exists  in  Brittany,  where  the  cases  of  Morvan's 
disease  described  in  recent  years  are  considered  by  Zambaco  to  be  cases  of  leprosy. 
More  important  centres  exist  in  Spain  and  in  Portugal  in  the  Baltic  provinces  of  Russia, 
and  in  Sweden  and  Norway,  where  prophylactic  measures  have  considerably  diminished 
the  number  of  cases  in  the  last  few  years.  The  most  important  exotic  centres  are  found 
in  Persia,  India,  China,  Tonkin,  the  Antilles,  Brazil,  Louisiana,  the  Sunda  Islands,  and 
the  Sandwich  Islands. 

iEtiology. — Leprosy  is  an  infectious  disease  caused  by  a  special  bacUlus. 
Heredity  and  contagion  are  considered  to  be  the  most  frequent  agents  ia 
the  propagation  of  the  parasite. 

Danielssen  laid  most  stress  upon  heredity.  As  a  matter  of  fact,  about 
a  third  of  the  patients  are  descended  from  lepers,  but  it  is  difficult  to  prove 
that  the  itidividual  has  not  been  infected  during  infancy  by  contact  with 
his  parents.  The  disease  may  be  transmitted  from  the  mother  to  the  foetus  in 
leprosy,  as  in  tuberculosis,  but  this  is  a  case  of  simple  direct  contamination. 

Heredity  is,  therefore,  possible,  but  contagion  is  certainly  the  usual 
cause  of  the  disease.  Leprosy  foUows  changes  of  domicile  and  large  migra- 
tions. It  entered  Europe  with  the  Crusaders,  and  the  Sandwich  Islands 
with  the  Chinese  immigration.  It  may  be  transmitted  by  direct  contact, 
as  by  sleeping  in  the  same  bed  or  following  on  a  cut  with  an  instrument 
soiled  by  the  discharge  from  a  leprous  ulcer.  Although  these  cases  are 
exceptional,  they  are  nevertheless  incontestable.  We  know  that  long  resi- 
dence among  leprous  patients  rarely  gives  rise  to  the  disease,  whence  comes 
the  immunity  of  physicians  and  of  hospital  attendants.  The  arrival  of 
lepers  in  localities  previously  free  from  the  disease  may  cause  an  outbreak 
among  the  population.  Lastly,  the  rapid  decline  of  leprosy  in  countries 
where  patients  are  rigorously  isolated  forms  a  decisive  argument  in  favour 
of  contagion.  Kalindero  (of  Bucharest)  in  1897  made  a  series  of  interesting 
communications  on  the  distribution  and  extension  of  leprosy  in  Roumania. 
Symptoms. — Leprosy,  although  a  specific  disease,  does  not  always 
present  an  identical  symptomatology.  We  meet  with  three  principal  forms ; 
tubercular,  anaesthetic,  and  mixed. 


lXFia:TU)rs  J)1SKASKS  rKol'KR  To    MAX  1827 

The  inuubation  period  is  always  very  long ;  it  may  be  as  long  as  thirty- 
two  years  (iralh>|i('au),  but  its  mean  duration  is  from  two  to  six  years. 

Tiu^  invasion  is  often  markcul  by  hissitu<U;,  rigors,  and  fever  at  night. 
The  patient  is  a  prey  to  a  physical  and  moral  apathy,  which  may  last  months 
and  years. 

Mariano  and  Wurtz  have  shown  that  the  affection  may  commence  with 
an  isolated  spot  some  years  before  other  symptoms.  In  the  stationary  stage 
the  symptoms  of  the  tubercular  form  differ  from  those  of  the  anajsthetic 
form. 

1.  The  Tubercular  Form. — We  find -two  phases — the  macular  and  the 
nodular. 

Macular  Stage.— The  macular  stage  is  essentially  characterized  by  the 
appearance  of  vascular  or  pigmentary  spots,  which  vary  in  colour  from  grey 
to  pale  rose  or  to  bright  crimson.  They  may  in  time  change  to  yellow  or 
even  to  brown.  Their  edges  are  polycyclical  and  slightly  prominent ;  their 
centre  is  often  shiny,  as  though  varnished.  Parts  which  are  uncovered 
(face,  hands),  or  parts  which  are  exposed  to  pressure  (elbows,  buttocks,  or 
knees),  form  their  seat  of  election. 

The  spots  are  sometimes  the  seat  of  sensory  and  trophic  troubles,  which 
become  more  marked  in  the  nodular  stage.  The  sensory  troubles  are  most 
varied,  and  characterized  by  hypersesthesia  and  hypo- anaesthesia.  The 
trophic  troubles  are  shown  by  persistent  alopecia  in  certain  regions,  such 
as  the  eyebrows,  by  hyperkeratinization  of  the  nails,  and  by  absence  of 
sweat. 

The  maculae  gradually  become  infiltrated,  and  the  disease  passes  pro- 
gressively into  the  second  stage. 

Nodular  Stage. — The  nodule  is  the  characteristic  lesion  of  the  second 
period.  It  attacks  both  the  skin  and  the  mucous  membranes,  and  develops 
either  in  the  maculae  above  described  or  in  the  healthy  skin.  It  corresponds 
to  the  tubercular  leproides  of  Bazin  and  to  the  leprides  of  Besnier.  The 
projections  formed  by  the  nodules  may  be  isolated  or  confluent.  They  may 
infiltrate  the  hypodermic  tissue  (hypodermic  leproma  of  Leloir)  or  the  dermis 
(pure  dermic  leproma  of  Leloir).  They  are  firm  and  elastic  in  consistency  ; 
they  vary  in  colour  from  red  to  \'iolet  and  bistre,  and  may  be  as  small  as  a 
pin's  head  or  as  large  as  a  small  nut.  Their  seat  of  election  is  the  face 
(tkroat,  outer  part  of  the  superciliary  region,  nose,  lips,  chin,  cheeks,  and 
especially  the  lobule  of  the  ear),  the  hands,  the  forearm,  and  the  lower 
limbs.  The  whole  thickness  of  the  skin  may  be  invaded.  When  the 
disease  has  reached  this  degree,  the  mucous  membranes  are  generally 
affected.  We  may  also  see  conjunctivitis,  keratitis,  and  iritis,  which  may 
end  in  indelible  opacities  and  even  in  panophthalmitis.  Hansen's  bacillus 
is  found  in  the  interstitial  keratitis  of  leprosy  (Jeanselme  and  Morax). 


1828  TEXT-BOOK  OF  MEDICIKE 

Beneatli  the  inflamed  pituitary  membrane  the  septum  is  perforated,  the 
cartilages  are  eroded,  and  foul-smelling  pus  flows  from  the  nasal  fossae. 
The  mucous  membrane  of  the  tongue  is  ulcerated  and  covered  with  vegeta- 
tions. The  changes  in  the  mucosae  of  the  pharynx  and  larynx  may  end  in 
more  or  less  complete  aphonia,  with  stridor,  dyspnoea,  and  attacks  of 
suflocation. 

Among  the  visceral  changes  orchitis  has  been  noticed  (HaUopeau  and 
Jeanselme),  and  lepromata  have  also  been  found  in  the  lungs  and  intestines. 

The  leper  presents  a  characteristic  facies,  due  to  the  mutilating  efiect  of 
the  disease.  The  bloated  face,  the  thickened  and  irregular  forehead,  the 
semipendent  eyelids,  the  swollen  and  flattened  nose,  the  enlarged  chin,  the 
thick  lips,  the  ears  with  large  infiltrated  lobules,  form  a  striking  symptom- 
complex,  which  includes  in  the  same  hideous  deformity  all  lepers,  whatever 
their  age,  their  sex,  or  their  race  may  be. 

The  course  of  the  disease  is  characterized  by  acute  febrile  attacks, 
interrupted  by  more  or  less  lengthy  periods  of  calm.  After  each  attack  the 
tubercles  increase  in  size  and  number.  The  lepromata  finally  break  down, 
and  form  deep  foul-smelling  ulcers.  Bones,  tendons,  and  joints  may  be 
exposed.  The  natural  tendency  of  the  disease  is  to  cause  destruction  of 
the  tissues  by  ulceration.  Death  occurs  ten,  twelve,  or  fifteen  years  after 
the  onset  of  the  infection,  either  from  marasmus  or  from  some  intercurrent 
malady,  tuberculosis  being  the  most  frequent. 

2.  AnsBSthetic  Form. — The  principal  symptoms  of  this  form  are  pig- 
mented spots,  bullous  eruptions,  trophic,  sensory  and  motor  troubles, 
thickening  of  the  nerves,  and  especially  of  the  ulnar  nerve,  the  lesions  being 
symmetrical. 

The  spots  at  the  commencement  of  this  stage  resemble  those  of  the 
preceding  period  in  their  morphology,  and  can  only  be  distinguished  by 
their  more  S5anmetrical  disposition,  by  their  greater  number  and  size,  by 
their  rapid  and  well-marked  pigmentation,  and  by  the  more  early  decolora- 
tion of  their  centres.  The  achromia  of  the  centre  and  the  hyperchromia 
of  the  edge  combine  to  give  them  the  appearance  of  vitiligo  or  of  black 
morphoea,  according  to  the  nomenclature  of  old  writers.  Bullous  eruptions 
may  develop  on  the  surface  of  these  spots,  and  form  a  leprous  pemphigus. 
The  bullee  may  continue  to  appear  for  months.  After  they  have  burst  they 
may  form  the  starting-point  of  intractable  ulcers  upon  the  limbs. 

The  sensory  troubles  are  very  marked  from  the  onset.  They  are  usually 
ushered  in  by  paroxysms  of  severe  pain  along  the  course  of  the  nerves,  by 
sensations  of  heat  and  of  cold,  and  by  cutting  and  gnawing  pains  in  the 
flesh.  The  patient  screams  with  pain  on  the  slightest  touch,  but  typical 
anaesthesia  may  accompany  or  may  follow  this  hyperanaesthesia.  The 
anaesthesia  is  often  so  marked  that  wounds  and  burns  are  unnoticed  by  the 


INFECTIDHS   DI.SEASES   I'KOPKR  TO  MAN  1829 

patient.  A  pin  may  be  pushed  into  the  tissues  or  the  cautery  point  may  be 
applied  to  the  skin  without  producing  the  least  suffering. 

The  trophic  troubles  are  the  most  interesting.  They  are  characterized 
by  thickening  of  the  nerve  trunks  and  amyotrophy.  The  ulnar  nerve, 
which  might  be  called  the  nerve  of  reaction  in  leprosy,  should  be  examined 
from  its  origin  in  the  brachial  j)lexus  as  far  as  the  olecranon  groove,  where 
we  can  feel  the  regular  or  moniliform  thickening  so  valuable  in  diagnosis. 

The  thenar  and  hypothenar  eminences  and  the  interossei  are  chiefly 
affected  by  the  amyotrophy.  The  hand  finally  presents  the  claw-hand  of 
the  Aran-Duchenne  syndrome.  The  flexors  of  the  feet,  the  peronei,  and 
the  extensors  of  the  toes  are  chiefly  affected  as  regards  the  lower  limbs. 
Finally,  as  in  syringomyelia,  amyotrophic  lateral  sclerosis,  or  progressive 
muscular  atrophy,  the  pectoral,  deltoid,  and  gluteal  muscles  may  be  affected 
simultaneously  or  progressively.  The  muscles  of  the  face  no  longer  remain 
free.  The  paralysis  of  the  orbicularis  palpebrarum,  characterized  by  ptosis 
of  the  upper  lid  and  by  ectropion  of  the  lower  lid,  is  of  great  importance  in 
diagnosis. 

We  may  see  lesions  in  the  skeleton,  and  especially  in  the  fingers,  shedding 
of  the  nails  and  teeth,  perforating  ulcer.s,  and  anaesthetic  lesions,  which  may 
destroy  whole  segments  of  the  limbs. 

The  motor  troubles  generally  depend  upon  the  muscular  atrophy,  and 
true  hemiplegia  or  monoplegia  is  rare.  Some  authors  have,  however, 
noticed  paralysis  of  the  extensors  of  the  lower  limbs,  giving  rise  to  the 
steppage  gait. 

The  patient  finally  succumbs  from  suppuration,  prostration,  and  stupor, 
or  may  be  carried  off  by  some  secondary  infection,  such  as  pneumonia  or 
tuberculosis. 

Mixed  Form. — This  form,  which  results  from  the  combination  of  the 
two  preceding  ones,  is  most  typical.  The  association  may  exist  at  the 
onset  of  the  affection,  but  in  most  cases  anaesthetic  leprosy  follows  the 
tubercular  form. 

Bacteriology. — The  bacillus  of  leprosy  was  fijst  discovered  by  Hansen 
in  1871,  stained  by  Neisser  in  1881,  and  has  since  been  studied  by  numerous 
bacteriologists,  and  especially  in  France  by  Cornil  and  Snchard,  Hillairet 
and  Gaucher,  and  by  Leloir. 

The  bacUlus  measures  from  3  to  5  //.  in  length,  and  1  /*  in  breadth.  It 
is  very  mobile,  straight  or  slightly  curved,  and  stains,  like  the  tubercle 
bacillus,  with  Ehrlich's  reagent.  Aiter  staining  it  shows  small  clear  points 
in  its  substance.  It  is  surrounded  by  a  capsule,  and  appears  either  alone 
or  grouped  in  masses. 

The  bacilli  are  enclosed  in  the  large  cells  of  the  dermis  and  in  the  interior 
of  the  nerve  cells.     They  closely  resemble  those  of  tuberculosis,  having 

n.  116 


1830  TEXT-BOOK  OF  MEDICINE 

nearly  the  same  form  and  staining  reaction.  The  bacilli  of  leprosy  fofm 
closely  packed  masses  in  the  centre  of  old  nodules. 

Attempts  at  inoculation  have  so  far  remained  inefiectual,  and  uncertain 
results  have  been  given  by  culture  experiments. 

Pathological  Anatomy.  —  The  lesions  of  leprosy  resemble  those  of 
tuberculosis  and  of  glanders.  The  tissues  are  infiltrated  with  leucocytes 
and  epithelioid  cells,  and  with  elements  comparable  to  the  giant  cells, 
although  the  nuclei  are  not  so  numerous.  Virchow's  cell  is  histologically 
characteristic  of  leprosy.  It  is  four  or  five  times  as  broad  as  a  leucocyte. 
Its  single  or  double  nucleus  is  large  and  clear,  and  closely  resembles  that  of 
the  epithelial  cells.  The  protoplasm  shows  numerous  small  vacuoles  {proto- 
plasma  en  ecumoire),  which  may  later  invade  the  whole  cell.  The  bacilli 
nearly  always  form  masses  of  five  or  six  rods  placed  side  by  side,  like  "  bundles 
of  cigars,"  or  more  compact  masses  are  seen,  in  which  the  bacilli  lie  in 
various  positions. 

The  bacilli  are  more  numerous  in  the  larger  and  older  cells.  In  the 
most  advanced  stage  the  protoplasm  is  replaced  by  the  bacilli.  Virchow's 
cell  is  always  present  in  the  central  and  oldest  parts  of  the  leproma.  It  is 
especially  frequent  in  the  lymphatic  glands,  the  bone-marrow,  and  the 
spleen. 

The  dermis  at  the  site  of  the  lepromata  is  infiltrated  throughout  its 
whole  extent  by  cells,  which  are  often  grouped  in  islets  along  the  blood- 
vessels and  lymphatics.  The  epidermis  is  generally  intact,  and  only  becomes 
afiected  when  the  tubercles  ulcerate.  Some  authors  have  found  baciUi  in 
the  sweat-glands  and  around  the  orifices  of  the  hair-follicles. 

The  baciUi  are  situated  in  the  interior  of  the  cells  which  make  up  the 
leproma.  They  often  form  emboli  in  the  central  vessels  of  the  erythematous 
spots,  and  are  sometimes  present  in  the  fluid  from  the  bullae.  They  have 
also  been  found  in  the  Pacinian  corpuscles,  in  the  epithelioid  cells  of  the 
cornea,  and  in  theic  interstices,  in  the  difEerent  layers  of  the  vessels,  and  in 
the  lymphatic  glands. 

The  changes  in  the  nerves  are  constant  in  the  anaesthetic  form.  They 
commence  in  the  cutaneous  nerves,  and  then  spread  to  the  nerve  trunks, 
which  become  enormously  enlarged.  The  swelling  of  the  nerves  is  some- 
times regular,  sometimes  uniform.  The  perineurium  is  inflamed,  and 
numerous  bacilli  are  found  in  the  cells  which  occupy  the  interstices.  These 
cells  may,  by  compression,  cause  atrophy  of  the  myelin  sheaths  and  of  the 
axis-cylinders. 

BaciUi  have  been  found  in  the  cells  of  the  seminiferous  tubules,  and  also 
in  the  cells  of  the  bone-marrow.  During  acute  attacks  Hoebna  fomid  them 
in  the  blood. 

As  regards  pathogenesis,  the  following  view  is  generally  adopted :  The 


INFECTIOUS  DISEASES  PROPER  TO  MAN  1831 

bacillus,  entering  by  the  lymphatic  channels,  multiplies  at  first  in  the  skin, 
where  it  forms  nodular  new  growths.  It  then  causes  changes  in  the  nerve 
endings,  and  finally  determines  ascending  iufiammation  of  the  nerve  trunks. 

Diagnosis. — The  diagnosis,  impossible  during  the  period  of  invasion 
and  dithcult  during  the  onset  of  the  disease,  becomes  easy  in  the  stationary 
stage.  The  chief  elements  in  diagnosis  are  :  present  or  former  residence  in  a 
country  where  the  disease  is  prevalent ;  sensory  troubles,  characterized 
especially  by  well-marked  anaesthesia  ;  the  presence  of  nodes  upon  the  ulnar 
nerve  ;  and  especially  the  discovery  of  the  bacillus  in  a  snip,  in  the  blood 
withdrawn  by  cupping,  in  the  serous  exudate  of  a  blister,  or  in  the  excised 
fragments  of  nerves  (Pitres  and  Sabrazes). 

During  the  period  of  onset  the  leprous  patches  may  be  confounded  with 
those  of  vitiligo,  morphoea,  and  mycosis  f  ungoides.  Leprosy  can  be  eliminated 
by  the  fact  that  sensation  is  preserved  in  the  first  case ;  the  discovery  of  the 
lilac  edge  in  the  second,  and  the  coincidence  of  eczematous  or  lichenoid 
eruptions  in  the  third,  will  prevent  error.  Syphilides  and  cutaneous  tuber- 
culosis may  at  first  sight  cause  confusion.  Careful  inquiry  into  the  previous 
history  and  close  examination  of  the  lesions  present  will  speedily  remove  all 
doubt. 

Between  anaesthetic  leprosy  and  Morvan's  disease,  or  syringomyelia,  the 
diagnosis  is  often  a  very  difficult  matter.  Anaesthesia  and  loss  of  the 
phalanges  are  present  in  both  diseases,  and  Zambaco  has  stated  the  identity 
of  the  two  diseases.  The  question  can  only  be  decided  by  repeated  bac- 
teriological examination. 

Sero-diagnosis  of  leprosy,  proposed  by  Spronck,  who  attempted  to  culti- 
vate Hensen's  bacillus,  is  an  interesting  method,  but  its  value  is  not  yet 
confirmed. 

Leprosy  ends  fatally  after  several  years.  Life  is  more  prolonged  in  the 
case  of  the  anaesthetic  form.  Besnier  and  Hallopeau  admit  attenuated 
forms,  characterized  by  simple  macules. 

Treatment. — We  possess  no  efficient  treatment  for  leprosy.  Chaul- 
mugra  oil  given  in  capsules  is  the  remedy  most  often  employed.  Chryso- 
phanic  and  pjTOgallic  acids  and  Guyun's  balsam  are  usually  employed  as 
local  remedies.  It  is  of  some  service  to  cover  the  affected  parts  with  a 
protective  sheath  in  order  to  avoid  the  exciting  action  of  air. 

Sero-Therapy  of  Leprosy — Cytotoxines — Haemolytlc  Serum  {al/jM, 
blood ;  \vaL<;,  dissolution). — Carrasqmlla,  employing  in  man  serum  from 
a  horse  treated  with  blood  from  lepers,  has  seen  diminution  in  the  size  of 
the  tubercles,  cicatrization  of  the  ulcers,  and  improvement  in  the  general 
condition.  Laverde  has  obtained  similar  results  by  employing  serum  from 
goats  treated  by  injections  of  finely  crushed  human  lepromata.  The  sero- 
therapy of  leprosy  has  been  taken  up  by  Metchnikoff.     His  results  are  so 

ilti— 2 


1832  TEXT-BOOK  OF  MEDICINE 

important  that  I  shall  describe  in  detail  his  method,  which  is  based  on  the 
knowledge  of  cytotoxines. 

Cytotoxines,  or  poisons  produced  by  the  cells,  have  attracted  much 
attention  in  the  medical  world.  Their  discovery  dates  from  the  experiments 
made  upon  the  transfusion  of  blood  from  the  mammiferas  to  man.  This 
form  of  transfusion  has  been  followed  by  fatal  results,  attributed  to  the 
solvent  action  of  the  animal  fluids  upon  the  corpuscles  of  hum.an  blood. 
The  phenomenon  is  really  due  to  natural  cytotoxines,  which  have  since  been 
described  by  Daremberg  and  Biichner, 

In  1898  Bordet,  at  the  instigation  of  Metchnikofi,  made  known  the 
first  artificial  cytotoxines.  He  found  that  the  serum  from  one  animal 
injected  into  an  animal  of  another  species  acquires  the  property  of  dis- 
solving the  red  corpuscles  in  the  latter.  Thus,  serum  from  the  guinea-pig 
dissolves  the  red  corpuscles  of  the  rabbit.  This  fact  led  M^tchnikofi  to 
think  that  it  might  be  possible  to  prepare  artificial  cytotoxines  which  would 
be  specific  against  the  corresponding  cells.  The  following  examples  will 
explain  this  idea  : 

If  spermatozoa  from  the  bull  are  injected  into  the  peritoneum  of  the  guinea-pig, 
they  are  digested  and  absorbed  aUve  by  the  white  corpuscles,  microphages,  and  macro- 
phages. A  substance  which  immobihzes  the  spermatozoa  is  formed,  therefore,  in  the 
peritoneal  fluid  and  in  the  blood-serum  of  the  guinea-pig. 

If  an  emulsion  of  a  rabbit's  kidney  is  injected  into  the  guinea-pig,  the  serum  of  the 
latter  becomes  toxic  as  regards  the  kidney  of  the  former,  and  it  is  quite  sufficient  to 
inject  into  the  rabbit  a  httle  of  this  serum  in  order  to  cause  marked  albuminuria  and 
death  from  urfemia.  Post  mortem  necrosis  and  marked  changes  in  the  tubuh  contorti 
are  found.  We  have,  therefore,  a  nephrolytic  serum  {ve(f>p6s,  kidney ;  Awts,  dissolu- 
tion). 

If  ducks  are  injected  with  an  emulsion  from  the  dog's  hver,  we  obtain  a  serum 
which  has  a  markedly  toxic  action  upon  the  hepatic  cells  of  the  dog  ;  injection  of  this 
serum  causes  rapid  death,  with  all  the  signs  of  hepatic  insufficiency  (diminution  of  urea, 
increase  of  ammonia  salts,  aUmentary  glycosuria,  etc.).  We  find  post  morten-  the 
lesions  of  acute  yellow  atrophy  of  the  liver  or  of  phosphorus-poisoning,  so  that  we  have 
here  a  true  hepatolytie  serum  [rj-irap,  hver  ;  Xilcns,  dissolution). 

Lastly,  if  an  emulsion  of  a  rat's  spleen  is  injected  under  the  skin  of  a  guinea-pig,  we 
obtain  a  serum  which  dissolves  the  leucocytes  of  the  rat  (Metchnikoff).  It  was  there- 
fore  reasonable  to  hope  that  the  macrophages  might  alone  be  destroyed,  without  injury 
to  the  microphages,  and  there  were  visions  of  the  possibihty  of  removing  the  macro- 
phages which  produce  fibrous  tissue,  and  perhaps  of  being  able  to  delay  the  appearance 
of  senile  atrophy  (Metchnikoff).  The  antiphagocytic  serum,  however,  destroys  all  the 
white  corpuscles  without  making  any  distinction. 

All  these  cytotoxines  are  specific.  They  dissolve  only  the  cells  which 
give  rise  to  them.  Thus,  nephrolytic  serum  attacks  the  kidney,  and  spares 
the  other  organs  ;  hepatolytie  serum  attacks  the  liver,  etc. 

The  application  of  hsemolytic  serum  in  man  depends  on  the  very  curious 
fact  that  cytotoxines  in  weak  doses  are  capable  of  producing  a  stimulating 
action  upon  tlie  corresponding  cells  (Metchnikofi).    Small  doses  of  hsemo- 


INFECTIOUS  DISEASES  PROPEn  TO  ^fAN■  1833 

lytic  serum  prepared  by  inoculation  of  rabbit's  blood  into  the  peritoneum 
of  the  guinea-pjfj  increase  the  number  of  corpuscles  and  tlie  quantity  of 
ha^noglobin  in  the  rabbit  (Cantacuzene).  Small  doses  of  leucocvtic  serum 
prepared  by  the  inoculation  of  an  emulsion  from  the  mesenteric  glands  of 
the  rabbit  into  the  peritoneum  of  the  guinea-pig  produce  in  the  former 
animal  a  marked  hyperleucocytosis  (Besredka). 

Metchnikoff  made  the  first  experiments  with  hsemolytic  senun  on  man, 
because  he  was  convinced  that  the  improvement  seen  in  the  treatment  of 
lepers  by  injections  of  Carrasquilla's  and  Laverde's  serum  must  be  attri- 
buted, "  not  to  some  products  of  Hansen's  bacillus,  but  to  the  cytotoxines 
developed  in  the  animal  organism  after  injections  of  blood  or  of  human 
tissues."  He  chose  lepers  from  the  St.  Louis  Hospital,  and  inoculated 
them  with  very  small  doses  of  haemoh'tic  serum  prepared  by  the  injection 
of  defibrinated  human  blood  into  the  goat.  These  injections,  given  only  in 
stimulating,  and  not  in  solvent,  doses,  in  every  case  brought  about  an 
increase  in  hsematopoiesis  and  in  the  haemoglobin. 

The  results  upon  leprous  lesions  have  not  been  as  weU  marked  as  the 
results  obtained  by  Carrasquilla  and  Laverde,  but  Metchnikoff  hopes  for 
improvement  by  employing  leucoc}i;ic,  and  not  hajmoh-tic,  senim.  In  anv 
case,  these  facts  prove  that  small  doses  of  cytotoxines  produce  hyper- 
activity of  the  corresponding  cells,  and  open  up  new  ^^stas  in  the  treat- 
ment of  the  ansemias.  It  is  not  rash  to  state  that  the  employment  of  small 
doses  of  cytotoxines  in  diseases  of  different  organs  may  be  a  new  departure 
in  therapeutics. 


CHAPTER  IV 
INFECTIOUS  DISEASES  COMMON  TO  MAN  AND  TO  ANIMALS 

I.  RABIES; 

iEtiology. — Rabies  in  man  does  not  develop  spontaneously.  It  is  always 
preceded  by  the  bite  of  rabid  animals  (dog,  wolf,  cat).  Many  people,  how- 
ever, are  bitten  by  a  rabid  animal  without  rabies  resulting,  because  they 
are  not  all  in  the  same  state  of  receptivity  ;  and,  moreover,  bites  upon  parts 
covered  by  clothing  are  much  less  dangerous  than  those  upon  the  hands  or 
upon  the  face. 

Up  to  1881  it  was  known  that  rabies  was  a  contagious  disease  usually 
communicated  from  one  animal  to  another  by  means  of  bites,  and  especially 
afEecting  dogs,  ruminants,  camivora,  rabbits,  and  guinea-pigs.  It  probably 
never  developed  spontaneously ;  it  appeared  after  a  variable  period  of 
incubation,  and  often  ended  in  death. 

Pasteur  has  succeeded  in  changing  this  gloomy  prognosis  by  his  excellent 
work  on  antirabic  vaccination.  I  shall  rapidly  sketch  the  various  stages 
which  have  led  to  this  marvellous  result. 

The  nervous  symptoms  are  so  constant  in  individuals  suffering  from 
rabies  that  the  attention  of  pathologists  had  long  been  fixed  upon  the  nerve 
centres,  though  without  much  result.  Duboue  had  put  forward  the  theory 
that  the  poison  reached  the  spinal  cord  by  way  of  the  nerves,  and  then 
involved  the  bulb ;  Jaccoud  had  placed  the  receptacle  of  the  poison  in  the 
mesencephalon ;  but  these  statements  were  not  sustained  by  any  experi- 
mental proofs.  Pasteur  conceived  the  idea  of  injecting  dogs  with  the 
diseased  spinal  cord,  which  had  been  diluted  in  sterile  broth.  When  injec- 
tions were  made  in  the  subcutaneous  cellular  tissue,  the  period  of  incuba- 
tion was  long  and  uncertain ;  when,  on  the  other  hand,  they  were  made 
under  the  dura  mater,  after  previous  trephining,  the  duration  was  shorter, 
and  the  animals  took  the  disease  within  a  definite  time. 

Seeking  for  a  convenient  and  expeditious  method  of  procedure,  he 
conceived  the  idea  of  comparing  the  virulence  of  spinal  cords  taken  from 
various  animals,  and  was  thus  able  to  prove  that  the  spinal  cord  of  a  monkey 
was  less  virulent  than  that  of  a  dog,  which,  again,  was  less  virulent  than 

1834 


INFECTIOUS  DISEASES  COMMON  TO  MAN  AND  ANIMALS    18J^r. 

the  cord  from  a  rabbit.  He  showed  also  that  the  vinilence  increased  in 
proportion  as  the  poison  passed  from  one  rabbit  to  another,  and  that  it 
diminished  in  proportion  as  it  passed  from  one  monkey  to  another.  The 
\'inilence  remained  stationary  in  each  series  after  reaching  a  certain 
point. 

Pasteur  thus  obtained  two  poisons,  the  one  attenuated  and  the  other 
exalted,  which  he  employed  fof  the  inoculation  of  dogs.  He  commenced 
by  inoculating  them  with  the  most  feeble  virus,  and  progressively  increased 
the  virulence  until  the  most  active  poison  was  inoculated. 

The  dogs  thus  prepared  were  brought  in  contact  with  dogs  suffering 
from  furious  rabies.  Though  bitten  on  several  occasions,  they  did  not  take 
the  disease  against  which  they  had  been  vaccinated.  These  experiments 
were  performed  before  a  Commission  nominated  by  the  Ministre  de  1' Instruc- 
tion Publique,  and  the  results  announced  by  Pasteur  were  confirmed. 

Pasteur  shortly  afterwards  discovered  another  method  of  antirabic 
vaccination,  which  was  simpler  and  quite  as  certain.  It  is  based  upon 
the  attenuation  of  the  \'irus  in  the  spinal  cords  of  rabbits  by  the  aid  of 
desiccation.  The  activity  of  the  virus  is  completely  destroyed  by  this 
procedure  at  the  end  of  a  fortnight,  but  this  attenuation  takes  place  pro- 
gressively, so  that  the  virulence  varies  inversely  as  the  time  of  desiccation. 
Pasteur  used  for  inoculation  cords  of  successively  greater  virulence,  and 
succeeded  in  rendering  a  series  of  dogs  absolutely  refractory  to  rabies. 

Such  was  the  condition  of  affairs  when  a  young  man  named  Meister, 
who  was  terribly  bitten  and  doomed  to  almost  certain  death,  came  to  Paris. 
Pasteur,  in  conjunction  with  Vulpian  and  Grancher,  treated  him  with  a 
series  of  subcutaneous  injections  from  rabid  cords  of  progressively  increasing 
virulence,  with  the  result  that  he  felt  no  inconvenience,  and  rabies  did  not 
develop. 

Numerous  individuals  bitten  by  rabid  animals  proceeded  to  Paris, 
attracted  there  by  the  hope  of  a  radical  cure. 

Some  failures  occurred,  especially  in  those  bitten  by  wolves,  and  it  was 
conclusively  proved  that  rabies  in  the  wolf  is  more  virulent  than  in  the 
dog,  and  that  the  most  active  treatment  must  be  employed  against  it. 
The  intensive  method  was  then  created. 

According  to  the  statistics  of  the  Institut  Pasteur,  the  mortality  from 
the  bite  of  rabid  dogs,  which  was  formerly  14  per  cent.,  fell  between  1886 
and  1889  to  0-67  per  cent.,  in  1890  to  0-57  per  cent.,  and  in  1892  to  0-22  per 
cent.  Between  1886  and  1899  23,245  bitten  persons  were  treated  at  the 
Institut  Pasteur,  with  a  total  mortality  of  103,  or  0'44  per  cent.  The 
mortality  following  bites  of  rabid  wolves  has  fallen  from  60  to  14  per  cent. 
(Dumesnil). 

From  the  present-day  knowledge  of  rabies,  of  its  course  and  propagation, 


1836  TEXT-BOOK  OF  MEDICINE 

and  the  attenuation  of  the  poison,  there  is  no  doubt  that  the  disease  is  a 
microbic  one,  although  the  special  micro-organism  is  as  yet  unknown. 

Eoux,  Bouchard,  and  Gibier  have  seen  extremely  fine  points  in  the 
tissue  of  the  spinal  cord,  bulb,  and  nerves.  Hermann  FoU  has  given  a 
description  of  this  microbe,  but  at  present  it  has  been  neither  isolated  nor 
cultivated. 

Description. — The  incubation  period  of  rabies  is  extremely  variable. 
Its  usual  duration  is  from  three  to  eight  weeks,  but  authentic  cases  have 
been  quoted  in  which  the  incubation  period  was  more  than  eighteen  months. 

Some  importance  has  been  given  to  the  presence  of  elliptical  vesicles 
which  develop  at  times  on  the  sides  of  the  frsenum  linguse,  but  these  vesicles,' 
called  lyssae  {\vcrcra,  rabies),  do  not  possess  the  properties  attributed  to 
them. 

After  its  incubation  period,  rabies  is  ushered  in  by  a  prodromal  stage, 
characterized  by  a  tendency  to  melancholia.  Patients  are  sad  and  depressed, 
even  though  they  are  ignorant  of  the  danger  which  threatens  them.  Those 
who  understand  the  situation  sufier  from  intense  restlessness,  with  insoronia, 
nightmare,  and  alternate  excitement  and  depression.  These  prodromata 
are  absent  in  some  cases,  and  the  disease  appears  suddenly,  with  the  fol- 
lowing symptoms  : 

The  patient  suffers  from  extreme  hypersesthesia,  so  that  light,  the  least 
noise,  and  smeUs  cause  much  distress.  Satyriasis  is  seen  in  some  cases. 
The  chief  symptom  is  hydrophobia,  which  does  not  mean  that  the  patient 
is  afraid  of  water,  as  the  term  would  appear  to  convey,  but  the  least  attempt 
at  swallowing  produces  such  painful  spasms  that  the  unhappy  patient 
prefers  the  torments  of  thirst  to  the  terrible  sense  of  strangulation  and 
suffocation  caused  by  the  laryngo-pharyngeal  spasm.  The  spasms  are 
sometimes  brought  on  by  the  sight  of  water  or  of  a  shining  object.  The 
saliva  is  instantly  spat  out  in  order  to  avoid  the  least  movement  of  swal- 
lowing. 

Later,  these  laryngo-pharyngeal  spasms  appear  spontaneously  in  the 
form  of  paroxysms.  Shivering  fits,  horripilations,  epileptiform  and  tetani- 
f orm  contractions  are  also  seen.  The  attacks,  which  are  exceedingly  painful, 
become  longer  and  more  numerous  ;  the  remissions  are  shorter  and  less 
frequent.  The  patient  is  a  prey  to  terror  between  the  attacks.  Attacks 
of  mania  or  ideas  of  suicide  are  sometimes  present,  but  the  affected  person 
has  no  tendency  to  bite  those  around  him,  contrary  to  the  common  belief. 
The  temperature  during  the  attack  rises  to  106°  F.,  and  may  remain  high 
after  death  (Peter). 

This  stage  usually  lasts  about  two  days.  The  next  stage — that  of 
paralysis  or  of  asphyxia — only  lasts  a  few  hours.  It  is  characterized  by 
a  loss  of  strength,  which  leads  to  collapse  and  death,  though  the  end  may 


INFECTIOUS  DISEASES  COMMON  TO  MAN  AND  ANIMALS    1837 

also  occur  diirinc;  the  precefliiijr  period  from  siifTocation.  In  some  cases 
the  course  of  rabies  appears  to  be  checked  for  a  few  days,  and  the  disease 
shows  several  successive  attacks. 

The  diagnosis  of  rabies  must  be  made  from  diseases  such  as  hysteria  or 
mental  alienation,  in  which  hydrophobia  may  be  present.  In  delirium 
tremens  the  dysphagia  and  spitting  are  not  accompanied  by  the  charac- 
teristic lar}Tigo-pharyngeal  spasms  of  rabies.  The  diagnosis  can  be  readily 
made  in  the  suspected  animal  by  histological  examination  of  the  spinal 
cord,  of  the  bulb  and  of  the  peripheral  cerebro-spinal  and  sympathetic 
ganglia.  The  spinal  cord  and  the  bulb  (Babes),  as  well  as  the  ganglia  (van 
Gehuchten),  show  nodules,  which  appear  to  be  characteristic  of  rabies. 
It  is  preferable,  however,  to  perform  intracerebral  inoculation  with  the 
nerve  tissue  from  the  suspected  animals. 

Pathological  anatomy  shows  but  few  changes.  The  congestion  of 
organs  (lung  and  meninges)  is  consecutive  to  the  convulsions  and  to  the 
respiratory  distress.  Some  writers  have  noted  a  granular  condition  and 
diffuse  myelitis  of  the  spinal  cord. 

Prophylactic  treatment  consists  in  immediately  destroying  any  rabid 
animal,  and  in  keeping  any  animal  suspected  of  rabies  in  close  confinement 
for  observation  purposes. 

The  following  measures  should  be  employed  for  an  individual  who  has 
been  bitten  by  a  mad  dog  :  The  wound  should  be  cleansed  with  especial 
care,  and  vigorously  cauterized  with  the  actual  cautery.  These  measures 
should  be  carried  out  as  quickly  as  possible.  The  mortality  in  wounds 
which  had  not  been  cauterized  was  84"84  per  cent.,  but  it  was  only  31'34: 
per  cent,  in  those  which  had  been  burnt  (Bouley).  Pasteur's  method  of 
treatment  by  vaccination  has  been  described  at  the  commencement  of  this 
section. 

II.  ANTHEAX. 

Bacteriology. — The  early  work  of  Pasteur  on  fermentation  led  Davaine 
to  ask  whether  the  disease,  studied  by  Chabert  from  the  symptomatic  point 
of  view,  was  not  produced  by  the  presence  of  a  low  form  of  organism  in  the 
blood.  Davaine,  in  his  early  researches  (1852),  noticed  the  presence  of  small 
transparent  rods,  which  he  called  bacteridia,  in  the  blood  of  infected  animals, 
and  he  established  a  causal  relation  between  the  existence  of  these  bacteridia 
and  the  development  of  anthrax. 

Some  years  later  Pollender  (1855)  and  BraueU  (1857)  confirmed  this  dis- 
covery, and  the  latter  deserves  the  honour  of  first  observing  the  bacillus  of 
anthrax  in  man.  Davaine  showed  that  inoculation  of  infected  blood,  even 
in  very  small  doses,  gives  rise  to  the  same  affection,  and  the  idea  of  contagion 
was  thus  experimentally  established. 


1838  TEXT-BOOK  OF  MEDICINE 

The  pathogenic  history  of  anthrax,  however,  did  not  advance  until 
Pasteur  and  Koch,  profiting  by  the  previously  acquired  knowledge  as  to 
the  microbic  nature  of  this  disease,  undertook  the  study  of  anthrax.  The 
results  obtained  by  these  two  observers  have  been  far  more  important 
than  was  at  first  supposed  ;  they  have  served  as  the  basis  for  the  bacterio- 
logical study  of  the  infectious  diseases. 

In  the  blood  the  bacteridia  form  short  rods,  with  clearly  marked  breaks ; 
in  broth  cultures  they  appear  in  the  form  of  long,  interwoven  filaments. 
The  bacilli  are  single,  or  are  placed  end  to  end  in  pairs  or  in  triplets.  Each 
bacillus  is  rectUinear,  flexible,  cylindrical,  and  immobile,  with  a  clearly- 
marked  fracture.  The  cement  substance  which  joins  the  bacillus  in  pairs 
(diplo-bacilli)  or  in  chains  (strepto-bacUli)  is  loose  and  incomplete. 

If  a  culture  is  made  upon  any  sort  of  nutritive  broth,  the  bacilli,  after 
some  hours  in  the  oven,  assume  the  form  of  very  long  and  much  interwoven 
filaments.     These  filaments  are  cylindrical,  wavy,  and  very  flexible. 

They  never  show  any  branches,  and  though  they  appear  to  be  long  and 
homogeneous,  they  are  reaUy  composed  of  a  series  of  bacilli,  placed  end  to 
end,  and  separated  from  one  another  by  clear  spaces,  remaining  unstained 
and  indicating  the  division  between  the  elements.  The  filaments  are  im- 
mobile, like  the  bacilli ;  they  stain  well  with  aniline  dyes,  and  in  cultures 
which  are  twenty-four  to  forty-eight  hours  old  they  show  spores. 

The  spores  do  not  appear  as  long  as  the  germ  is  in  living  blood.  After 
forty-eight  hours  on  a  culture  medium  ovoid  granules  are  seen  at  the  centre 
of  each  small  segment  of  the  filament.  The  bacteridium  arises  from  the 
spore,  which  often  passes  unnoticed,  so  that  the  blood  of  an  infected  animal 
may  at  first  sight  appear  to  be  free  from  infective  elements,  when  in  reality 
it  contains  them. 

Cultures  on  gelatine  plates  at  a  temperature  of  from  15°  to  20°  C.  yield 
sinuous  colonies,  which  after  thirty-six  hours  (magnification  of  60  diameters) 
resemble  a  cluster  of  threads,  and  after  three  to  four  days  the  lashes  of  a 
whip. 

The  bacteridia  are  found  in  the  blood,  in  the  lymph,  in  the  urine,  and, 
indeed,  in  aU  the  fluids  of  the  body.  They  are  essentially  aerobic — that  is 
to  say,  they  absorb  oxygen  readily  whenever  they  come  in  contact  with  it. 
The  blood  thus  deoxygenated  assumes  a  brownish  colour,  which  gives  a 
cyanotic  tint  to  the  tissues. 

The  bacteridia  are  very  easily  cultivated,  providing  the  experimental 
media  are  kept  at  a  temperature  of  about  40°  C.  They  no  longer  multiply 
below  12°  and  above  45°  C.  In  solutions  of  glycerinated  peptone  they 
produce  a  toxine  which  may  prove  fatal  to  animals  (Marmier). 

Pathogenesis. — The  spores  are  very  resistant  and  preserve  their  infective 
properties  for  some  years,  and  they  are  usually  the  cause  of  the  infection. 


INFECTIOUS  DISEASES  COMMON  TO  MAN  AND  ANIMALS    1839 

Animals  are  infected  from  the  corpses  of  dead  animals  buried  in  the  earth 
and  from  the  fluids  which  may  have  escaped  from  the  body  before  burial. 
In  fields  where  the  burials  have  taken  place  earthworms  bring  to  the  surface 
particles  of  earth  loaded  with  bacteridia  and  spores,  which  are  spread  over 
the  pasture  lands.  The  persistence  of  anthrax. in  an  endemic  state  in 
les  chamfs  maudits,  as  well  as  the  possibility  of  apparontly  spontaneous 
epidemics,  are  thus  explained.  The  germs  enter  in  animals  through  small 
wounds  of  the  throat  caused  by  the  leaves  of  dried  thistles,  by  the  beards 
on  the  ears  of  barley,  by  the  dried  leaves  of  almond  trees,  and  also  by  the 
introduction  of  the  elements  of  contagion  into  the  digestive  tube.  This 
mode  of  contagion  is  very  rare  in  man  and  has  even  been  denied,  but  yet 
undoubted  examples  exist  (Bouisson).  Inoculation  in  man  usually  occurs 
through  a  scratch  upon  the  skin. 

It  was  long  held,  as  the  residt  of  Brauell-Davaine's  opinion,  that  the 
bacteridia  of  anthrax  do  not  pass  through  the  placenta,  but  this  is  not  so, 
as  Straus  and  Chamberland  have  proved. 

Let  me  also  mention  that  in  chicken  cholera  Pasteur  employed  the 
bacteridia  of  anthrax  in  order  to  study  the  attenuation  of  the  virus  and 
the  preventive  vaccination  of  infectious  diseases.  This  attenuation  of  the 
vims  in  anthrax  is  everywhere  admitted,  although  it  was  at  first  rejected  by 
Koch,  and  vaccination  against  anthrax  has  for  several  years  been  performed 
by  the  farming  community  in  numerous  countries. 

In  the  study  of  anthrax  it  is  important  to  distinguish  the  disease  which 
Chabert  had  described  under  the  name  of  symptomatic  anthrax.  Arloing, 
Comevin,  and  Thomas  have  shown  that  the  latter  is  quite  a  distinct 
disease. 

Malignant  pustule,  malignant  anthrax,  and  malignant  oedema  may  be 
united  in  a  single  description  as  manifestations  of  the  same  disease. 

Anthrax  is  particularly  common  in  sheep  (blood  of  the  spleen),  bullocks, 
goats,  and  horses,  but  here  I  shall  describe  only  the  disease  in  the  human 
race.  Anthrax  is  transmitted  from  animals  to  man  in  many  ways.  Farmers 
and  shepherds  who  look  after  infected  animals,  butchers  who  skin  them, 
and  knackers  are  more  liable  than  others  to  contract  anthrax.  The  dried 
hides  of  infected  animals,  the  skins,  the  wool,  and  the  hairs  may  harbour 
the  infection  for  years,  so  that  tanners,  workmen  who  handle  skins, 
dressers  and  curriers,  and  mattress  carders  are  especially  liable  to  con- 
tract the  disease.  I  may  quote  the  following  examples  :  A  young  woman 
who  had  worked  for  six  weeks  in  a  hair  factory  was  pricked  by  a  hair  in  the 
right  cheek ;  a  malignant  pustule  developed,  and  death  followed  in  a  few 
days  (Straus).  A  malignant  pustule  ended  fatally  in  an  individual  whose 
work  was  to  pull  the  old  hair  stufl&ng  out  of  cushions  in  the  railway  carriages 
(Orth).     These  cases  prove  that  the  spores  which  reproduce  the  bacteridium 


1840  TEXT-BOOK  OF  MEDICINE 

are  endowed  with  great  resistance  to  changes  of  temperature  and  to  desicca- 
tion (Pasteur). 

The  transmission  of  the  poison  also  takes  place  indirectly,  and  flies  may 
carry  and  deposit  it. 

In  the  cases  above  qu,oted  the  anthrax  entered  the  economy  by  a  breach 
of  surface,  and  a  chafe  or  a  wound  of  the  skin  was  always  present.  This 
mode  of  entrance,  which  is  the  rule  in  human  beings,  is  exceptional  in 
animals.  The  latter  are  especially  subject  to  internal  or  spontaneous 
anthrax.  They  become  infected  after  eating  food  (sainfoin,  maize)  im- 
pregnated with  spores  or  after  feeding  in  fields  where  infected  animals  have 
been  buried.  Experiments  have  been  undertaken  in  order  to  elucidate  the 
question  of  this  so-called  spontaneous  anthrax,  and  it  has  been  found  that 
foods  soaked  in  fluid  containing  bacteria  are  more  likely  to  cause  anthrax 
if  the  beards  of  barley  or  of  thistles  are  added,  because  these  plants  are 
capable  of  causing  wounds  and  abrasions  of  the  digestive  tract. 

Whatever  theory  we  may  adopt,  anthrax  of  external  origin  is  the  rule 
in  man,  while  that  of  internal  origin  is  the  rule  in  animals.  The  latter  form 
has  so  far  been  seen  only  in  a  few  rope-makers  (Wagner),  in  a  leather- 
dresser  (Bouisson),  and  in  certain  cases  of  pulmonary  or  of  gastric  anthrax. 
In  every  case  the  spores  are  absorbed  together  with  the  dust  in  which  they 
are  contained  (Bouisson),  thus  allowing  them  to  escape  the  noxious  action 
of  the  gastric  juice. 

Description. — After  the  poison  has  been  introduced  into  the  economy 
the  disease  shows  an  incubation  which  varies  from  a  few  hours  to  six  days. 
In  nearly  every  case  (I  speak  of  man)  the  malignant  pustule  is  the  first 
manifestation,  and  precedes  the  general  symptoms.  Intense  itching  com- 
mences at  the  point  of  inoculation,  followed  by  the  appearance  of  a  vesicle. 
This  vesicle  has  the  appearance  of  a  small  phlyctena  or  pustule,  and  bursts, 
leaving  in  its  place  an  ulcer  with  a  livid  or  with  a  blackish  base,  which  is 
sometimes  covered  by  a  smaU  eschar.  The  scab  is  usually  only  a  few  milli- 
metres in  diameter.  The  cellular  tissue  beneath  it  is  indurated,  and  an 
inflammatory  areola,  studded  with  small  vesicles,  develops  at  the  periphery. 
The  neighbouring  tissues  are  swoUen  and  oedematous ;  the  oedema  in 
anthrax  sometimes  extends  to  a  great  distance.  In  some  cases  lymphangitis 
is  seen,  and  the  neighbouring  glands  are  swollen.  The  above  description 
pertains  to  the  malignant  pustule  ;  it  is  not  painful,  and  has  its  seat  of 
election  upon  the  face,  the  neck,  or  the  hands — that  is  to  say,  upon  the 
uncovered  parts. 

The  local  lesion  does  not  always  present  the  foregoing  appearance. 
The  charhon  is  only  a  malignant  pustule  in  which  the  dark  and  bulky  eschar 
is  surrounded  by  a  highly  coloured  areola. 

A  true  pustule  is  not  present  in  some  cases  ;  we  may  see  simply  an 


INFECTIOUS  DISEASES  COMMON  TO  MAN  AND  ANIMALS    1841 

abrasion  of  tho  Hkin.  with  dilTuse  redness,  swellini,'.  and  lymphangitis.  In 
otlior  oases  the  oedema  is  the  ehief  feature  (malignant  oedema),  and  the 
pustule  passes  practically  unnoti(;ed,  or  may  even  be  absent  (malignant 
cedenui  of  the  evelids). 

The  general  symptoms  ajjpcar  within  one  to  three  days  after  the 
appearance  of  the  pustule  ;  nausea  and  vomiting  are  sometimes  present, 
the  face  is  covered  with  sweat,  the  pulse  is  small  and  irregular,  the  patient 
complains  of  prostration,  and  in  some  cases  the  temperature  is  raised. 
The  clinical  picture  is  characterized  by  prostration,  dyspnoea,  asphyxia, 
cyanosis,  and  anaesthesia,  and  the  patient  dies  in  an  adynamic  condition. 
The  general  symptoms  may  precede  or  may  accompany  the  appearance  of 
the  malignant  pustule  in  exceptional  cases. 

Pulmonary  anthrax  nearly  always  commences  suddenly  with  rigors, 
headache,  vertigo,  vomiting,  and  pains  in  the  side  or  in  the  epigastrium. 
The  cyanosis  is  very  marked,  and  is  accompanied  by  acute  dyspnoea  ;  the 
pulse  is  small,  rapid,  and  irregular.  Auscultation  at  first  reveals  only  moist 
rales,  but  pleuro-pulmonary  signs  soon  appear,  indicating  an  effusion,  which 
is  often  bilateral.  The  temperature,  which  may  be  as  high  as  104°  F.  at 
the  onset,  falls  progressively  to  subnormal  by  the  third  day.  The  sputum 
is  bloodstained  and  swarms  with  bacilli.  The  disease  runs  a  very  rapid 
course,  and  death  occurs  between  the  third  and  sixth  days  (Schottmuller). 

Anthrax  of  the  tongue  presents  the  general  characters  of  the  disease. 
The  tongue,  which  is  ulcerated  at  one  point,  much  swollen,  and  of  a  li\ad 
colour,  protrudes  from  the  mouth,  and  is  locked  between  the  teeth.  The 
tonsils,  the  uvula,  the  velum  palati,  the  floor  of  the  mouth,  and  the  face  are 
enormously  swollen.  The  bacilli  are  found  in  the  ulcerated  parts.  The 
affection,  although  very  serious,  may  end  in  recovery  (Rammstedt). 

Intestinal  anthrax  very  closely  resembles  cholera.  The  chief  symptoms 
are  cyanosis,  asphyxia,  vomiting,  and  diarrhoea.  Cramps  appear,  the  urine 
is  suppressed,  and  the  patient  dies  in  an  algid  condition  (Bouisson).  Anthrax 
of  the  stomach  presents  practically  the  same  symptoms ;  it  is  often  found 
as  a  surprise  at  the  autopsy  (Nebolioubov). 

The  diagnosis  of  the  malignant  pustule  is  based  upon  the  signs  alreadv 
enumerated.  The  pustule  is  not  painful  and  does  not  suppurate,  while  the 
bacteridia  are  found  both  in  the  pustule  and  in  the  serous  effusioii  of  the 
neighbouring  tissue.  These  signs  constitute  the  points  of  difference  between 
anthrax  and  boils,  carbuncles  and  wasp-stings.  The  diagnosis  is  more 
difficult  when  the  pustule  is  ill-developed  and  the  oedema  is  the  chief  lesion, 
and  careful  inquiry  must  therefore  be  made  as  to  the  patient's  occupation. 

The  prognosis  is  very  grave.  Anthrax,  when  untreated,  is  nearly  always 
fatal.  Death  supervenes  between  the  second  and  fourth  days,  sometimes 
even  within  twenty -four  hours. 


1842  TEXT-BOOK  OF  MEDICIKE 

Pathological  Anatomy. — The  pustule  and  the  surrounding  oedematous 
tissue  are  poor  in  leucocytes  ;  we  know  also  that  the  malignant  pustule  has 
no  tendency  to  suppurate,  but  that  the  chief  lesion  in  the  oedematous  tissue 
is  an  excess  of  coagulable  lymph.  The  bacteridia  are  not  found  in  uniform 
numbers  in  all  the  organs ;  the  malignant  pustule,  which  is  the  initial  seat 
of  the  disease,  and  the  gelatiniform  oedema  which  surrounds  the  pustule, 
contain  but  few  bacUli,  while  the  neighbouring  lymphatic  glands,  which 
communicate  directly  with  the  seat  of  the  primary  infection,  are  swollen 
and  hypersemic,  and  their  sinuses  and  follicles  are  packed  with  bacilli.  The 
infective  germ  jfinds  in  their  tissue  its  first  centre  for  multiplication,  and  its 
progress  is  for  a  moment  retarded  by  them  (Toussaint). 

The  mucous  membrane  of  the  stomach  and  of  the  intestine  presents 
prominent  ecchymotic  patches,  which  are  usually  situated  on  the  free 
edge  of  the  valvulse  conniventes  of  the  smaU  intestine.  The  tissue  of  the 
villi,  the  submucous  connective  tissue,  the  bundles  of  the  muscular  coat, 
and  the  subserous  cellular  layer  are  infiltrated  by  the  baciUi.  A  similar 
condition  is  found  in  the  coats  of  the  stomach. 

In  the  spleen,  liver,  kidneys,  pancreas,  breast,  and  salivary  glands  the 
bacilli  are  distributed  in  and  remain  confined  to  the  capillary  vessels,  and, 
accordingly,  the  cells  of  the  liver  and  the  canaliculi  of  the  kidney,  together 
with  the  tubuli  recti  and  tubuli  contorti,  are  unafiected,  while  the  capillary 
vessels  and  the  glomeruli  are  invaded.  The  blood,  both  before  and  after  death, 
presents  special  characters  :  the  red  corpuscles  agglutinate,  and  have  little 
tendency  to  form  rouleaux,  the  white  corpuscles  are  exceedingly  numerous, 
and  the  bacteria,  in  more  or  less  large  numbers,  are  found  in  the  serum. 

Treatment. — The  prophylactic  measures  consist  in  the  destruction  and 
the  deep  burial  of  infected  animals. 

The  pustule  in  man  must  be  promptly  treated  by  injections  around  the 
pustule,  and  for  this  purpose  a  solution  of  50  per  cent,  carbolic  acid  or  a 
solution  of  iodine  may  be  employed.  The  pustule  is  cauterized,  either  by 
the  thermocautery  or  with  sublimate  of  mercury. 

Serum,  which  is  preventive  and  curative  in  experimental  anthrax  (Mar- 
choux),  may  perhaps  be  of  service  in  man. 

III.  GLANDEKS— FAECY. 

Glanders  is  an  infectious  disease  fairly  common  in  ungulate  animals 
(horse,  ass,  mule),  and  transmissible  from  man  to  animals,  from  animals  to 
man,  and  from  man  to  man.  Farcy,  formerly  described  as  a  separate 
disease,  should  be  included  under  glanders. 

Bacteriology. — Glanders  is  a  microbio  disease.  The  bacillus,  which 
was  discovered  at  the  same  time  by  Bouchar,  Capitan  and  Charrin,  and  by 


INFECTIOUS  DISEASES  COMMON  TO  MAN  AND  ANIMALS    1843 

Loffler  and  Schiily,  presents  the  form  of  a  small  rod,  with  straii^'ht  or  Rlip^htly 
curved,  rounded  ends ;  it  is  a  little  thicker  than  the  tubercle  bacilluw,  to 
which  it  bears  a  close  resemblance.  It  grows  well  on  the  ordinary  culture 
media,  but  the  growth  on  potato  is  characteristic.  The  culture,  after  three 
days  in  the  oven  at  37*^  C,  assumes  an  amber  colour,  and  during  the  next 
few  days  a  reddish  colour,  with  greenish-l)lue  edges — a  feature  not  seen  in  the 
cultures  of  any  other  microbe. 

The  virulence  of  the  cultures  is  not  great ;  it  becomes  attenuated  on 
exposure  to  the  air  for  a  few  days  ;  in  vacuo  it  may  last  for  three  or  foui 
months  (Loffler,  Sanarelli).  Of  animals,  the  donkey,  the  mule,  the  horse 
and  the  guinea-pig  are  the  most  sensitive  to  inoculation.  Li  the  male 
guinea-pig  we  find,  after  two  or  three  days,  enormous  swelling  of  the  testes, 
which  is  of  use  in  the  early  diagnosis  of  glanders  (Straus).  The  early 
diagnosis  can  also  be  made  in  suspected  animals  by  the  injection  of  mallein, 
which  is  a  soluble  product  of  the  cultures  of  the  bacillus.  Mallein  has  as  great 
a  diagnostic  importance  in  glanders  as  tuberculin  has  in  tuberculosis 
(Nocard). 

etiology. — Transmission  from  animals  to  man  takes  place  by  inocula- 
tion or  by  infection.  The  nasal  discharge  in  animals  and  the  secretion  from 
the  farcy  buds  or  ulcers  may  impregnate  the  straw  or  the  blankets,  and 
become  a  powerful  agent  of  contagion. 

Inoculation  requires  a  scratch  or  an  abrasion  of  the  skin  or  of  the  mucous 
membranes.  Stablemen  become  inoculated  with  the  disease  from  the 
straw,  the  blankets,  and  the  bandages  soiled  by  the  nasal  discharge  of  the 
glandered  horses.  The  secretion  of  the  farcy  buds  or  ulcers,  and  the  skin 
and  hides  of  animals  which  have  died  from  glanders,  contain  the  bacillus. 
Indirect  transmission  probably  takes  place  by  absorption  of  the  dried  nasal 
discharge. 

Description. — In  man  glanders  is  usually  acute,  and  farcy  is  more  often 
chronic. 

Let  us  first  study  acute  glanders.  In  some  cases,  after  an  incubation 
which  varies  from  two  to  eight  days,  the  disease  commences  with  lymphan- 
gitis, adenitis,  and  diffuse  inflammation,  which  correspond  to  the  seat  of 
inoculation,  and  are  often  found  on  the  hands  or  on  the  feet.  The  disease, 
however,  more  usually  begins  with  general  symptoms,  like  those  of  acute 
septicaemia.  The  patient  is  seized  with  a  rigor,  fever,  headache,  vomiting, 
and  pains  in  the  muscles  and  joints,  which  at  first  sight  resemble  rheuma- 
tism. Erythematous  patches  soon  appear  on  the  face  and  in  the  neighbour- 
hood of  the  joints  ;  they  take  on  a  livid  tint,  and  are  converted  into  blebs, 
with  a  tendency  to  sloughing.  A  pustular  eruption,  which  is  generally 
discrete,  appears  on  the  face  about  the  twelfth  day  (Rayer) ;  it  may  spread 
to  the  trunk,  the  limbs,  and  the  respiratory  tract. 


1844  TEXT-BOOK  OF  MEDICINE 

Before  or  at  the  same  time  as  this  eruption,  ulcers,  with  foetid  discharge 
of  blood  and  of  mucus  similar  to  that  seen  in  horses,  may  develop  in  the 
nasal  fossae.  The  enlargement  of  the  maxillary  glands,  which  is  almost  con- 
stant in  horses  (glandage),  is  wanting  in  man.  As  the  eruption  afiects 
various  parts  it  may  cause  dysphagia,  dyspnoea,  cough,  and  expectoration 
of  blood-stained  sputum. 

The  fever  is  continuous,  with  an  evening  rise,  the  dyspnoea  is  progressive, 
and  the  patient  dies  with  adynamia  or  with  delirium  from  the  twelfth  to  the 
twentieth  day. 

Acute  farcy  differs  from  glanders  in  the  local  troubles,  which  are  more 
marked,  and  include  suppurating  angioleucitis,  ulcers,  the  presence  of  farcy 
buds  in  the  muscles  and  in  the  subcutaneous  tissue,  and  in  the  absence  of 
nasal  discharge. 

Primary  chronic  glanders  is  very  rare ;  it  usually  follows  farcy  {morve 
chronique  farcineuse  of  Tardieu).  This  description  will,  therefore,  deal  with 
chronic  farcy,  rather  than  with  the  acute  form.  Farcy  in  the  chronic  con- 
dition is  a  disease  which  is  at  times  purely  local,  so  that  we  may  see  a  chronic 
angioleucitis  which  ends  in  recovery,  or  a  chronic  ulcer  which  also  recovers, 
unless  the  increasing  cachexia  carries  the  patient  off  (Tardieu).  In  other 
cases  chronic  farcy  is  characterized  by  abscesses,  with  or  without  ulceration, 
and  by  general  symptoms  of  fever,  diarrhoea,  wasting  and  hectic,  which 
render  the  prognosis  fatal.  The  symptoms  of  chronic  glanders  resemble 
those  of  very  mild  acute  glanders,  and  appear  during  the  course  of  chronic 
farcy. 

The  diagnosis  of  these  affections  is  generally  revealed  by  the  occupation 
of  the  patient.  In  acute  glanders  the  nasal  discharge  is  a  valuable  symptom, 
but  it  appears  late  in  man,  and  is  sometimes  absent.  In  difficult  cases 
inoculation  of  a  male  guinea-pig  (Straus)  wiU  rapidly  clear  up  the  diagnosis. 

Pathological  Anatomy.— The  pustules  of  glanders  and  those  of  variola 
are  almost  identical  in  structure.  The  inflammatory  process  in  the  former 
is  more  extensive,  and  affects  all  the  layers  of  the  dermis,  as  well  as  the 
subjacent  cellular  tissue.  Ulcers  are  also  present  in  the  swollen  nasal  mucous 
membrane.  The  lesions  of  the  laryngeal  and  tracheal  mucosa  are  less  marked 
than  those  of  the  nose.  The  abscesses  in  the  lung  resemble  the  metastatic 
abscess  of  septicaemia.  In  the  parenchyma  of  the  lung  we  find  yellowish  or 
greyish  areas,  which  resemble  the  lesions  of  lobular  pneumonia.  The 
tubercles  in  glanders,  which  resemble  true  tubercle  in  their  anatomical 
characters,  are  not  found  in  man.  Bloody  or  purulent  fluid  is  found  in  the 
abscesses  of  the  cellular  tissue  and  of  the  muscles.  The  bacillus  is  found 
in  all  these  lesions. 

Treatment. — The  prophylactic  measures  consist  in  the  isolation  and 
destruction  of  horses  suffering  from  glanders  or  from  farcy.     Their  corpses 


INFECTIOUS  DISEASES  COMMON  TO  MAN  AND  ANIMALS.  1845 

bIioiiM  Ix'  Idirifd  deeply  in  Mm-  soil,  aiul  the  stable  furniture  should  be  burnt. 
In  man  any  suspicious  scratch  should  be  immediately  burnt  with  the  actual 
cautery. 

IV.  ACTINOMYCOSIS. 

Parasitology. — Actinomycosis  (Harz)  is  an  infectious  disease  common  to 
man  and  to  many  domestic  animals.  The  infective  agent  is  a  fungus,  which 
resembles  the  rays  of  a  star,  whence  the  name  "  actinomyces  "  (a/cTt''?,  star ; 
and  fivKTj'i,  fungus)  given  to  it  by  Harz  in  1876.  In  the  tissues  and  in  the 
fluids  from  the  infected  regions  the  actinomyces  is  present  in  the  form  of 
yellow  grains,  which  may  be  as  large  as  a  pin's  head.  The  elementary 
granule,  or  the  actinomyces,  is  composed  of  a  central  part  made  up  by  an 
inextricable  network  of  filaments.  This  network  is  the  mycelium.  The 
peripheral  part  is  formed  of  divergent  rays,  set  like  a  crown  around  the 
central  network.  Each  of  these  rays  is  bent  at  its  extremity  into  the  form 
of  a  club. 

These  two  parts,  however,  vary  in  importance.  The  constant  element 
is  the  mycelium.     The  rays  are  a  superadded  element,  and  the  result  of  a 


Fig.  82.— Actinomyces:  Tufts  without  Clubs. 

defensive  reaction  on  the  part  of  the  actinomyces.  For  this  reason,  the 
clubs  are  practically  constant  in  the  grains  taken  from  the  tissues,  while 
they  are  usually  absent  in  cultures  where  the  actinomyces  is  not  in  the 
presence  of  live  cells,  and  therefore  has  no  need  of  defence  by  a  crown  of 
clubs. 

The  essential  part,  therefore,  is  the  mycelium,  which,  occupies  the  centre 
of  the  grain.  The  crown  of  clubs  is  the  rampart.  We  often  find  tufts  of 
mycelium  without  clubs  in  the  infected  tissues  or  in  the  discharge  from  them. 

According  to  certain  writers,  the  club  is  said  to  be  due  "  to  a  product 
of  hyaline  degeneration  of  the  exoplasm  condensed  at  the  edges  of  the 
mycelimu  filament,  and  appearing  to  constitute  a  sheath,  which  in  reality 
does  not  exist  in  the  plain  state.  Each  club  is  at  first  hung  on  to  a  filament, 
which  pierces  it  like  a  pedicle  ;  later,  the  extremity  of  the  filament  is  destroyed 
and  the  club  is  set  free  "  (Poncet  and  Berard). 

II.  117 


1846 


TEXT-BOOK   OF   MEDICINE 


As  the  mycelmm  is  converted  into  clubs,  tlie  staining  reactions  change. 
Instead  of  staining  with  blue  and  violet  dyes,  as  the  mycelium  does,  the  club 
takes  up  the  red  colours.  In  specimens,  therefore,  the  mycelium  is  stained 
blue  or  violet  (gentian  violet),  and  the  crown  of  clubs  is  coloured  red  (eosin). 

I  have  said  that  the  mycelium  is  composed  of  entangled  filaments.  The 
filaments  are  larger  and  two  or  three  times  longer  than  Koch's  bacillus. 
If  these  filaments  are  placed  in  a  suitable  broth  culture,  they  become  longer 
stiU,  giving  ofi  branches,  breaking  up  into  segments,  and  producing  numerous 
spores. 

The  parasite  develops  in  the  ordinary  culture  media.  It  assumes  the 
form  of  greyish  tubercles,  which  penetrate  into  the  depth  of  the  substratum, 
and  do  not  form  spores.  The  latter  develop  almost  always  in  broth  cultures 
of  a  month  old.  On  this  medium  Sauvageau  and  Radais  have  obtained  a 
"  thin  superficial  pellicle,  which  soon  showed  an  appearance  like  white 
velvet,  and  became  a  pale,  clear  yellow,  following  the  formation  of  the  spores." 


Fig.  83. — Actinomyces. 


On  potato  cultures  the  fungus  forms  large  masses,  which  are  very  prominent, 
and  covered  by  a  pale  yellowish  dust,  characteristic  of  the  presence  of  spores, 
and  clearly  marked  from  the  deep  parts,  which  are  of  a  rusty  colour.  The 
spores  may  be  single  or  united  in  chains  ;  the  latter  may  hang  from  the  end 
of  the  filaments  or  remain  quite  free,  so  that  the  actinomyces  can  be 
definitely  classed  among  the  Oospora. 

Fig.  83  is  taken  from  Cranwell's  work  on  Actinomycosis.  The  figure 
on  the  left  shows  the  section  of  a  grain  without  clubs.  The  mycelium  is 
very  scanty  in  the  central  part  of  the  section.  It  is  almost  absent  at 
some  points. 

The  other  shows  a  section  with  the  mycelium  and  the  radiating 
crown  of  clubs.  The  mycehimi  is  somewhat  rarefied  at  the  centre,  and 
much  tufted  at  the  periphery.  At  one  point  a  tuft  of  mycelium  is  escaping 
through  the  crown  of  clubs. 

The  parasite  can  be  inoculated  in  calves,  rabbits,  and  guinea-pigs,  but 
its  transmission  is  somewhat  difficult,  as  actinomycosis  becomes  attenuated 


INFPXTIOUS  DISEASES  COMMON  To  MAN  AND  ANIMALS    \H\7 

in  its  passage  through  the  human  body  and  through  animals.  In  some 
cases  it  is  necessary  to  pass  it  through  a  plant  before  it  becomes  pathogenic 
(Liebman). 

The  special  appearance  of  actinomycosis  is  not  always  confined  to  this 
affection  alone ;  it  has  been  met  with  in  certain  cases  of  tuberculosis  due 
to  favus,  as  well  as  in  cultures  from  human  tuberculosis  (Metchnikoff)  and 
in  aspergillary  tuberculosis,  when  it  sometimes  indicates  spontaneous  cure 
of  the  disease. 

etiology. — This  disease  is  fairly  frequent  in  Russia,  Germany,  and 
especially  in  Austria.  It  was  very  rare  in  France,  where  only  fourteen 
cases  were  recorded  in  1894.  Since  this  period  many  more  cases  have  been 
seen,  and  the  Lyons  School  of  Medicine  has  succeeded  in  collecting  several. 
Although  it  is  much  more  common  in  animals  (bovine)  than  in  man,  the 
same  aetiology  holds  good  in  both  cases.  Contagion  from  animals  is  excep- 
tional, in  spite  of  the  frequency  of  the  disease  in  homed  cattle  and  its 
existence  in  other  domestic  animals.  The  contagion  usually  results  from 
grasses  impregnated  with  the  parasite,  and  actinomycosis  may  sometimes 
result  from  a  splinter  of  corn  or  oats  getting'under  the  skin,  into  the  pharynx 
or  into  the  cavity  of  a  hollow  tooth,  from  scratches  or  abrasions  received 
during  harvest-time,  from  contact  of  a  wound  with  a  mouldy  mattress,  or 
from  inhalation  of  hay-dust. 

Poncet  and  Berard  record  the  following  cases  : 

A  child  swallowed  a  small  ear  of  barley,  and  after  a  while  felt  severe  pains  in  the 
back.  Abscesses  formed  between  the  spine  and  the  scapula.  On  opening  the  abscesses, 
the  remains  of  the  ear  of  barley,  covered  with  actiaomycotic  granules,  were  found.  In 
three  cases  of  actinomycosis  of  the  tongue,  Schartan  and  Jiiriaka  foimd,  on  incising  the 
affected  tissue,  small  fragments  of  barley-ears,  covered  with  the  actinomyces.  In  five 
cases  Bostrom  has  found  the  vegetable  fragment  buried  in  the  yellow  grains  or  in  the 
masses  of  myceUum.  In  a  case  of  actinomycosis  of  the  ovary  of  intestinal  origin 
sheaves  of  myceUum  were  seen  bursting  from  an  ear  of  barley. 

The  fungus  may  also  be  present  on  large  plants  and  on  a  piece  of  worked- 
up  wood,  which  explains  the  inoculation  from  a  prick  with  a  fragment  of 
wood  or  with  a  splinter  from  a  shrub  (Poncet). 

The  time  of  year  appears  to  have  some  influence  on  the  evolution  of  the 
disease.  It  is  much  more  frequent  between  August  and  January,  during 
the  thrashing  of  the  harvest  (Bostrom). 

Pathological  Anatomy. — The  lesions  of  actinomycosis  sometimes  take 
the  form  of  a  sarcomatous  or  myxomatous  tumour  (Bollinger),  at  other 
times  that  of  a  sero-purulent  pocket  containing  chocolate-brown  pus.  The 
yellow  granules  of  the  actinomyces  are  found  in  the  interior  of  the  tumour 
and  in  the  pus.  The  bones,  lungs,  mouth,  pharynx,  intestine  (Chiari),  and 
testis  may  be  affected,  and  the  parasite  may  extend  to  the  pleura,  medias- 
tinum, peritoneum,  spinal  meninges,  and  spinal  cord  (Dor,  Macaigne,  and 

117—2 


1848  TEXT-BOOK  OF  MEDICINE 

Eaingeard).  Abscesses  have  also  been  noted  in  the  Fallopian  tube,  in  the 
ovaries,  in  the  bladder,  in  the  kidneys,  etc. 

When  the  patient  dies  of  pulmonary  actinomycosis,  the  lesions  found 
post-mortem  are  :  "  The  affected  lobe  appears  atelectatic,  as  though  affected 
by  grey  hepatization.  On  section,  we  find  upon  a  congested  ground,  studded 
with  islets  of  chronic  broncho- pneumonia  and  of  sclerosis,  prominent 
resistant  nodules,  of  yellowish  or  rosy-white  colour,  and  readily  detached 
with  the  point  of  the  knife ;  some  are  already  softened  or  are  resolved 
into  a  pap,  wherein  we  can  stain  the  fungus,  but  can,  rarely,  isolate  typical 
yellow  grains.  In  some  cases  cavities  are  seen  in  the  lung "  (Poncet, 
Berard), 

Description. — The  disease  presents  such  different  aspects  that  its 
description  is  a  matter  of  great  diificulty.  In  some  cases  a  neoplasm  is 
found  in  the  temporo-maxillary  region,  and  presents  a  close  analogy  with 
a  sarcoma  ;  in  other  cases  we  find  inflammation  of  the  cervical  region, 
Ludwig's  angina  (Roser,  Kapper),  or  a  tumour  of  the  inferior  maxilla,  of 
the  parotid  gland,  or  of  the  tongue  (Hochenegg).  The  neighbouring  parts 
are  as  a  rule  invaded.  The  skin  becomes  ulcerated,  sanious  material  and 
pus  making  their  escape.  In  more  rare  cases,  actinomycosis  gives  rise  to 
bronchitis,  pseudo-tuberculosis,  enteritis,  typhlitis,  appendicitis,  abscess  of 
the  liver  (Boari),  and  meningitis.  I  have  described  actinomycosis  of  the 
ileo-c8ecal  appendix  under  Hypertrophic  Tuberculoma  of  the  Csecum.  The 
skin  may  be  affected  from  the  first  by  the  parasite,  and  the  affection  then 
resembles  either  ordinary  tubercular  lupus,  with  or  without  ulceration,  or 
certain  ulcers  of  hot  climates,  such  as  madura-foot  (Roux,  Brocq). 

When  the  actinomyces,  carried  by  infected  plant-dust,  enters  the  air- 
passages,  it  causes  primary  lesions  in  the  lungs  and  bronchi.  The  bronchial 
and  pulmonary  symptoms  are  then  the  first  to  appear.  For  months  the 
patient  coughs  and  expectorates  as  if  he  had  chronic  bronchitis  or  tuber- 
cular lesions.  Auscultation  reveals  rales  of  all  kinds,  tubular  breathing, 
bronchophony,  and  even  signs  of  a  cavity.  At  a  later  date  the  actino- 
myces invades  the  pleura,  chest-wall,  and  skin. 

Infection  through  the  oesophagus  is  fairly  common.  "  In  many  cases  it 
determines  the  distribution  of  the  thoracic  lesions,  even  more  than  does 
infection  through  the  lung.  In  Soltinann's  case,  a  small  boy,  after  swallow- 
ing an  ear  of  barley,  suffered  from  retrosternal  pain.  After  some  weeks 
abscesses  appeared  between  the  spine  and  the  scapula.  Death  followed  at 
the  end  of  fifteen  months.  Slight  lesions  were  found  in  the  lungs,  and  very 
large  abscesses  in  the  mediastinum,  vertebrse,  and  muscles  "  (Poncet  and 
.  Berard). 

The  entrance  of  the  actinomyces  through  the  oesophagus,  says  Cranwell, 
is  quite  in  agreement  with  the  clinical  facts,  for  we  could  not  otherwise 


INFECTIOUS  DISEASES  COMMON  TO  MAN  AND  ANIMALS    1849 

explain  the  prolonged  absence  of  pulmonary  symptoms  when  the  neigh- 
bouring organs — the  pleura,  the  pericardium,  etc. — are  so  often  invaded. 

In  one  of  my  patients  at  the  Hotel-Dieu,  the  actinomyces,  after  entering 
the  cellular  tissue  of  the  mediastinum,  spread  in  two  directions.  On  the 
one  hand  it  prov^oked  lesions  in  the  pleura  and  in  the  thoracic  wall  ;  on  the 
other  hand  it  tracked  up  along  the  spine,  infecting  the  vertebrae,  and  giving 
rise  to  multiple  abscesses  and  lumbar  fistulse.* 

As  Cranwell  observes,  one  of  the  characters  of  actinomycotic  infection 
is  its  tendency  to  spread  to  a  distance.  As  regards  thoracic  actinomycosis, 
starting  from  the  pharynx  or  cesophagus,  it  may  track  in  all  directions. 
We  find  fistulae  in  the  mediastinum,  lungs,  and  pleura.  In  one  of  Adler's 
cases  the  anterior  mediastinum  was  converted  into  a  lardaceous  block  of  a 
milky  colour,  and  studded  with  yellow  abscesses.  Clear  or  purulent  effusion 
may  be  present  in  the  pleural  cavity.  Actinomycotic  pleurisy  may  simulate 
pleurisy  of  quite  a  different  nature,  and  the  pathogenic  diagnosis  may  be 
impossible  unless  the  actinomyces  is  found. 

Actinomycosis  is  a  terrible  malady.  It  may  be  limited  to  regions  in 
which  surgical  intervention  is  possible  (face,  appendix,  and  skin).  When 
the  lesions  are  widespread,  and  deep  or  inaccessible,  the  patient  dies  from 
the  onslaught  of  the  little  fungus. 

Diagnosis. — The  diagnosis  is  very  difficult,  if  we  remember  all  the 
diseases  which  actinomycosis  may  simulate.  When  the  disease  is  limited 
to  the  mouth,  neck,  face,  or  pharynx,  we  may  debate  the  possibility  of 
dental  periostitis,  sarcoma,  syphilis,  epithelioma,  and  scrofulo-tuberculosis 
of  these  regions.  If  the  tongue  is  affected,  it  is  difficult  to  distinguish 
this  disease  from  gumma,  tuberculosis,  or  from  cancer.  In  the  thoracic  forms, 
doubts  may  be  present  between  this  disease  and  such  lesions  as  tuberculosis, 
pulmonary  aspergillosis,  broncho-pneumonia,  purulent  pleurisy,  cancer  of 
the  lung  and  pleura,  etc.  The  abdominal  forms  may  simulate  local  peri- 
tonitis, tubercular  typhlitis,  appendicitis,  and  bone  lesions  of  the  pelvis. 
Actinomycosis  of  the  spine  may  simulate  Pott's  disease.  In  spite  of  the 
distinctive  signs,  which  may  help  in  making  a  differential  diagnosis,  we  are 
often  in  doubt  until  ulceration  takes  place,  and  the  discovery  of  the  actino- 
myces clears  up  the  diagnosis.  The  same  difficulty  occurs  in  actinomycosis 
of  the  chest- wall,  which  simulates  osteosarcoma  or  a  cold  abscess  of  a  rib. 
Doubt  may  occur  until  the  discovery  of  the  fungus  is  made.  Lastly,  when 
actinomycosis  runs  an  acute  course,  it  may  simulate  typhoid  fever,  purulent 
infection,  or  acute  miliary  tuberculosis. 

When  we  see  these  clinical  varieties,  of  which  the  cause  appears  to  be 
obscure,  we  must  always  think  of  actinomycosis,  and  undertake  a  bacterio- 
logical examination  of  the  pus  and  of  the  various  secretions.     The  presence 

*  Cliuique  Medicalede  V Hotel-Dieu,  '•  Actinoinycose  lomhaire  et  thoraeiqne,"  1906, 
IB""*  le9on. 


1850  TEXT-BOOK  OF  MEDICINE 

of  the  characteristic  yellow  granules  will  confirm  the  diagnosis.  In  doubtful 
cases  cultures  will  be  indispensable.  In  ordinary  practice  there  is  no  need 
to  reckon  the  rare  cases  of  pseudo-actinomycosis,  due  to  bacilli  (Coppen, 
Jones,  Svotchenko)  or  to  myocotic  fungi  (Dor).  Sporotrichotic  coaggluti- 
nation  and  cofixation  may  be  employed  in  the  diagnosis  of  actinomycosis. 

Botryomycosis,  formed  by  inflammatory  neoplasms,  and  due  "  to  the 
fungus  of  castration  "  in  the  horse,  has  been  met  with  in  man  (Poncet  and 
Dor,  Ten  Siethoff).  The  neoplasm  resembles  a  fleshy  bud  or  a  vascular 
papilloma,  deprived  of  its  epidermic  covering.  It  is  rounded,  mammillated, 
and  assumes  the  appearance  of  a  strawberry,  connected  with  the  surrounding 
tissues  by  a  pedicle.  In  cultures,  botryomycosis  is  present  in  the  form  of 
microbes  resembling  staphylococci ;  in  the  tissues  it  assumes  the  appearance 
of  granules  collected  into  a  bunch. 

Treatment. — Contagion  must  be  avoided  by  the  complete  covering  of 
wounds  and  ulcers.  Grains,  stalks,  and  ears  of  cereals  must  not  be  put 
into  the  mouth. 

Incision,  scraping,  and  curetting  of  the  abscess  are  brought  to  a  happy 
ending  by  the  employment  of  iodide  of  potassium.  This  drug  is,  however, 
not  a  specific  in  actinomycosis.  In  my  patient  at  the  Hotel-Dieu  it  pro- 
duced no  improvement.  Poncet  and  Berard  speak  as  foUows :  "  Out  of 
twenty-five  grave  cases  of  actinomycosis  in  man,  iodide  of  potassium  was 
quite  useless  in  eighteen." 


V.  SPOEOTEICHOSIS. 

Sporotrichosis  is  a  mycotic  affection,  common  to  man  and  to  animals. 
Its  parasite  has  not,  as  yet,  an  exact  place  in  botanical  classification. 

The  first  case  was  published  in  1898  by  Schenk,  in  America. 

In  1903,  de  Beurmann  and  Eamond  described  the  first  case  in  France, 
but  the  parasite  differed  from  that  found  by  Schenk ;  it  was  named  the 
SpoTotrichum  Beurmanni.  Nattan-Larrier  and  Loeper,  in  1904  and  1905, 
working  in  my  clinic,  described  a  sporotrichum,  which  they  had  isolated. 

Parasitology. — The  Sioorotrichum  Beurmanni  shows  two  distinct 
forms ;  in  the  pus  and  in  the  tissues,  it  takes  the  form  of  oblong  rods, 
broader  in  the  middle  than  at  the  ends,  "  from  3  to  bfi  in  length  and  from 
2  to  3/1  in  breadth,  basophile,  finely  granular,  and  encircled  by  a  very  fine 
colourless  membrane  "  (De  Beurmann  and  Gougerot).  These  short  forms, 
when  sown,  develop  and  give  rise  to  a  mycelium  of  fine  filaments  (2//), 
which  are  colourless,  entangled,  and  very  irregularly  branched.  The  latter 
are  covered  over  all  their  surface  by  pigmented  oval  spores  (3  to  4/^  by  5 
to  6/i),  which  are  fixed  by  such  short  pedicles,  that  they  appear  to  be 


INFECTIOUS  DISEASES  COMMON  TO  MAN  AND  ANIMALS    1851 

sessile,  but  ■Nvliicli  are  grouped  in  branches  at  the  ends  of  the  filaments. 
Tlie  best  way  to  study  the  parasite  consists  in  cultivating  it  on  a  dry  slide 
or  in  a  hanging  drop  and  examining  it  directly  under  the  microscope. 

The  best  medium  for  making  cultures  is :  water,  1000  gr. ;  peptone 
Chassaing,  10  gr.  ;  crude  glucose,  37  gr. ;  agar,  15  to  18  gr.  The  culture 
tubes,  of  slanting  agar,  should  not  be  capped  and  must  be  kept  at  the 
temperature  of  the  laboratory  ;  the  fungus  then  develops  more  quickly 
than  in  the  oven.  When  this  medium  is  sown  with  sporotrichotic  pus,  we 
find,  after  five  or  six  days,  small  pearly-white  colonies,  buried  in  the  agar 
and  difficult  to  detach.  As  they  extend,  the  centre  becomes  first  brown 
and  then  black,  until  the  appearance  is  quite  characteristic  at  the  tenth 
or  twelfth  day.  At  this  time,  the  colonies  look  like  cerebral  convolutions 
of  small  size.  The  culture  may  extend  all  over  the  agar ;  when  it  becomes 
old,  we  see  a  kind  of  grey  down  on  the  surface.  The  other  varieties  of 
sporotrichum  differ  from  this  form  in  that,  on  Sabouraud's  medium,  they 
become  black  more  or  less  rapidly,  or  indeed,  they  may  not  become  black 
at  all. 

On  peptone,  glucose,  and  maltose  bouillon,  it  forms  on  the  surface  of 
the  liquid  a  thick  film,  first  whitish,  then  blackish,  while  whitish  flocculi 
fall  to  the  bottom  of  the  tube; 

In  order  to  expedite  the  diagnosis,  Gougerot  allows  a  few  drops  of  pus 
to  trickle  down  the  side  of  the  tube  opposite  the  agar ;  then,  by  the  second 
or  third  day,  we  can  see  under  the  microscope,  on  the  tube  itself,  fine  stars 
formed  by  the  parasite.  Soluble  toxines  have  been  extracted  from  the 
fungus. 

The  study  of  the  parasite  has  been  completed  by  inoculations  in 
animals.  Spontaneous  sporotrichosis  had  already  been  noted  in  the  rat, 
the  dog,  the  mule,  and  the  horse.  The  rat  appears  to  be  the  reactive 
animal.  All  the  lesions  found  in  man  have  been  reproduced  experi- 
mentally :  chancre,  and  cutaneous,  subcutaneous,  mucous,  muscular,  osseous, 
and  articular  gummata,  and  also  generalized  sporotrichosis. 

Pathological  Anatomy. — The  lesions  seen  in  man  and  in  animals  are 
identical.  The  typical  element  is  the  gumma,  which  is  usually  softened 
in  the  centre.  The  central  part  of  this  abscess  is  made  up  of  polynuclear 
cells  and  microphages ;  at  the  periphery,  in  a  proliferated  and  infiltrated 
connective-tissue,  we  find  either  miliary  abscesses  or  masses  of  epithelioid 
and  giant  cells.  The  short  forms  of  the  parasite,  though  rare  in  human 
lesions,  are  fairly  common  in  inoculated  animals. 

.ffltiology. — The  sporotrichum,  found  as  a  saprophyte  on  vegetables, 
appears  to  develop  in  man  on  wounds,  caused  or  soiled  by  plant  debris. 
Inoculation  generally  occurs  on  the  skin.  More  rarely  on  a  mucous 
membrane.   In  some  cases,  the  stings  of  insects  or  the  bites  of  animals  (rat. 


1852  TEXT-BOOK  OF  MEDICINE 

mule),  appear  to  have  been  the  cause  of  infection.  Contamination  by 
means  of  food-stuffs  may,  perhaps,  play  some  part.  The  dissemination  of 
the  parasite  takes  place  either  by  the  arterial  or  by  the  lymphatic  path. 
Its  presence  in  the  blood  has  been  remarked  (Widal  and  Weill). 

Description. — Sporotrichosis,  though  it  may  attack  healthy  persons, 
usually  strikes  those  who  are  enfeebled  by  disease  (tuberculosis,  syphilis, 
cancer,  cirrhosis  of  the  liver,  diabetes).  The  subcutaneous  tissue  is  the 
common  starting-point.  Sporotrichosis  appears,  either  in  the  form  of 
multiple  gummata  (3-5),  localized  in  one  region  of  the  body,  the  limbs 
in  particular,  and  preceded  by  a  chancre,  which  may,  however,  be  absent,  or 
in  the  form  of  disseminated  gummata,  this  being  the  more  usual  condition. 
This  septicsemic  form  is  ushered  in,  as  a  rule,  before  the  appearance  of  the 
subcutaneous  nodules  by  fever  with  lassitude  and  bronchitis. 

The  gumma  begins  as  a  small,  hard,  mobile  nodule,  which  gradually 
softens  and  finally  opens,  giving  exit  to  viscid  pus.  Nevertheless,  some 
gummata  do  not  open  spontaneously. 

The  fistula  results  in  a  rounded  or  oval  ulcer,  with  more  or  less  thickened, 
undermined  edges,  and  with  a  floor  that  exudes  transparent  yellowish 
serum.  In  many  cases,  the  diagnosis  is  rendered  difficult  because  this 
ulcer  closely  resembles  a  syphilitic  or  tubercular  lesion. 

These  ulcers  are  painless  ;  they  are  secondarily  infected ;  they  become 
covered  with  thick  crusts  which  modify  their  appearance,  they  often  serve 
as  starting-points  for  re-inoculation,  or  again  they  may  heal,  leaving  flat 
scars,  more  or  less  pigmented  and  at  times  stained  a  brownish  colour.  In 
very  rare  instances,  sporotrichosis  assumes  the  form  of  the  large  cold 
abscess.  On  the  other  hand,  it  may  invade  the  epidermis  and  simulate 
Tricopliyton  circinatum  or  kerion. 

These  localized  or  disseminated  subcutaneous  gummata  run  their  course 
without  pain  or  fever  ;  they  may  be  accompanied  by  deep  gummata.  De 
Beurmann  and  Gougerot  have  seen  ulceration  of  the  tonsil ;  LetuUe  has 
found  pharyngo-laryngeal  changes  in  a  fatal  case  of  sporotrichosis.  Gum- 
mata have  been  met  with  in  the  muscles.  Several  cases  of  sporotrichosis 
in  the  bones  have  been  noted ;  in  a  woman  under  my  care,  we  found  a 
flstula  of  the  first  metatarsal  bone,  which  resembled  a  spina-ventosa. 
Two  cases  of  joint  sporotrichosis  have  been  published.  The  glands  are 
rarely  affected  in  the  course  of  the  cutaneous  lesions  of  sporotrichosis. 
Lesions  in  the  viscera  have  not,  as  yet,  been  discovered,  if  we  except  a 
pyonephrosis  in  which  the  sporotrichum  was  present  and  two  cases  in 
which  it  was  recognized  in  the  sputum. 

Diagnosis. — At  the  present  time,  more  than  a  hundred  cases  of  sporo- 
trichosis have  been  published.  Its  resemblance  to  tuberculosis  (cutaneous, 
bony,  articular,  and  glandular  lesions)  and  to  syphilis  (cutaneous  lesions) 


INFECTIOUS  DISEASES  COMMON  TO  MAN  AND  ANIMALS    1S53 

demand  an  exact  diaf»nosis,  the  more  so,  because  tlie  profjuosis  is  good  and 
recovery  is  rapid.  The  diagnosis  may  be  based  on  tho  Iblhjwing  charac- 
teristics :  mulLiplioity  of  the  gummata,  appearance  of  the  ulcers,  frequency 
of  auto-inoculation,  course  afebrile  and  painless,  cicatrices,  and  absence,  as 
a  rule,  of  adenitis.  These  signs  and  symptoms  will  also  allow  us  to 
exclude  general  microlipomatosis,  riccklinghausen's  disease,  and  also  leprosy. 

Nevertheless,  the  diagnosis  will  not  be  certain  unless  cultures  give  a 
positive  result.  As  the  parasite  grows  very  slowly  even  on  its  chosen 
medium,  we  must  have  recourse  to  sporo-agglutinatiou  and  to  the  reaction 
of  fixation  (Widal  and  Abrami).  These  authorities  have  shown  that  the 
serum  of  persons  suffering  with  sporotrichosis  contains  an  agglutinin  and 
a  sensibilisatrix  specific  for  the  sporotrichum.  Sporo-agglutination  con- 
sists in  mixing  serum  from  the  suspected  case  with  an  emulsion  of  the 
spores  of  the  fungus,  obtained  by  crushing  in  physiological  serum  a  culture 
of  sporotrichum  six  weeks  to  three  months  old  and  filtering  through 
Chardin  paper ;  the  spores  alone  pass  through  the  filter.  Positive  aggluti- 
nation occurs  in  ratios  of  ^^  and  4^^. 

The  reaction  of  fixation  is  simply  the  application  of  Bordet  and 
Gengou's  reaction  to  sporotrichosis.  These  two  reactions  allow  of  a  retro- 
spective diagnosis,  the  serum  preserving  its  properties  after  the  patient's 
recovery. 

Widal  and  Abraim  have  further  obtained,  with  the  spores  of  the  sporo- 
trichum and  the  serum  of  persons  suffering  from  thrush  or  from  actino- 
mycosis, a  coagglutination  and  a  conJBjKation,  in  much  weaker  ratios  than 
in  the  case  of  sporotrichosis  (-^  to  Y5o)y  ^^^  serving,  nevertheless,  in  the 
diagnosis  of  these  two  affections.  Opsonins  and  precipitins  ha^-e  been 
found  in  the  serum  of  persons  suffering  with  sporotrichosis. 

The  presence  of  the  sporotrichum  being  proved,  it  is  necessary  to  know 
whether  this  parasite  is  really  the  cause  of  the  lesions  found.  Although 
the  sporotrichum  is  often  the  sole  pathogenic  agent,  it  is,  at  times,  merely 
a  saprophyte  in  individuals  affected  with  tuberculosis  or  with  syphilis. 

Treatment. — Sporotrichosis,  considered  per  se,  is  a  benign  affection. 
Iodide  of  potassium  is  a  quasi-specific  agent,  and  in  doses  of  sixty  to 
ninety  grains  daily  causes  the  rapid  and  permanent  disappearance  of  the 
lesions,  provided  the  drug  be  exhibited  for  at  least  a  month  after  apparent 
recovery.     Local  dressings  or  injections  of  iodine  have  been  recommended. 

VI.  PSITTACOSIS. 

The  term  psittacosis  (i//(VraKoc,  parrot)  is  applied  to  an  infectious 
disease  transmitted  to  man  by  parrots.  The  infection  is  due  to  a  special 
microbe — Nocard's  bacillus. 


1854  TEXT-BOOK  OF  MEDICINE 

etiology. — Psittacosis  has  become  endemic  since  the  Paris  epidemic 
of  1892.  The  direct  transmission  from  the  parrot  to  man  has  often  been 
recognized.  A  bird  aSected  with  psittacosis  is  listless  and  sleepy ;  the 
feathers  stand  on  end,  and  the  wings  droop.  This  condition  lasts  from  a 
week  to  a  fortnight,  during  which  period  diarrhoea  and  anorexia  are  present. 
The  wasting  is  rapid,  and  the  disease  ends  fatally  ia  nearly  every  case. 
Contamination  from  the  bird  to  man  takes  place  in  various  ways.  Thus, 
in  order  to  make  the  sick  bird  eat,  the  evil  habit  of  feeding  from  mouth 
to  beak  is  employed— a  dangerous  method,  which  explains  the  frequent 
onset  of  the  affection,  with  transient  oedema  of  the  face  and  diphtheroid 
patches  in  the  mouth  or  the  pharynx,  or  else  with  angina.  Other  persons 
do  not  go  so  far  as  to  gavage,  but  they  fondle  the  sick  creature,  and  warm 
it  under  their  clothes— a  practice  that  exposes  them  the  more  readily  to 
contagion,  as  the  feathers  of  the  bird  are  soiled  by  the  infected  excreta. 

Transmission  may  occur  indirectly  through  objects  soiled  by  the  dejecta 
(cages  and  perches).  The  disease  very  rarely  spreads  from  man  to  man 
(Dujardin-Beaumetz,  Peter,  NicoUe). 

Bacteriology. — Nocard's  microbe,  isolated  in  1892  from  the  bone- 
marrow  of  the  wings  of  parrakeets  which  died  during  the  voyage  from 
America  to  France,  is  a  short,  truncated  bacillus  with  rounded  ends.  It 
does  not  stain  by  Gram.  It  is  endowed  with  great  mobility,  and  possesses 
from  ten  to  twelve  cilia.  It  is  readily  cultivated  on  the  usual  media,  and 
is  both  aerobic  and  anaerobic.  It  rapidly  makes  broth  turbid,  producing  a 
thin  pellicle  on  its  surface.  It  does  not  liquefy  gelatine,  and  it  does  not 
cause  fermentation  in  lactose  or  coagulation  in  nulk.  Lastly,  it  does  not 
give  the  reaction  of  indol.  It  grows  slowly  on  Eisner's  medium,  and  forms 
small  colonies.  It  does  not  develop,  like  the  Bacillus  coli,  on  agar,  from 
which  colonies  of  the  Bacillus  typhosus  have  been  scraped  away  ;  and,  lastly, 
it  multiplies  in  broth,  together  with  the  Bacillus  coli.  These  last  two 
characteristics  distinguish  it  from  the  Bacillus  typhosus. 

In  short,  Nocard's  bacillus  resembles  both  the  Bacillus  coli  and  the 
Bacillus  typhosus,  although  it  preserves  its  autonomy.  It  is  agglutinated  by 
typhoid  serum,  but  to  a  much  less  marked  degree  than  Eberth's  baciUus 
(Gilbert  and  Fournier,  Widal  and  Sicard).  This  difference  in  the  agglutina- 
tive power  is  such  that  Widal  has  set  it  down  as  one  of  the  best  differential 
points  between  the  bacillus  of  Eberth  and  that  of  Nocard. 

The  bacillus  is  extremely  virulent  in  parrakeets,  parrots,  mice,  pigeons, 
and  rabbits.  These  animals  can  be  infected  by  mixing  cultures  with  their 
food,  or,  better  stiU,  by  inoculating  them. 

Gilbert  and  Fournier  have  isolated  a  bacillus  which  closely  resembles 
that  of  Nocard,  from  the  intestinal  contents  of  healthy  parrakeets  or  parrots. 
This  fact  permits  the  two  following  hypotheses  as  to  the  nature  and  origin 


INFECTIOUS  DISEASES  COMMON  TO  MAN  AND  ANIMALS   18r,5 

of  psittacosis  :  Either  the  bacillus  of  healthy  parrots  and  Nocard's  bacillus 
are  derived  from  a  common  source,  in  which  case  the  former,  though  harm- 
less in  the  normal  state,  may  become  virulent,  and  cause  psittacosis  ;  or 
these  two  bacilli  have  nothing  in  common  as  regards  their  origin,  and  may 
be  considered  as  radically  distinct. 

Nocard's  bacillus  has  been  found  only  once  in  man  (Gilbert  and 
Foumier) — in  a  cultivation  from  the  blood  of  a  woman  who  died  from 
psittacosis. 

Description. — The  general  character  of  the  disease  is  that  of  a  typhoid 
infection,  rapidly  complicated  by  pulmonary  troubles.  I  shall  divide  its 
course  into  four  periods  :  incubation,  onset,  stationary  stage,  and  decline. 

The  incubation  seems  to  last  from  seven  to  twelve  days.  In  a  case 
published  by  Dubief,  this  period  was  found  to  be  exactly  nine  days. 

The  onset  is  insidious.  The  patient  complains  of  malaise,  anorexia, 
lassitude,  and  pains  in  the  limbs,  kidneys,  and  trunk.  The  morbid  process 
commences  with  peribuccal  oedema,  prostration,  and  headache,  which  may 
be  accompanied  by  epistaxis,  nausea,  and  vomiting.  Rigors  are  constant, 
and  the  temperature  may  exceed  104°  F.,  with  a  slight  morning  remission. 

After  four  or  five  days  the  stationary  stage  declares  itself.  The  symp- 
toms of  the  onset  become  more  marked ;  the  patient  is  prostrated,  and  lies 
in  a  state  of  muttering  or  of  violent  deUrium,  with  restlessness  and  inco- 
ordinate movements.  The  tongue  is  coated,  the  thirst  is  acute,  and  the 
loss  of  appetite  is  absolute  and  lasts  until  the  fever  falls.  Vomiting  of  food 
and  of  bile  is  frequent,  the  stomach  is  slightly  distended,  and  diarrhoea  or 
constipation  may  be  present.  The  liver  is  normal,  but  the  spleen  is  generally 
enlarged. 

Pulmonary  troubles  are  early  and  of  the  highest  importance.  At  the 
onset  the  cough  is  paroxysmal,  and  distresses  the  patient  greatly.  The 
dyspnoea  is  severe  if  the  pulmonary  lesions  are  extensive.  According  to 
the  case,  we  may  find  on  auscultation  general  bronchitis,  lobar  or  lobular 
pneumonia,  or  pleural  effusion.  The  urine  is  scanty,  dark-coloured,  and  often 
albuminous.  Nervous  troubles  (headache  and  delirium)  increase  during 
the  course  of  the  disease,  especially  when  thoracic  complications  appear ; 
and  we  may  then  note  hallucinations,  carphologia,  and  subsultus  tendinum. 

The  disease  remains  stationary  for  eight  to  ten  days,  and  then  in 
favourable  cases  the  fever  diminishes,  the  other  symptoms  improve,  the 
patient  passes  out  of  his  stupor,  and  enters  on  convalescence,  although  he 
remains  feeble  and  anaemic  for  several  weeks.  In  unfavourable  cases  the 
patient  falls  into  a  state  of  deep  stupor,  and  succumbs  a  few  days  later, 
without  having  regained  consciousness.  In  most  cases  death  results  from 
pulmonary  complications,  such  as  double  congestion,  pneumonia,  or  broncho- 
pneumonia. 


1856  TEXT-BOOK  OF  MEDICINE 

Psittacosis  may  assume  several  clinical  forms :  the  slight  form,  especially 
among  young  people  and  children ;  the  nervous  form,  exceedmgly  grave, 
and  ataxic  or  ataxo- adynamic  ;  and  the  pulmonary  form,  marked  by  the 
severity  of  the  thoracic  symptoms  and  by  the  almost  total  absence  of 
sputum.  In  old  people,  psittacosis  is  especially  grave  when  the  heart  and 
arteries  are  diseased.  The  disease  is  always  exceedingly  dangerous  in 
diabetic  and  cardiac  patients. 

Diagnosis. — The  diagnosis  of  psittacosis  is  based  on  the  clinical  char- 
acters of  the  disease,  and,  above  all,  upon  the  information  furnished  by 
inquiry  as  to  the  cause.  We  shall  not  confound  psittacosis  with  infective 
pneumonia,  which  is  also  seen  as  an  epidemic  in  families  and  houses,  because 
the  pulmonary  phenomena  in  psittacosis  supervene  as  complications,  and 
are  not  the  substratum  of  the  disease.  The  aetiological  conditions  must 
also  be  inquired  into  carefully.  Typhoid  fever,  however,  is  the  disease 
which  has  most  often  to  be  excluded.  In  its  regular  forms,  typhoid  fever 
is  easily  distinguished  from  psittacosis.  The  course  of  the  disease,  the 
temperature  curve  (the  temperature  chart  in  psittacosis  resembles  that  of 
pneumonia),  the  abdominal  symptoms,  and  the  lenticular  spots,  are  evidence 
in  favour  of  typhoid  fever.  We  see,  however,  abnormal  cases  and  septi- 
casmic  forms  of  typhoid  fever,  in  which  the  course  diSers  much  from  the 
classical  type.  The  agglutinative  reaction  (Widal)  wiU  be  of  great  assistance 
in  diagnosis.  Influenza  begins  in  the  same  way  as  psittacosis,  and  the 
respiratory  troubles  have  the  same  importance  in  both  diseases  ;  but  in 
psittacosis  we  do  not  see  the  oculo-nasal  catarrh,  which  is  one  of  the  most 
constant  s}'mptoms  in  influenza.  The  diagnosis  becomes  very  difficult  if 
influenza  is  complicated  with  severe  pulmonary  trouble.  A  decision  can 
be  reached  only  after  the  most  careful  ^etiological  inquiry,  completed,  if 
need  be,  by  bacteriological  examination  of  the  bone-marrow  from  the 
suspected  bird. 

Eesearches  as  to  the  agglutinative  property  of  serum  in  patients  suflering 
from  psittacosis  at  first  gave  negative  results  (Gilbert  and  Foumier,  Achard 
and  Bensaude,  Sicard).  Psittacosis  runs,  in  most  cases,  such  a  rapid  course 
that  the  blood  has  scarcely  time  to  acquire  any  agglutinative  power.  The 
researches  of  XicoUe,  however,  show  that  sero-diagnosis  is  possible  in 
psittacosis.  The  agglutinative  power  was  manifest  in  two  patients;  it 
reached  a  fiftieth  in  one  case  and  a  tenth  in  the  other.  The  method  is 
carried  out  in  a  similar  manner  to  Widal's  reaction. 

Prognosis. — The  mortality  amounts  to  30  per  cent.,  and  the  prognosis 
is  made  worse  by  pulmonary  complications.  The  age  of  the  patient  must 
also  be  taken  into  account.  The  disease  is  relatively  benign  in  children, 
but  is  very  deadly  in  old  people. 

Treatment. — Prophylaxis  depends  upon  general  measures,  such  as  the 


INFECTIOUS  DISEASES  C(JMM0N  TO  MAN  AND  ANIMALS    1857 

examination  of  panakeets  and  parrots  on  arrival,  nnd,  among  special 
measures,  it  is  im])ortant  to  buy  neither  parrots  nor  parrakeets  from  hawkers. 
It  is  always  unwise  to  feed  a  parrot  from  one's  own  mouth.  When  the 
creatures  are  sick,  they  should  be  left  in  their  cage,  especially  if  they  have 
been  recently  bought.  If  they  die,  they  must  be  disposed  of  at  once,  and 
the  cages  disinfected.  If  the  disease  declares  itself  in  a  family,  it  must  be 
treated  as  an  infectious  malady.  We  must  insist  upon  the  danger  of  con- 
tagion, isolating  the  patient,  and  carefully  carrying  out  the  disinfection  of 
all  articles  which  in  any  way  may  come  near  him.  Milk  diet,  cold  baths, 
and  injections  of  serum,  comprise  the  chief  methods  employed. 


PART   VI 

DISEASES  OF  THE  SPLEEN 

HYDATID  CYSTS  OF  THE  SPLEEN— DIAGNOSIS  OF  ENLARGE- 
MENTS  OF  THE  SPLEEN 

Before  I  describe  the  history  of  hydatid  cysts  of  the  spleen,  I  will  quote 
cases  from  two  of  my  cluiical  lectures  on  this  subject.* 

Clinical  Oases. — On  January  7,  1899,  Dr.  Gillebert-Dhercourt  sent  me  a  patient 
with  tke  following  note  :  "  Kindly  examine  the  poUceman  who  brings  my  card.  There 
is  a  question  of  splenomegha  and  surgical  intervention.  I  should  hke  to  have  your 
opinion  before  it  is  carried  out."  I  told  the  man  to  take  oflE  his  clothes,  and  I  examined 
him. 

The  bulgiag  of  the  left  hypochondrium  struck  me  at  one© ;  the  tumour  was 
evident  both  ia  full  face  and  ia  profile.  The  ribs  were  bent  outwards,  the  hypochon- 
drium and  left  flank  showed  deformity,  and  the  projection  affected  both  the  thorax 
and  the  abdomen,  although  it  was  rather  thoracic  than  abdominal. 

In  order  to  appreciate  the  lesions  causing  this  projection,  it  was  necessary  to  examiae 
the  patient  in  the  upright,  supiae,  and  right  lateral  positions.  On  palpation  of  the 
abdomen,  I  found,  in  the  left  flank,  an  oval,  painless  tumour.  Its  indented  edge  gave 
the  feeling  of  two  lobes.  This  tumour,  which  could  be  circumscribed  by  the  hand 
below  and  internally,  measured  4  inches  in  a  vertical  direction.  It  extended  inwards 
nearly  to  the  hnea  alba.  It  was  not  mobUe.  Above,  the  tumour  passed  up  behind  the 
left  ribs,  which  it  pushed  outwards  ;  the  diaphragm  and  the  lungs  were  pushed  up  as 
far  as  the  third  intercostal  space,  and  the  heart  was  displaced  to  the  right  of  the  sternum. 
In  its  vertical  diameter  the  tumour  gave  a  total  dullness  of  11  inches — that  is  to  say, 
8  inches  in  its  thoracic  portion  behind  the  ribs,  and  3  inches  in  its  abdominal  portion. 
The  thoracic  portion  of  the  tumour  was,  therefore,  much  larger  than  the  abdominal 
one. 

What  was  the  nature  of  this  tumour,  and  in  what  organ  was  it  situated  ?  It  was 
not  in  the  liver,  which  normally  takes  up  the  right  hypochondrium,  but  it  was  necessary 
to  eliminate  the  kidney,  which  did  not  appear  to  have  left  the  lumbar  region  of  the 
left  side.  Everything,  therefore,  pointed  to  a  tumour  of  the  spleen,  which  accounts 
for  most  of  the  tumours  in  the  left  hypochondrium.  It  remained  to  be  seen  what 
was  the  nature  of  this  tumour.  Speaking  generally,  very  large  spleens,  due  to  malaria, 
leukaemia,  tuberculosis,  and  primary  splenomegha,  are  especially  abdominal  tumours. 
They  commence  in  the  left  hypochondrium,  and  their  weight  and  their  size  drag  them 
downwards  towards  the  abdomen,  while  their  upper  part  is  situated  behind  the  ribs 
in  the  hypochondrium,  where  they  cause  deformity.     In  any  case,  only  the  smaller 

*  Glinique  Medicde  de  VHotd-Dieu,  "  Les  Kystes  Hydatiques  de  la  Rate,"  1899, 

1858 


DISEASES  OF  'J'HK  Sl'LKKN  1859 

portion  of  tho  tumour  is  aituatod  hero,  tho  principal  pari  hiiu^  in  tho  holly.  The 
shape  of  tho  tumour  in  my  patient  wjis  (|uito  different,  and  in  tho  abdomen  I  felt  only 
the  small  partof  tho  tumour,  which  meinured  3  inches,  wliile  tho  large  part  of  the  tumour, 
which  measured  8  inches,  was  hidden  behind  tho  ribs,  bending  them  outwards,  pushing 
up  the  diaphragm  and  the  limg,  and  displacing  the  heart  to  tho  right  of  tho  sternum. 
The  tumour  was  therefore  abdomino-thoracic  ;  but  it  was  much  more  thonicic  than 
abdominal.  Such  is  not  the  case  in  tho  oolargemonts  of  the  spleen  wliich  I  have  just 
enumerated. 

If  the  tumour  had  been  on  the  right  instead  of  on  the  left  side,  there  would  have 
been  no  hesitation  in  diagnosing  hydatid  cyst  of  the  liver,  and  I  should  have  thought 
of  those  large  cysts  on  the  convex  surface  of  the  liver  which  pu.sh  up  the  thoracic  organs, 
so  as  to  simulate  pleural  effusion.  In  this  patient,  as  the  tumour  was  situated  on  the 
left  side,  it  seemed  logical  to  diagnose  hydatid  cyst  of  tho  spleen,  the  abdominal  portion 
of  tho  tumour  being  formed  by  the  spleen  and  by  tho  cyst,  the  thoracic  portion  being 
formed  by  the  cyst  alone.  One  more  point,  however,  remained  to  be  cleared  up.  Was 
it  quite  certain  that  the  patient  had  not  a  large  effusion  in  the  left  pleura  ?  He  showed 
all  the  principal  signs  :  Dullness,  reaching  as  high  as  the  third  intercostal  space  ;  dis- 
appearance of  resonance  in  Traube's  space ;  absence  of  tactile  fremitus ;  silence  on 
auscultation  ;  and  displacement  of  the  heart,  which  was  felt  to  the  right  of  the  sternum. 

I  put  aside  the  idea  of  a  pleural  effusion  for  two  reasons :  first,  the  bulging  of  the 
lower  ribs  was  better  explained  by  a  tumour  of  the  hypochondrium  than  by  fluid  in 
the  pleural  cavity  ;  and,  second,  the  left  nipple  was  1  inch  higher  than  the  right  one. 
In  the  case  of  pleural  effusion,  however  much  the  heart  may  be  displaced,  the  two 
nipples  remain,  practically,  in  the  same  horizontal  line.  In  the  case  of  hydatid  cysts 
of  the  spleen,  as  the  pressure  acts  from  below  upwards,  the  whole  of  the  skin,  including 
the  nipple,  is  affected,  and  hence  the  marked  difference  of  level  between  the  two  nipples 
in  this  patient. 

Many  other  reasons  were  in  favour  of  hydatid  cyst  of  the  spleen.  There  could  be 
no  question  of  malaria,  because  he  had  never  shown  any  symptoms  of  this  disease. 
We  could  also  reject  the  hypothesis  of  leukaemia,  because  the  blood  was  normal  and  the 
corpuscles  numbered  5,180,000  red,  and  6,800  white.  Further,  the  general  symptoms 
agreed  with  the  diagnosis  of  hydatid  cyst,  which  is  for  a  long  time  compatible  with  good 
health.  The  disease  in  this  man  had  commenced  four  years  previously,  with  pain  in 
the  hypochondrium  and  the  left  shoulder.  He  could  not  exactly  state  the  time  when 
the  thoracic  bulging  appeared,  but  the  increase  iu  size  had  become  so  marked  in  the 
past  six  months  that  his  clothes  did  not  fit,  and  movement  was  difficult.  Subse- 
quently the  chief  symptoms  had  been  dyspnoea  and  pain. 

The  man  was  fairly  well,  apart  from  the  pain  and  dyspnoea  ;  his  appetite  was  good, 
and  the  wasting  was  slight.  I  therefore  made  a  diagnosis  of  hydatid  cyst  of  the  spleen, 
which  had  extended  upwards.  It  had  displaced  the  ribs  outwards,  forming  a  marked 
bulging  in  the  left  hypochondrium,  pushing  up  the  diaphragm  and  the  lung,  and  dis- 
placing the  heart  to  the  right  of  the  sternum,  just  as  a  large  pleural  effusion  would  do, 
but  the  pleura  was  free.  The  absence  of  fever  and  of  any  infective  symptoms  showed 
that  the  cyst  was  not  suppurating,  and  that  the  fluid  would  be  as  transparent  as 
water. 

I  was  careful  not  to  perform  an  exploratory  punctm'e,  in  order  to  confirm  my  diag- 
nosis, because  the  so-caUed  exploratory  pimctures  (extraction  of  a  few  ounces  of  fluid) 
should  be  forbidden  in  hydatid  cysts.  Exploration  of  a  cyst,  even  though  made  with 
a  fine  aspirating  needle,  may  have  the  most  terrible  results.  It  is  a  control  method  in 
diagnosis  which  should  be  left  alone,  because  the  hydatid  fluid,  being  under  pressure, 
may  pass  into  the  peritoneum,  through  the  breach  left  by  the  needle,  and  give  rise 
to  the  fatal  troubles  described  in  detail  under  Hydatid  Cysts  of  the  Liver. 

1  gave  a  favourable  prognosis  and  ad\'ised  immediate  operation.      Delay  would 


1860  TEXT-BOOK  OF  MEDICINE 

be  fatal  in  such  a  case,  for  there  was  nothing  to  prove  that  the  cyst,  already  of  long 
standing,  might  not  become  infected,  and  thus  make  the  prognosis  far  worse.  More- 
over, there  was  nothing  to  prove  that  the  cyst,  in  its  expansion  upwards,  might  not 
perforate  the  diaphragm  and  pleura,  and  thus  bring  about  formidable  complications. 

The  operation  was  performed  by  Gerard  Marchant,  who  agreed  with  me  as  to  the 
diagnosis  of  hydatid  cyst  of  the  spleen.  After  opening  the  abdomen,  we  found  that  the 
spleen  was  free  from  adhesions  and  reached  very  low  down  in  the  abdominal  cavity. 
It  was  large  and  partly  surmounted  by  an  enormous  cyst,  which  extended  up  under 
the  ribs  and  encroached  upon  the  thorax,  by  pushing  up  the  diaphragm.  Through 
the  wide  incision  we  perceived  the  lower  end  of  the  spleen  and  the  cyst,  which  bulged 
hke  a  hemisphere  between  the  spleen  and  the  stomach.  The  cyst  was  inlaid  in  the 
spleen,  and  was  only  adherent  at  the  hilum.  The  finger  could  be  passed  all  roxmd  the 
spleen,  except  at  the  hilum,  where  the  cyst  originated.  The  cyst-wall  was  slate-coloured, 
and  so  thin  as  to  be  translucent. 

A  large  trocar  plunged  into  the  cyst  gave  exit  to  about  4  pints  of  clear  fluid.  The 
patient  was  then  turned  on  to  the  left  side,  and  another  quart  of  fluid  evacuated,  so 
that  at  least  3  quarts  of  fluid  were  contained  in  this  unilocular  cyst.  After  the  fluid 
had  been  evacuated,  Gerard  Marchant  at  first  thought  of  seizing  the  spleen  and  drawing 
it  out,  together  with  the  greater  portion  of  the  cyst.  Splenectomy,  followed  by  incision 
of  a  portion  of  the  pocket,  appeared  to  be  impracticable,  because  of  the  thinness  of  the 
wall,  as  well  as  from  its  deep  situation  and  its  adhesion  to  the  deep  parts.  He  found 
it  better  to  marsupialize  the  pouch  to  the  waU,  although  this  was  a  difficult  task,  because 
of  the  friability  and  the  depth  to  which  the  wall  extended.  The  results  of  the  operation 
were  excellent,  and  the  patient  recovered. 

By  one  of  those  chances  which  are  not  rare  in  clinical  medicine,  we  had,  in  the 
St.  Christopher  ward,  another  patient  also  suffering  from  hydatid  cyst  of  the  spleen. 
There  were,  however,  some  differences  between  the  second  and  the  first  cases.  In 
my  second  patient  the  bulging  of  the  hypochondrium  was  much  less  marked  than  in 
the  first,  but  the  abdominal  tumour  was  very  much  larger.  It  could  be  taken  in  both 
hands,  and  reached  below  the  umbihcus  and  to  the  right  of  the  linea  alba.  The  dullness, 
indicating  the  upper  Mmit  of  the  tumour,  did  not  reach  as  high  as  in  the  first  patient, 
and  only  extended  as  far  as  the  fifth  rib  instead  of  the  third.  The  heart  was  not  dis- 
placed, and  the  two  nipples  were  practically  on  the  same  level. 

The  symptoms  included  pain  in  the  chest  and  abdomen,  heaviness  and  dragging 
sensations,  of  three  years'  duration.  The  deformity  of  the  hypochondrium  and  the 
swelling  of  the  abdomen  had  been  noticed  for  only  about  a  year.  From  this  period 
onward,  dyspepsia,  loss  of  appetite,  pain,  and  constipation  had  been  present.  With 
the  exception  of  these  symptoms,  the  general  health  remained  good,  the  patient  had 
wasted  but  Uttle,  and  had  never  suffered  from  fever.  I  made  a  diagnosis  of  hydatid 
cyst  of  the  spleen,  and  was  careful,  for  the  above-mentioned  reasons,  not  to  perform 
exploratory  puncture.  I  felt  that  it  was  necessary  to  intervene  without  delay,  and 
asked  Gerard  Marchant  to  undertake  the  operation. 

The  abdominal  waU  was  opened  by  an  incision  on  the  left  side,  extending  from  the 
false  ribs  to  1  inch  below  the  level  of  the  umbihcus.  We  then  found  an  enormous 
spherical  cyst,  covered  almost  entirely  by  the  spleen,  which  was  spread  over  it  hke 
an  envelope.  Adhesions  were  present  only  at  the  level  of  the  phrenico -splenic  hga- 
ment.  The  cyst  was  punctured  at  its  thinnest  pomt.  It  contained  4  pints  of  typical 
fluid,  in  which  booklets  were  foimd.  In  proportion  as  the  cyst  became  empty,  it  was 
pulled  out  of  the  incision,  and  after  some  manipulation  the  spleen  was  removed.  The 
operation  resulted  in  recovery. 

Such,  then,  was  my  second  case  of  hydatid  cyst  in  the  interior  of  the  spleen.  From 
its  tendency  to  extend  downwards  into  the  abdomen,  it  belonged  to  the  chnical  variety 
which  I  have  called  cysts  of  the  descending  type. 


DISEASKS  OV  TIIK  SI'I-KI'.X  1861 

I  may  hero  recivll  its  chief  oharautors.  It  dififered  from  tho  proceding  cshc  in  that 
the  tumour  did  not  rciurh  so  higli  into  tho  thorax,  and  causud  less  displacement  of  the 
ribs,  so  that  tho  biil^inj^  in  tho  hypochi  iidrium  was  less  marked.  On  tho  other  hand, 
in  tho  abdonun  it  formed  an  enormous  tumour  which  invaded  tho  iUatt  fossa,  and 
reached  beyond  tho  hnoa  alba.  Tho  symptoms  wore  therefore  <>i  tho  abdominal  rather 
thou  of  tho  thoracic  type. 

Anatomical  Classification. — iVll  hydatid  cysts  of  the  spleen  are  far 
from  being  alike,  aud  we  have  just  seen  the  proof  in  the  history  of  my 
patients,  iii  whom  the  cysts  from  the  anatomical  and  clinical  point  of  view 
were  absolutely  different.  The  cyst  developed  in  the  pulp  of  the  spleen, 
in  the  second  case,  aud  the  splenic  tissue  was  pushed  aside  cxcentrically, 
so  as  to  form  a  cap  ;  Marchant  was  therefore  obliged  to  perform  splenectomy. 
In  the  first  patient,  on  the  other  hand,  the  cyst  was  only  attached  to  the 
spleen,  and  had  commenced  in  the  hilum,  leaving  the  rest  of  the  organ  free. 
The  spleen  was  therefore  left  alone  by  the  surgeon.  It  is  evident,  then, 
that  the  anatomical  conditions  may  lead  to  different  indications  as  regards 
treatment.  Accordingly,  it  appears  advisable  to  class  cysts  of  the  spleen 
according  as  they  answer  to  the  nature  of  the  facts,  rather  than  to  unite 
them  in  one  description. 

From  the  anatomical  point  of  view,  I  may  describe  three  varieties. 
In  the  first  variety  the  cyst  develops  in  the  tissue  of  the  spleen,  more  or  less 
near  to  the  centre  of  the  organ.  In  this  case  the  spleen  tissue  is  pushed 
aside  excentrically,  forming  a  cap  for  the  cyst.  A  tumour  results,  formed 
at  its  centre  by  the  cyst  and  at  its  periphery  by  the  spleen  tissue.  Such 
was  the  case  in  my  second  patient,  where  the  spleen  was  spread  out  over 
the  cyst,  and  formed  an  envelope,  thin  at  certain  spots,  but  elsewhere 
much  hypertrophied.  The  hypertrophy  in  this  case  (compensatory  hyper- 
trophy) was  so  great  that  the  spleen  tissue  weighed  25  ounces. 

I  have  been  able  to  collect  cases  of  hydatid  cysts  which  commenced  in 
the  spleen  tissue,  and  pushed  it  aside  like  an  envelope.  The  following  case  is 
reported  by  Rambeau  : 

A  woman  was  admitted  to  the  Hopital  de  la  Charite,  under  Velpeau,  for  dyspnoea, 
fever,  and  pain  in  the  left  flank.  On  examination  of  the  patient,  it  was  found  that 
the  left  hypochondiium  and  flank  were  bulging  outwards.  This  bulging  formed  a 
tumour  -^vith  ill-defined  limits.  The  patient  said  that  the  tumour  had  increased  three- 
fold in  eight  months.  The  pain,  dyspncea,  and  fever  were  only  of  a  fortnight's  duration. 
The  patient  died  some  weeks  later,  and  the  autopsy  gave  the  folloAving  results  :  The 
spleen  was  converted  into  an  enormous  tumour,  which  filled  the  left  half  of  the 
abdomen.  It  yielded,  on  examination,  the  feehng  of  a  thin  covering,  formed  of  the 
spleen  tissue,  and  spread  out  over  a  fluid  tumour  in  the  centre  of  tho  organ.  The 
organ  was  punctured,  and  3  pints  of  pm-ulent  fluid  came  out.  The  finger  was  intro- 
duced into  the  cavity,  and  withdrew  a  large  spherical  membrane,  which  was  really 
the  covering  of  a  hydatid  cyst.  The  spleen  tissue  was  expanded  over  the  surface 
of  the  cyst,  and  formed  an  adventitious  tissue,  more  or  less  thickened  at  different 
points. 

II.  118 


1862  TEXT-BOOK  OF  MEDICINE 

The  following  case  was  published  by  Hartmann  : 

A  woman,  twenty-nine  years  of  age,  was  suffering  from  an  abdominal  tumour,  with 
pain,  dyspepsia,  and  dyspncea.  Examination  of  the  abdomen  showed  a  large  tumour, 
resembling  the  shape  of  a  bean.  Its  convexity  corresponded  to  the  left  iliac  fossa, 
and  its  hilum  looked  towards  the  umbOicus.  On  palpation  the  tumour  presented  a 
rounded  outHne  with  marked  nodulations.  In  its  left  superior  portion  it  was  tense, 
painless,  and  very  mobile  in  aU  directions.  When  it  was  pushed  upwards,  or  when  the 
patient  was  placed  in  the  Trendelenburg  position,  the  tumour  was  partly  hidden  in  the 
left  hypochondrium.  The  sensation  of  baUottement,  comparable  to  that  of  the  kidney, 
was  felt,  with  this  difference,  that,  instead  of  being  caused  by  succussion  at  the  costo- 
vertebral angle,  the  baUottement  was  produced  by  pushing  in  the  costo-ihac  space. 
The  tumour,  which  encroached  upon  the  hypochondrium,  fell  back  as  soon  as  the  patient 
sat  down,  and  the  patient  then  experienced  a  dragging  sensation.  It  was  possible  to 
push  the  tumour  considerably  to  the  right  of  the  umbiUcus,  but  not  quite  so  far  as  the 
right  hypochondrium.  When  the  tumour  wd,s  drawn  forcibly  downwards,  pain  to  the 
left  of  the  umbilicus  resulted.  From  these  various  sjonptoms  Hartmann  made  a 
diagnosis  of  a  cyst  in  a  movable  spleen.  The  blood-examination  was  practically 
normal. 

Hartmann  performed  splenectomy.  The  tumour  was  formed  by  a  hydatid  cyst 
of  the  spleen,  which  had  pushed  aside  the  spleen  tissue  in  an  eccentric  manner,  so  as  to 
form  an  incomplete  cap.  At  the  upper  end  of  the  cyst  the  spleen  tissue  had  the  appear- 
ance of  a  small  flattened  tongue,  resembling  in  shape  the  end  of  a  bullock's  tongue. 
The  spleen  tissue  was  thin  over  an  extent  of  two  fingers'  breath,  and  was  spread  out 
beyond  into  a  large  roimded  and  lobular  mass.  The  whole  inferior  part  of  the  splee» 
was  spread  out,  and  contained  a  large  hydatid  cyst  with  numerous  small  hydatids. 

Sneguirew  (of  Moscow)  has  seen  a  case  which  comes  under  the  category  of  intra- 
splenic  cysts.  After  the  abdomen  had  been  opened  in  the  hnea  alba,  a  splenic  tumour, 
as  large  as  a  man's  head,  was  withdrawn.  He  caused  the  spleen  tissue  to  shrivel  up 
by  means  of  a  jet  of  steam,  and  then  made  an  incision,  3  inches  long,  across  the  spleen. 
By  this  incision  he  opened  up  the  interior  of  a  hydatid  cyst,  situated  in  the  depth  of 
the  organ.  After  removal  of  the  cyst,  the  spleen  was  two  or  three  times  its  normal 
size.  He  decided  to  remove  the  spleen.  The  task  was  difl&cult,  but  recovery  resulted 
without  any  febrile  reaction. 

In  Jejebherg's  case  the  spleen  formed  a  sac  around  the  cyst.  The  wall  of  this  sac 
was  composed  of  two  layers :  an  external  thickened  layer  of  splenic  tissue,  and  an 
internal  thin  layer  of  fibrous  tissue.  After  opening  the  sac,  numerous  hydatids  of 
various  sizes  escaped. 

Lyons  has  reported  the  case  of  a  young  woman  suffering  from  an  abdominal  tumour 
which  extended  from  the  epigastrium  to  the  left  iliac  region.  On  opening  the  abdomen, 
he  found  an  enormous  spleen,  which  was  incised  and  about  8  pints  of  hydatid  fluid 
drawn  off.  This  case  was  also  one  of  intrasplenic  cyst,  as  the  spleen  "  was  completely 
hollowed  out  by  the  cyst,  and  resembled  the  uterus  after  accouchement." 

I  have  applied  the  name  of  "intrasplenic  hydatid  cyst"  to  this 
anatomical  variety,  in  which  the  cyst  develops  near  the  centre  of  the  spleen, 
and  ia  its  growth  pushes  aside  the  spleen  pulp,  which  forms  a  cap  of  unequal 
thickness.  In  the  specimen  from  my  second  patient  the  thin  parts  of  the 
cap  were  partly  converted  into  fibrous  tissue ;  elsewhere  the  splenic  tissue 
was  considerably  thickened. 

The  hydatid  cyst  during  its  intra;splenic  development  preserves  a  spherical 
form.     The  whole  tumour  may  be  oblong,  curved,  and  nodular  at  its  ex- 


DISEASES  (J¥  THE  Sl'LKEN  1863 

tromities  through  the  unequal  amount  of  spleen  tinsue  over  the  surface 
of  the  cyst,  but  the  cyst  preserves  its  spherical  form. 

Let  us  now  consider  another  anatomical  variety  of  liydatid  cyst  in  the 
spleen.  In  this  form  the  cyst  does  not  develop  at  the  centre  of  the  organ, 
but  at  the  periphery,  at  one  end,  or  at  the  edge,  and  not  far  from  the  surface. 
In  such  a  case  the  splenic  tissue  is  not  spread  out  over  the  cyst  like  a  cap, 
for  it  is  affected  in  only  a  small  portion  ;  the  cyst  expands  outwards,  and  the 
spleen  practically  preserves  its  normal  shape,  with  or  without  subsequent 
hypertrophy.  I  have  been  able  to  find  a  few  cases  which  come  under  this 
category.  Gras  writes  :  "  The  hydatid  cyst  developed  at  the  upper  end 
and  at  the  posterior  portion  of  the  spleen,  which  was  hypertrophied." 

In  a  case  published  by  Jayle,  the  spleen  was  much  hypertrophied  (apart  from  the 
cj^t),  measm'ing  7  by  6  inches.  It  assumed  a  triangular  form,  Avith  its  apex  downwards 
and  its  base  up-wards,  supporting  an  enormous  hydatid  cyst,  which  was  "  implanted 
upon  the  upper  and  internal  part  of  the  organ."  The  splenic  tissue  was  spread  out 
over  the  cyst  for  a  distance  of  4  inches.  I  find,  in  a  case  published  by  Fink,  that  the 
hydatid  cyst  developed  "  at  the  lower  part  of  the  spleen,"  while  the  upper  part  was 
normal. 

The  tumours  in  this  second  variety  are  generally  bilobular  and  of  an 
irregular  shape.  The  larger  part  of  the  tumour  is  formed  by  the  cyst, 
which  grows  externally,  and  the  smaller  part  belongs  to  the  spleen,  which  is 
sometimes  hypertrophied.  I  have  reserved  for  this  variety  the  term  of 
exteriorized  hydatid  cyst  of  the  spleen. 

In  the  third  variety  I  have  placed  hydatid  cysts  which  develop,  not  in 
the  tissue  of  the  spleen,  but  in  contact  with  it,  either  at  the  hilum  or  under 
the  capsule,  and  I  have  given  to  this  variety  the  name  of  juxtasplenic 
cyst,  in  order  to  distinguish  it  from  intrasplenic  and  exteriorized  cysts. 

In  the  case  quoted  above,  a  juxtasplenic  hydatid  cyst  surmounted  the 
spleen,  and  appeared  at  first  sight  to  be  a  part  of  that  organ ;  but  the 
spleen  was  affected  only  as  regards  its  pedicle,  and  its  tissue  was  free,  as 
the  cyst  had  originated  in  the  hilum. 

James  Oliver  has  published  a  case  which  belongs  to  the  category  of 
juxtasplenic  cysts  : 

A  lady  came  to  consult  him  for  a  tumour  which  filled  the  lower  part  of  the  abdomen. 
It  was  palpable  in  the  left  cul-de-sac  on  vaginal  examination.  Bimanual  palpation 
gave  the  feeUng  that  it  was  the  same  tumom*.  As  the  pains  were  very  acute  in  the  left 
ovarian  region,  the  tumour  was  thought  to  be  a  cyst  of  the  broad  hgament,  and  an 
operation  was  decided  upon.  The  abdominal  incision  revealed  aa  enormous  cyst, 
bound  down  to  the  interior  wall  of  the  abdomen  by  dense  adhesions,  which  extended 
from  the  pubes  to  the  umbilicus.  On  dissection  it  was  found  that  the  tumour  was 
adherent  to  the  omentum  in  the  left  hypochondrium.  The  cyst,  which  was  of  the  shape 
of  a  leather  bottle,  was  firmly  bound  down  by  a  pedicle  to  the  right  edge  and  to  the 
lower  part  of  the  spleen.  The  cyst  was  first  evacuated,  and  contained  5  or  6  pints  of 
fluid  with  several  hydatid  vesicles,  of  which  some  were  as  large  as  a  nut.     The  wall 

118—2 


1864  TEXT-BOOK  OF  MEDICINE 

of  the  cyst  was  clearly  felt,  passing  into  the  pedicle  adherent  to  the  spleen.  The  case 
was  therefore  one  of  pedunculated  juxtasplenic  cyst.  The  psdicle  was  Kgatured  and 
cut  off,  as  in  an  ovarian  cyst,  and  the  patient  recovered  without  mishap. 

This  variety  of  juxtasplenic  hydatid  cyst  is  analogous  with  cysts  of  the 
kidney,  as  the  following  case  proves  : 

A  young  girl  consulted  a  physician  for  acute  paras,  and  a  tumour  was  found  in  the 
left  hypochondrium.  Two  years  later  the  tumour,  which  was  very  painful,  caused 
a  bulging  in  the  flank  and  in  the  left  hypochondrium.  The  diagnosis  remained 
donbtful  between  a  tumour  of  the  left  kidney  and  one  of  the  spleen,  but  an 
operation  was  not  even  thought  of,  which  is  not  astonishing,  as  the  case  occurred  some 
sixty  years  ago.  The  unfortimate  patient  died,  and  at  the  autopsy  a  tumour  as  large 
as  the  foetal  head  was  foimd  in  the  left  flank  and  hypochondrium.  It  weighed  2  poiuids, 
and  was  a  hydatid  cyst  of  the  kidney  which  had  developed,  not  in  the  renal  tissue,  but 
between  the  capsule  and  the  tissue  proper  of  the  kidney,  which  Avas  atrophied,  so  that 
the  cyst  was  only  separated  from  frhe  cahces  and  pelvis  by  a  very  thin  layer  of  tissue. 
The  case  was  therefore  a  juxtarenal  cyst,  analogous  to  the  juxtasplenic  cysts  which 
I  have  just  described. 

I  therefore  propose  to  admit,  from  the  anatomical  point  of  view,  three 
varieties  of  hydatid  cysts  of  the  spleen.  The  first  variety,  which  is  the 
most  numerous,  comprises  the  intrasplenic  cyst  of  the  spleen.  The  spleen, 
pushed  back  in  an  excentric  fashion  by  the  cyst,  forms  a  cap  or  envelope, 
atrophied  in  some  places  and  hypertrophied  in  others. 

In  the  second  variety  the  cyst  develops,  not  in  the  deep  tissue  of  the 
spleen,  but  at  some  point  near  the  surface  ;  it  grows  outwards,  and  forms  a 
bilobed  tumour,  of  which  the  large  lobe  is  formed  by  the  cyst,  and  the  small 
lobe  is  formed  by  the  spleen.     The  cyst  is  exteriorized. 

The  third  variety  concerns  the  juxtasplenic  cyst,  which  is  sessile  or 
pedunculated.  It  develops  under  the  capsule  of  the  spleen,  at  the  ends, 
at  the  edges,  or  in  the  kilum,  but  the  splenic  tissue  remains  free.  The 
tumour  is  irregular  and  bilobed  ;  the  large  lobe  is  formed  by  the  cyst,  and 
the  small  lobe  is  formed  by  the  spleen. 

Pathological  Anatomy. — There  is  no  need  for  me  to  describe  here  the 
formation  and  the  structure  of  the  hydatid  cyst,  with  its  coverings,  its 
vesicles,  its  fluid,  and  its  echinococci ;  these  details  are  given  under  Hydatid 
Cysts  of  the  Liver.  I  need  not  dwell  upon  the  adhesions,  the  suppurations, 
and  the  perforation,  which  may  result  during  the  evolution  of  the  cyst, 
but  there  are  some  pathological  peculiarities  which  I  desire  to  mention. 
Whatever  the  general  shape  of  the  tumour  may  be,  whether  it  be  oval, 
elongated,  or  fusiform,  the  cyst  itself  remains  absolutely  spherical,  in  spite 
of  the  resistance  of  the  tissue  in  which  it  develops. 

In  my  case  the  pericystic  tissue  of  the  spleen  was  not  of  the  same  thick- 
ness at  all  points.  The  tissue  was  very  thin  and  reduced  to  a  cap  at  the 
centre  of  the  spleen,  while  it  had  undergone  such  hypertrophy  at  the 


PTSEASES  OF  THE  SPLEEN  IRP.n 

extremities  that  the  spleen,  after  removal  of  the  cyst,  still  weighed  four  times 
its  normal  weight. 

Tn  the  thin  portion  forming  the  cap,  fibrous  tissue  (peiisplenitis)  had 
taken  the  place  of  the  normal  splenic  tissue,  but  at  the  extremities  of  tho 
spleen  the  tissue  had  hypertrophiod  to  a  considerable  extent,  and  tho 
two  histological  preparations  reproduced  in  my  clinical  lectures  show  the 
hypertrophy  of  the  spleen  pulp  and  the  fibrosis  of  the  capsule  (perisplenitis). 

What  is,  then,  the  signification  of  this  hypertrophy  which  more  than  com- 
pensates for  the  partial  loss  of  spleen  tissue,  due  to  atrophy  ?  This  variety 
of  hypertrophy,  which  has,  as  far  as  I  know,  not  as  yet  been  described  in 
the  spleen,  is  comparable  to  the  compensatory  hypertrophy  of  the  liver 
described  by  Hanot,  ChaufEard,  and  Kahn  in  several  diseases  of  the  liver 
(large  alcoholic  liver  and  hydatid  cysts) ;  and  in  some  diseases  of  the  kidney 
(Albarran,  ChaufFard).  These  conditions  are  described  in  the  sections  on 
these  diseases. 

The  spleen,  when  it  contains  a  hydatid  cyst,  appears  to  me  to  undergo 
marked  compensatory  hypertrophy.  Further,  this  variety  of  splenic 
hypertrophy  cannot  be  rare,  if  I  judge  by  the  few  remarks  regarding  it  in 
cases  of  hydatid  cysts  of  the  spleen,  as  observers  have  not  specially  dwelt 
on  it.  Sneguirew's  case  :  after  removal  of  the  cyst  the  spleen  was  double 
or  treble  the  normal  size  ;  Robert's  case  :  the  spleen  was  hypertrophied ; 
Jayle's  case  :  the  spleen  was  hypertrophied,  and  measured  17  by  14  centi- 
metres ;  Arnozan's  case  :  the  spleen  was  hypertrophied,  and  weighed 
250  grammes  after  removal  of  the  cyst. 

Compensatory  hypertrophy  of  the  spleen  in  the  case  of  cysts  appears 
to  me,  therefore,  to  be  clear,  and  it  must  take  its  place  with  the  compensa- 
tory hypertrophy  of  the  liver  and  of  the  kidney. 

Haematology. — An  interesting  question  is  the  comparative  study  of 
the  blood  before  and  after  splenectomy.  Wlaeff,  professor  at  the  Military 
Academy  of  St.  Petersburg,  has  kindly  communicated  to  me  some  in- 
teresting researches  which  he  made  while  my  first  patient  was  under  Gerard 
Marchant's  care  : 

After  removal  of  the  spleen,  examination  of  the  blood  yielded  4,400,000  red  cor- 
puscles and  10,560  white  corpuscles.     Relative  proportion,  1  in  417. 

Twenty-four  hours  after  splenectomy,  3,820,000  red  corpuscles  and  21,200  white 
corpuscles.     Relative  proportion,  1  in  181. 

Five  days  after  operation,  3,610,000,  red  corpuscles  and  12,600  white  corpuscles. 
Relative  proportion,  1  in  286. 

Twelve  days  after  operation,  3,520,000  red  corpuscles  and  13,600  white 
corpuscles.     Relative  proportion,   1  in  258. 

Twenty-eight  days  after  operation,  3,500,000  red  corpuscles  and  8,400  white  cor- 
puscles.    Relative  proportion,  1  in  410. 

Tliirty-tive  days  after  operation,  3,637,000  red  corpuscles  and  12,000  white  cor- 
pMseles.     Relative  proportion,  1  in  303. 


1866  TEXT-BOOK  OF  MEDICINE 

Forty-six  days  after  operation,  3,800,000  red  corpuscles  and  11,700  white  corpuscles. 
Relative  proportion,  1  in  324. 

Sixty-one  days  after  operation,  4,000,000  red  corpuscles  and  12,000  white  corpuscles. 
Relative  proportion,  1  in  310. 

Eighty-six  days  after  operation,  4,250,000  red  corpuscles  and  14,000  white  corpuscles. 
Relative  proportion,  1  in  304. 

This  comparative  table  shows  that  the  number  of  red  corpuscles  is 
considerably  lowered  directly  after  the  removal  of  the  spleen  ;  the  number 
of  white  corpuscles  is  doubled.  During  the  next  few  days  the  red  corpuscles 
continue  to  diminish  up  to  the  twentieth  day ;  they  then  increase  progres- 
sively until  the  eighty-sixth  day,  when  they  regain  their  normal  count. 
The  white  blood-corpuscles,  on  the  contrary,  are  not  diminished  in  propor- 
tion, and  their  number  remains  decidedly  higher  after  the  operation. 

For  some  weeks  after  splenectomy  Wlaafi  found  in  the  patient  a  transient 
enlargement  of  the  thyroid  body,  as  weU  as  transient  hypertrophy  of  the 
lymphatic  glands  in  the  neck,  axiUa,  and  groin. 

The  examination  of  the  blood  in  my  patient  also  dealt  with  the  con- 
dition of  the  red  corpuscles,  and  the  relative  numbers  of  their  different 
varieties. 

The  enumeration  and  the  relative  proportions  of  the  elements  of  the 
blood,  counted  before  splenectomy,  gave  practically  normal  results  :  Red 
corpuscles,  4,400,000 ;  white  corpuscles,  10,560.  The  white  corpuscles 
were  divided  as  follows  :  Small  mononuclear  leucocytes  (lymphocytes  of 
the  Germans),  and  large  mononuclear  leucocytes,  15*4  per  cent.  ;  inter- 
mediary leucocytes,  7*6  per  cent.  ;  polynuclear  leucocytes,  77  per  cent.  ; 
eosLQophile  cells,  4  per  cent. 

For  the  better  understanding  of  the  changes  in  the  blood  cells  figured  in 
the  figures  on  p.  1868,  it  is  necessary  to  remember  the  varieties  of  white  blood- 
corpuscles  in  the  normal  condition.  In  order  to  avoid  repetition,  I  would 
ask  the  reader  to  turn  to  the  section  on  Leucocythaemia,  where  he  will  find 
a  detailed  description. 

In  Fig.  84,  which  shows  the  blood  films  before  removal  of  the  spleen, 
we  see  that  the  condition  is  normal,  both  as  regards  the  number  and  the 
relative  proportions  of  red  and  white  corpuscles.  We  also  see  some  lympho- 
cytes (small  mononuclear  leucocytes),  as  well  as  the  mononuclear,  inter- 
mMiary,  polynuclear,  and  eosinophile  forms. 

In  Fig.  85,  which  shows  the  blood  film  a  month  after  removal  of  the 
spleen,  we  see  an  absolute  change  as  regards  the  red  and  white  corpuscles. 

The  former  have  diminished  in  number  (3,820,000),  and  the  shape  of 
some  is  altered.  Their  outline,  instead  of  being  circular,  assumes  the 
appearance  of  an  almond,  a  pear,  a  comma,  and  a  heart. 

Nucleated  red  blood  cells  are  also  present  in  the  proportion  of  1  to  20,000. 

The  variations  in  the  leucocytes  chiefly  affect  the  mononuclear  cells 


DISEASES  OF  THE  SPLEEN"  18f.7 

and  the  staining  reactions  of  their  protoplasm ;  while  some  remain  well 
stained,  the  others  no  longer  take  the  dye. 

A  white  blood-corpuscle  undergoing  karyokinesis,  which  is  not  found 
in  all  blood,  is  also  seen. 

Fig.  80  represents  an  examination  of  the  blood  three  months  after 
splenectomy,  and  shows  that  the  normal  appearance  has  been  regained. 

It  is  evident  that  a  substitution  has  taken  place  in  the  blood-forming 
organs. 

The  normal  forms  of  the  red  blood  cells,  as  well  as  the  deformed  and 
nucleated  corpuscles,  and  the  abnormal  forms  of  white  corpuscles  showing 
karyokinesis,  have  disappeared.  The  relations  between  the  different 
varieties  are  normal,  as  Fig.  94  shows. 

I  shall  refrain  from  drawing  conclusions  as  to  the  formation  and  changes 
in  the  red  and  white  corpuscles.  It  is,  however,  certain  that  after  removal 
of  the  spleen  a  disturbance  occurred  both  in  the  quantity  and  quality  of 
red  corpuscles,  and  it  is  also  certain  that  this  disturbance  was  only  transient, 
that  substitution  took  place  in  the  blood-forming  organs,  and  that  in  three 
months  the  blood  regained  its  normal  morphology,  the  equilibrium  being 
re-established. 

Description. — Let  us  first  consider  the  clinical  side  of  the  question. 
We  find  hydatid  cysts  in  the  spleen,  just  as  in  the  liver,  but  we  cannot  say 
when  they  commence  to  develop,  because  in  both  cases  there  is  a  latent 
period  of  indefinite  duration.  Pain  is  generally  the  first  symptom.  It 
lasted  four  years  in  my  first  case,  and  several  years  in  my  second.  Similar 
facts  obtain  in  most  of  the  cases  which  I  have  collected.  It  is  rarely  early, 
but  more  often  occurs  late.  The  pain,  especially  at  the  onset,  is  neither 
acute  nor  continuous  ;  it  is  rather  duU  and  deep-seated,  with  paroxysms  and 
periods  of  calm.  Its  situation  is  variable.  In  one  case  it  may  simulate  left 
intercostal  neuralgia ;  in  a  second  it  is  abdominal ;  and  in  a  third  the  left 
shoulder  and  scapular  region  are  painful,  especially  if  the  cyst  lies  close  to 
the  diaphragm.  The  pain  in  some  cases  becomes  very  acute,  and  requires 
special  treatment — antipyrine,  morphia,  blisters,  or  applications  of  iodine. 

The  course  of  events  proceeds  in  this  manner  for  one  or  two  years,  or 
longer,  as  in  my  patients,  with  feelings  of  weight  and  dragging  in  the  left 
hypochondrium  and  in  the  abdomen,  but  without  the  appearance  of  clearly 
defined  signs.  During  this  lengthy  period  the  appetite  remains  good  and 
the  strength  does  not  diminish  ;  slight  dyspepsia  or  dyspnoea  may  be  present. 
The  cyst,  however,  grows,  pushes  aside  the  neighbouring  organs,  hampers 
their  function,  gives  rise  to  deformity,  and  excites  fresh  symptoms.  From 
this  time,  according  as  the  cyst  develops  in  one  direction  or  another,  the 
clinical  picture  becomes  so  modified  that  it  is  desirable  to  classify  cysts  of 
the  spleen  in  two  categories. 


1868 


TEXT-BOOK  OF  MEDICINE 


Fia.  84. — Before  Splenectomy. 

A,  Small  mononuclear  lymphocytes  ;  h,  large  mononuclear  leucocytes  ;  c,  intermediary 
leucocytes  ;  d,  polynuclear  leucocytes  ;  e,  eosinopMle  cells. 


/      rf 


Pig.  85. — A  Month  after  Splenectomy. 
A,  Small  mononuclear  lymphocytes  ;  h,  large  mononuclear  leucocytes  ;  c,  intermediary 
leucocytes  ;  d>,  polynuclear  leucocytes  ;  e,  leucocyte  showing  karyokinesis  ;  /,  eosino- 
phile  cells ;  g,  nucleated  red  corpuscle. 


!Pia.  86. — Three  Months  after  Splenectomy. 
Small  mononuclear  lymphocytes  ;  To,  large  mononuclear  leucocytes  ;  c,  intermediary 
leucocytes  ;  A,  poljmuclear  leucocytes  ;  e,  eosinophile  cells. 


inSEASES  OF  TTTK  RTM,7<:EN  l.SHO 

When  the  hydatid  cyst  of  the  spleen  has  comniencod  to  grow,  it  may 
take  several  directions.  If  the  f^rowth  is  downwards,  we  have  a  cyst  of  the 
descending  type.  Tn  this  case  the  tumour  ])rnjcc,ts  into  the  belly,  and  is 
especially  abdominal,  while  the  u])per  portion  hidden  Ixliind  tlif  ril).s  is 
of  minor  importance.  If  the  cyst,  on  the  other  hand,  grows  in  an  upward 
direction,  it  belongs  to  the  ascending  type.  It  pushes  up  the  diaphragm, 
and  displaces  the  thoracic  organs.  The  bulging  is  chiefly  found  in  the  left 
hypochondriac  region  and  the  lower  portion  of  the  thorax.  The  lower 
portion  of  the  tumour,  situated  in  the  abdomen,  is  then  of  minor  importance. 

It  is  therefore  necessary  to  study  the  evolution  and  the  symptoms  of 
hydatid  cysts  of  the  spleen,  according  as  they  grow  downwards,  towards 
the  abdomen  (descending  type),  or  upwards  towards  the  thorax  (ascending 
type).  I  feel  the  more  justified  in  admitting  these  two  clinical  varieties, 
as  they  form  a  faithful  reproduction  of  the  two  cases  above  described. 

Cyst  of  the  Ascending  Type. — Let  us  first  take  the  case  in  which  the 
splenic  cyst  grows  upwards  from  the  left  hypochondrium  towards  the 
thorax  (ascending  type).  The  hypochondrium,  in  this  .case,  first  feels  the 
effect.  The  tumour,  in  its  development,  raises  the  diaphragm  and  dis- 
places the  lower  ribs  outwards.  The  patient  complains  of  thoracic  and 
scapular  pains,  simulating  intercostal  neuralgia  and  scapulalgia.  At  the 
same  time  the  thorax  becomes  deformed,  and  its  base  is  enlarged  ;  the 
lower  ribs  bulge  outwards.  So  far  the  changes  are  evidently  confined  to 
the  hypochondrium  ;  nevertheless,  the  tumour  commences  to  become 
abdominal,  and  forms  a  prominence  in  the  flank. 

As  the  cyst  continues  to  grow,  the  symptoms  become  more  marked. 
The  breathing  is  hampered,  and  the  oppression  is  greater  the  more  the  dia- 
phragm and  the  lungs  are  pushed  up,  and  the  bulging  of  the  lower  part  of 
the  thorax  is  the  more  marked  in  proportion  as  the  ribs  are  more  pushed 
outwards.  Moreover,  by  this  time,  the  tumour  is  no  longer  retrocosta\ 
and  thoracic  ;  it  has  become  abdominal,  and  may  be  felt  in  the  belly.  It 
is  painless,  with  a  regular  outline,  and  is  only  slightly  movable,  being  clamped 
above  in  the  thorax. 

At  length  the  time  comes,  as  in  my  first  case,  when  the  symptoms  reach 
their  maximum.  The  cyst,  by  reason  of  its  upward  growth,  pushes  up  the 
left  lung,  as  far  as  the  upper  intercostal  spaces,  and  displaces  the  heart  to 
the  right  of  the  sternum.  The  dyspnoea  is  severe,  and  interrupted  by 
attacks  of  oppression,  which  coincide  or  alternate  with  crises  of  neuralgia. 
Certain  movements  become  very  painful.  As  regards  the  abdomen,  the 
tumour  increases  in  size,  and  causes  dyspepsia.  The  bulging  is  no  longer 
confined  to  the  hypochondrium,  but  also  affects  the  flank.  When  we  place 
the  patient  in  the  upright  position  and  take  a  full-face  view,  the  bulging  and 
the  deformity  become  more  apparent  on  making  him  turn  to  his  left  side. 


1870  TEXT-BOOK  OF  MEDICIN'E 

In  stort,  tlie   dominant   feature   in    a  cyst  of   tlie  ascending  type  is 

not  tlie  abdominal  symptoms,  but  the  thoracic  ones.  At  first  sight  the  cyst 
may  simulate  a  pleural  efiusion,  since  it  pushes  up  the  diaphragm,  compresses 
the  lung,  and  displaces  the  heart.  We  find,  on  percussion,  dullness  as  high 
as  the  fourth,  or  even  the  third,  intercostal  space,  according  to  the  size  of 
the  cyst.  Dullness  is  also  present  in  the  axiUa  and  at  the  back  of  the  chest, 
although  it  does  not  coincide  exactly  with  the  anterior  limit  of  dullness. 
The  thoracic  vibrations  are  absent  over  the  whole  of  the  dull  area.  On 
auscultation,  we  can  hear  neither  the  normal  respiration  nor  any  abnormal 
sounds.  There  is  complete  silence.  Rales,  due  to  pulmonary  congestion, 
are  heard  both  in  front,  behind,  and  above  the  dull  region.  In  a  word, 
the  examination  of  the  chest  yields  the  signs  of  a  large  pleural  effusion. 

Certain  slight  differences,  however,  give  the  diagnosis  between  effusion 
into  the  left  pleura  and  displacement  of  the  thoracic  organs  by  a  splenic 
cyst.  In  pleural  effasion  the  thorax  may  undergo  an  enlargement  which  is 
perceptible  both  on  inspection  and  on  mensuration.  Some  other  cause 
than  pleural  effusion,  such  as  a  tumour  of  the  hypochondrium,  is,  however, 
necessary,  in  order  to  push  out  the  lower  ribs  and  form  a  bulging  limited  to 
the  lower  part  of  the  thorax.  i^gophony,  pectoriloquy,  and  tubular 
breathing,  which  are  the  usual  signs  of  pleural  effusion,  are  absent  or  excep- 
tional  when  the  thoracic  organs  are  displaced  by  a  cyst  of  the  spleen. 

In  both  pleural  effusion  and  in  a  cystic  tumour  the  heart  may  be  dis- 
placed beyond  the  right  edge  of  the  sternum ;  but  in  pleural  effusion  the 
two  nipples  remain  practically  on  the  same  level,  whereas  in  the  case  of  a 
cyst  the  left  nipple,  which  is  raised  up  together  with  the  skin,  is  found  to  be 
higher  than  the  right  nipple. 

Such  are  the  chief  symptoms  in  a  case  of  hydatid  cyst  of  the  ascending 
type.  They  are  somewhat  more  striking  than  the  abdominal  signs,  of  which 
I  shall  now  speak.  While  the  cyst  encroaches  upon  the  cavity  of  the  thorax, 
it  is  also  dragged  down  towards  the  abdomen  by  reason  of  its  weight  and  its 
growth.  We  find,  therefore,  an  oblong  or  a  rounded  tumour  in  the  flank 
or  in  the  belly.  This  tumour,  which  is  not  movable,  because  it  forms  part 
of  the  cyst  clamped  under  the  thorax,  does  not  assume  a  large  size  in  the 
abdomen.  It  rarely  descends  lower  than  the  umbilicus  or  beyond  the 
line  a  alba. 

We  find,  on  palpation  and  percussion,  that  the  abdominal  and  thoracic 
tumours  are  really  one,  and  measure  10  or  12  inches  in  length,  the  sub- 
costal portion  being  much  more  limited  than  the  supracostal  portion.  This 
feature  permits  the  elimination  of  splenic  enlargement  due  to  malaria, 
leukaemia,  or  to  bacillary  infection,  etc.,  for  the  principal  trait  of  these 
enlarged  spleens  is  that  they  do  not  reach  high  up  into  the  thorax,  but 
descend  low  down  into  the  abdomen,  forming  tumours  which  are  abdominal 


PTSKASKS  OF  T7TE  STTJ'.KN"  1871 

rather  than  tlioracic.  When  we  come  to  the  Rubject  of  the  descending 
type  of  splenic  cyst,  we  shall  have  to  distinguish  between  a  cyst  and  these 
various  forms  of  splenomegaly. 

I  do  not  like  to  leave  the  description  of  splenic  cysts  of  the  ascending  type 
without  speaking  of  certain  severe  complications  which  may  result.  These 
cysts,  in  their  upward  growth  towards  the  thorax,  sometimes  cause  such 
complications  as  perforation  of  the  diaphragm,  invasion  of  the  pleura  and 
lung  by  the  hydatids.     The  following  cases  are  excellent  examples  : 

The  first  of  those  cases  deals  'wath  a  young  woman  admitted  to  hospital  imder 
Amozan's  care  for  acuto  and  long-standing  pain  on  the  left  side  of  the  chest. 

Marked  bulging  of  the  loft  hypochondrium  was  found.  This  region  was  dull,  and 
tactile  fremitus  was  absent.  The  breathing  was  scarcely  perceptible  on  auscultation  ; 
bronchophony  and  cegophony  were  not  audible.  The  heart  was  displaced  to  the  right 
side  of  the  sternum.  Exploration  of  the  abdomen  revealed  a  large,  painless  tumour, 
which  extended  to  within  two  fingers'  breadth  of  the  ihac  crest,  wliile  the  sharp  edge 
reached  almost  to  the  umbiUcus.  Percussion  showed  that  this  abdominal  tumour, 
diagnosed  as  splenic,  was  continuous  with  the  dull  area  in  the  thorax.  A  puncture 
was  made  in  the  eighth  left  intercostal  space,  and  a  few  drops  of  purulent  fluid  drawn 
off,  the  cannula  being  obhterated  by  a  whitish  membrane.  On  microscopic  examination 
the  membrane  showed  hydatid  structure,  and  the  purulent  fluid  contained  booklets 
of  the  echinococcus. 

Arnozan  and  Demons,  considering  the  situation  and  the  abdomino-thoracic  develop- 
ment of  the  tumour,  made  the  diagnosis  of  suppurating  cyst  of  the  spleen.  An  operation 
was  therefore  decided  upon,  and  Demons  performed  it.  After  resection  of  the  ninth 
rib,  the  incision  of  the  subjacent  tissue  led  into  a  cavity  from  which  an  enormous 
quantity  of  purulent  fluid,  with  numerous  hydatids,  flowed  out.  The  finger,  intro- 
duced into  this  cavity  in  order  to  explore  the  vault  of  the  diaphragm,  passed  into  a 
hiatus,  which  was,  in  part,  obhterated  by  hydatid  membrane.  The  membrane  was 
drawn  out  with  forceps,  the  orifice  of  communication  was  enlarged,  and  the  hand  then 
passed  into  an  abdominal  cavity.  A  quantity  of  hydatid  vesicles  were  withdrawn, 
the  cavity  was  washed  out,  and  two  drainage  tubes  introduced — one  into  the  pleural 
cavity,  and  the  other  into  the  abdominal  cystic  cavity. 

The  patient  died  a  few  days  later,  and  the  autopsy  revealed  a  suppurating  cyst, 
which  had  developed  in  the  upper  three-quarters  of  the  spleen.  The  tumour,  in  its  as- 
cending course,  had  perforated  the  diaphragm,  and  opened  into  the  left  pleura.  The 
left  lung  contained  numerous  hydatids.  As  regards  our  anatomical  classification,  the 
case  was  a  typical  one  of  intrasplenic  cyst,  and  the  spleen  tissue  covered  it  everywhere, 
except  at  the  perforation.  Furthermore,  the  spleen  had  undergone  a  certain  amount 
of  compensatory  hypertrophy,  since  it  weighed  8  ounces  after  removal  of  the  cyst. 

A  woman  had  suffered  for  four  years  from  a  tumour  in  the  left  hypochondrium. 
A  large  tumour  occupied  the  flank,  the  left  hypochondrium,  the  hypogastric,  and 
umbihcal  regions,  and  descended  into  the  ihac  fossa.  The  tximour  was  most  prominent 
at  the  epigastrium  and  the  umbiUcus.  It  reached  upwards  under  the  false  ribs,  causing 
dullness  in  the  fifth  intercostal  space.  Tactile  fremitus  and  breath  sounds  were  absent 
over  the  whole  of  the  dull  region,  which  corresponded  to  the  lower  part  of  the  thorax. 
The  diagnosis  of  a  splenic  cyst  invading  the  left  pleura  was  made. 

The  operation  was  performed  by  Reboul.  The  abdominal  incision  revealed  an 
enormous  tumour  beneath  the  ribs  in  the  left  hypochondrium.  The  tumoiir  fluctuated, 
and,  in  the  parts  accessible  to  view,  its  covering  was  formed  of  spleen  tissue.  Puncture 
of   the  tumour  gave  exit  to   a  large  quantity  of  sero-purulent  fluid,  with  hydatid 


1872  TEXT-BOOK  OF  MEDICmE 

debris.  The  wall  of  the  tumour  was  incised  with  the  thermo-cautery.  The  cavity  was 
then  explored,  and  the  operator  found  that  the  cyst  reached  upwards  under  the  dia- 
phragm, and  communicated  with  the  thoracic  cavity  by  a  large  opening.  After  alternate 
periods  of  improvement  and  relapse,  the  situation  became  defuiitely  better,  when  left 
hemiplegia  and  apoplexy  set  in  and  ended  fatally. 

At  the  autopsy  the  spleen  was  found  to  be  hypertrophied  (compensatory  hyper- 
trophy). The  hydatid  had  developed  at  the  upper  end  of  the  organ,  thus  explaining 
its  tendency  to  push  up  the  diaphragm  and  the  thoracic  organs.  Sections  of  the  brain 
revealed,  on  the  inner  surface  of  the  right  hemisphere,  two  suppurating  hydatid  cysts, 
which  opened  into  the  lateral  ventricle.     The  apoplexy  and  death  were  thus  explained. 

Splenic  Cysts  of  the  Descending  Type.— Cysts  of  the  descending  type 
spread  downwards,  and  involve  the  abdominal  cavity.  The  ribs  in  this 
case  are  less  displaced,  the  hjrpochondrium  does  not  bulge  as  much  as  in 
the  preceding  variety,  and  the  chief  growth  of  the  cyst  takes  place,  not  in 
the  hypochondrium  or  in  the  thorax,  but  in  the  abdomen.  The  tumour, 
as  a  whole,  is  abdomino-thoracic,  but  it  is  more  abdominal  than  thoracic. 
The  tumour  commences  in  the  left  hypochondrium,  and  spreads  chiefly  to 
the  abdomen.  In  a  few  years  it  may  acquire  an  enormous  size,  filling  up 
the  flank,  and  encroaching  upon  the  epigastrium  and  the  umbilical  region, 
or  descending  into  the  iliac  fossa.  The  tumour  is  generally  somewhat 
irregular,  resistant,  and  painless — at  any  rate  in  the  early  stages.  It  is 
usually  mobile  and  less  bound  down  by  adhesions.  On  palpation  and 
percussion  we  find  that  the  tumour  reaches  behind  the  ribs,  but  does  not 
cause  the  great  displacement  of  the  diaphragm  and  of  the  thoracic  organs 
seen  in  cysts  of  the  ascending  type. 

The  sjonptoms  of  this  variety  are  chiefly  abdominal :  dyspepsia, 
nausea,  and  vomiting,  with  pain  in  the  stomach  and  intestines ;  digestion 
is  delayed,  and  constipation  is  the  rule.  The  patient  complains  of 
heaviness  and  weight  in  the  abdomen,  and  notices  that  his  stomach 
becomes  larger,  that  his  clothes  feel  too  tight,  and  that  his  movements 
are  hampered. 

The  chief  symptoms  of  hydatid  cysts  of  the  abdominal  type  are  as 
above.  If  the  cysts  spread  upwards  (ascending  type)  as  weU  as  downwards 
(descending  type),  we  find  a  combination  of  thoracic  and  abdominal 
symptoms. 

Diagnosis. — I  have  discussed  the  diagnosis  of  splenic  cysts  which  grow 
upwards  towards  the  thorax  and  simulate  pleural  eflusion  ;  let  us  now 
discuss  the  diagnosis  of  cysts  which  closely  resemble  other  tumours  of  the 
abdomen.  The  diagnosis  between  a  cyst  of  the  spleen  and  one  of  the 
kidney  is  by  no  means  simple.  Thus  Nelaton  was  twice  wrong,  and  mis- 
took a  cyst  of  the  spleen  for  one  of  the  kidney,  and  Potain  diagnosed  a  cyst 
of  the  spleen,  when  the  lesion  was  really  a  left  hydronephrosis.  These 
quotations  are  sufficient  to  show  the  great  difiiculty  in  diagnosis. 


DISKASKS  OF  THM  Sl'LKKN  1873 

SplfMiio  cysts  have  nmiiy  ]K>iuts  in  coniuKHi  with  t lioso  of  Ww.  nnjsfiito.ry. 
Bra(|iiehiiye  lias  thus  prescnlt'd  tliis  «[iuistion  :  If  the,  siirgooii  has  to  deal 
with  an  abdominal  tumour  wliidi  was  ])riinarily  lateral,  but  which  has 
rapidly  become  median,  growing  towards  the  umbilicus,  and  especially  if 
the  tumour  is  accomi)anied  by  Tillaux's  three  signs  (free  mobility  in  every 
direction,  resonant  zone  between  the  walls  and  the  tumour,  and  another 
resonant  zone  above  the  pubes),  it  is  highly  probable  that  the  tumour  is 
mesenteric.  I  may  add  that  a  splenic  cyst  arises  in  the  left  hyj)ochondriurn  ; 
tumours  of  the  mesentery  have  not  this  origin. 

What  are  the  diagnostic  elements  between  hydatid  cysts  of  the  spleen 
and  the  splcnii;  enlargements  due  to  malaria,  leuka3mia,  and  tuberculosis  ? 
As  a  general  rule,  every  enlarged  spleen,  whether  due  to  malaria,  to  leukaemia, 
or  to  tuberculosis,  shows  a  natural  tendency,  by  reason  of  its  weight  and  of 
its  size,  to  extend  from  the  hypochondrium  into  the  abdominal  cavity. 
Every  enlarged  spleen  forms  a  well-developed  timaour,  of  which  the  smaller 
part  is  situated  behind  the  ribs  in  the  hypochondrium,  and  of  which  the 
larger  portion  projects  into  the  abdomen.  The  portion  of  the  tumour 
hidden  behind  the  ribs  in  the  left  hypochondrium  cannot  be  palpated. 
It  reveals  itself  by  dullness  and  by  bulging  of  the  hypochondrium.  The 
abdominal  portion  of  the  tumour  can  be  easily  palpated,  and  we  are  thus 
enabled  to  estimate  exactly  the  situation,  shape,  consistency,  size,  and 
degree  of  mobility  of  the  tumour. 

These  facts  are  equally  applicable  to  abdominal  cysts  of  the  spleen 
and  to  other  enlargements  of  the  organ.  In  both  cases  the  smaller  portion 
of  the  tumour  is  hidden  behind  the  ribs,  and  the  larger  portion  forms  a 
marked  projection  in  the  abdomen.  How,  then,  can  the  diagnosis  between 
splenic  cyst  and  splenomegaly  be  decided  ?  In  order  to  do  so  let  us  review 
the  different  enlargements  of  the  spleen,  and  see  what  are  their  distinctive 
characters. 

Let  us  commence  with  the  malarial  spleen.  The  spleen  may  be 
enormously  enlarged  in  persons  suffering  from  malaria,  especially  in  the 
chronic  forms  and  in  cachexia.  The  organ  bulges  in  the  left  hypochondrium, 
and  forms  in  the  abdomen  a  tumour,  which  is  sometimes  exceedingly  large. 
The  malarial  spleen,  although  it  is  much  hypertrophied,  practically  pre- 
serves its  form,  and  is  not  bilobed,  in  contradistinction  to  the  splenic  cyst. 
Further,  while  the  cyst  runs  its  course  without  fever  and  without  affecting 
the  general  health  for  a  long  while,  the  malarial  spleen  is  preceded  by  attacks 
of  fever  of  different  kinds,  and  becomes  larger  with  the  febrile  attacks  and 
with  the  appearance  of  cachexia  ;  and  the  liver  is,  moreover,  generally 
hj'^ertrophied. 

Let  us  consider  the  enlarged  spleen  of  leucocythaemia.  I  had  a  remark- 
able example  under  my  care  some  years  ago  : 


1874  TEXT-BOOK  OF  MEDIOHSTE 

The  patient  was  admitted  to  hospital  in  an  advanced  stage  of  cachexia.  His 
appearance  resembled  that  of  a  cancerous  patient :  earthy  tint  and  colourless  mucous 
membranes,  cedema  of  the  legs  and  purpura.  The  patient  complained  of  extreme 
weakness  and  felt  ill.  On  examination  we  found  in  the  abdomen  an  enormous  tumour. 
It  was  hard  and  painless,  and  caused  deformity  of  the  left  flank  and  the  hypochondrium. 
It  reached  almost  as  low  as  the  umbilicus,  and  was  wedged  in  above,  beneath  the  ribs, 
where  the  duUness  extended  as  high  as  the  fifth  intercostal  space.  The  diagnosis  of  an 
enlarged  spleen  was  made,  but  it  remained  to  determine  the  nature  of  this  tumour. 
If  the  cachectic  patient  with  this  enormous  spleen  had  also  presented  glandular  swell- 
ings in  the  neck,  groin,  and  axilla,  we  should  at  once  have  thought  of  leucocyth^emia, 
but  he  had  no  apparent  glandular  hypertrophy.  And  yet  this  fact  was  not  a  reason 
for  abandoning  the  diagnosis  of  leucocythsemia,  for  examples  of  splenic  lymphadenia 
exist,  without  apparent  glandular  tumours. 

In  order  to  decide  the  question,  Apert  examined  the  blood,  and  the  diagnosis  of 
a  leucocythsemic  spleen  was  confirmed.  The  patient  had  50,000  white  corpuscles  to 
1,900,000  red  corpuscles,  or  a  proportion  of  1  to  40,  instead  of  1  to  500  ia  the  normal 
condition.  Nevertheless,  ia  leucocythsemia  it  is  not  sufficient  to  find  considerable 
excess  of  the  white  corpuscles  ;  we  must  also  know  to  which  variety  they  belong.  This 
case  was  one  of  leukemia,  with  small  mononuclear  leucocytes  (the  lymphocytes  of 
Grerman  authors,  and  the  globulins  of  the  old  French  authors).  The  diagnosis  was 
verified  at  the  autopsy.  The  hydatid  cyst  of  the  spleen  is  for  a  long  while  compatible 
with  good  health,  and  does  not  modify  the  normal  condition  of  the  blood.  The  leuco- 
cythffimic  spleen,  on  the  other  hand  (with  or  without  participation  of  the  lymphatic 
glands),  is  accompanied  by  considerable  excess  of  white  corpuscles  ia  the  blood,  with 
predominance  of  leucocytes,  or  of  lymphocytes  according  to  the  case. 

Let  us  now  see  kow  it  is  possible  to  arrive  at  a  diagnosis  between  hydatid 
cysts  of  tbe  spleen  and  primary  tubercular  splenomegalia.  In  addition  to 
the  secondary  infection  of  the  spleen  resulting  from  other  localizations  of 
the  tubercle  bacillus  (broncho-pneumonia,  miliary  tuberculosis,  micro- 
polyadenia,  etc.),  primary  tuberculosis  of  the  spleen  has  been  described  by 
Rendu  and  Widal,  Moutard-Martin  and  Lefas,  and  by  Guiliani.  This 
disease  does  not  appear,  as  was  formerly  supposed,  in  the  course  of  advanced 
phthisis ;  it  develops  during  good  health  in  persons  whose  tubercular  taint 
has  passed  unnoticed.  The  only  symptoms  for  some  time  are  pain  in  the 
left  hypochondrium,  and  a  sensation  of  weight  and  dragging ;  but  dyspnoea 
may  also  appear  in  some  cases. 

After  this  indefinite  phase  has  lasted  for  some  months,  the  splenic  tumour 
has  become  large  ;  it  projects  into  the  hypochondrium,  descends  into  the 
flank,  and  invades  the  abdomen,  forming  an  ovoid  or  oblong  mass,  which  is 
indurated  and  nodular.  The  hjrpochondrium  and  the  flank  bulge.  The 
disease,  sometimes  apyretic  and  at  other  times  febrile,  may  last  for  several 
years  and  end  fatally.  The  autopsy  reveals  an  enormous  spleen,  weighing 
from  3  to  8  pounds.  Its  shape  is  practically  normal,  its  large  diameter  is 
from  6  to  12  inches,  and  its  surface  presents  nodular  masses,  varying  in  size 
from  a  cherry  to  an  orange.  The  cut  section  of  the  tumour  shows  fibrous 
tissue,  infiltrated  with  caseous  masses.     It  is  rare  to  find  Koch's  bacilli. 

How  are  we  to  diagnose  a  tubercular  spleen  from  a  hydatid  cyst  ?     The 


PrSEASES  OF  THE  SPLEEN  187.', 

differential  sif^ns  are  :  The  tubercular  spleen  is  more  nodular  than  the 
cyst ;  it  afl'ects  the  health  much  more  quickly,  and  is  accompanied  by  hyper- 
trophy of  the  liver.  Lastly,  though  this  might  not  be  expected,  it  some- 
times excites  such  an  increase  in  red  corpuscles  that  the  count  shows 
8,000,000  to  the  cubic  centimetre,  with  or  without  leucocytosis.  It  is  true, 
however,  that  in  a  case  reported  by  Achard  and  Castaigne  this  increase  of 
red  corpuscles  was  not  present. 

Let  us  now  consider  the  diagnosis  between  hydatid  cyst  of  the  spleen 
and  so-called  primary  splenomegaly.  In  the  first  place,  what  is  meant 
by  splenomegaly  ?  This  term,  coined  by  Debove,  is  applied  to  an  affection 
characterized  by  hypertrophy  of  the  spleen,  followed  later  by  enlargement 
of  the  liver,  by  absence  of  glandular  tumours,  and  by  progressive  diminution 
of  the  red  blood  cells,  without  notable  increase  in  the  leucocytes.  Anaemia, 
loss  of  strength,  and  wasting  coincide  with  the  enlargement  of  the  spleen, 
which  may  weigh  from  4  to  6  pounds.  Certain  rare  cases  of  this  "  hyper- 
trophic cirrhosis  of  the  spleen  "  have  been  confounded  with  the  lesion 
formerly  described  by  Gaucher  under  the  name  of  primary  epithelioma 
or  idiopathic  hj^ertrophy  of  the  spleen  without  leukaemia.  In  any  case 
primary  splenomegaly  is  distinguished  from  hydatid  cyst  of  the  spleen  by 
the  following  signs  :  In  splenomegaly  the  surface  and  outlines  of  the  spleen 
do  not  present  the  deformity  of  the  cystic  spleen  ;  the  liver  is  enlarged,  the 
anaBmia  is  constant,  and  the  general  health,  which  remains  good  for  a  long 
time  during  the  development  of  the  splenic  cyst,  is  rapidly  affected  in 
primary  splenomegaly. 

There  are  certain  cases  of  greatly  enlarged  spleens  which  do  not  enter 
into  any  of  the  preceding  categories.  A  lady  student  of  medicine  re- 
counted her  own  case  to  me  : 

For  eleven  years  the  spleen  had  increased  in  size,  until  it  became  as  large  as  the 
head  of  a  three-year-old  child,  but  it  never  caused  any  symptoms.  She  had  no  pain, 
no  oedema,  no  signs  of  pressure,  and  no  change  in  the  composition  of  blood.  As  the 
tumoiur  was  becoming  troublesome,  it  was  removed  by  Routier,  and  was  found  to  be  a 
spleen  weighing  8  pounds.  The  splenic  tissue  was  semi  transparent  on  section.  Histo- 
logically the  hypertrophy  was  due  to  a  primary  fibrous  degeneration,  probably  dependent 
upon  some  unknown  infective  process.  Haemorrhages,  which  were  most  hkely 
secondary,  were  found  in  the  spleen  tissue.  Such  a  case  of  splenomegalia  is  not  always 
easy  to  differentiate  from  a  hydatid  cyst. 

In  making  a  diagnosis  of  hydatid  cysts  of  the  .spleen,  it  is  useful  to 
employ  the  method  of  deviation  of  the  complement  by  the  hydatid  anti- 
bodies, or  Weinberg's  reaction. 

After  having  reviewed  the  enlarged  spleens,  which  simulate  more  or  less 
closely  a  hydatid  cyst  of  this  organ,  let  me  say  a  few  words  as  to  its  evolu- 
tion, which  is  very  slow,  the  first  phase  being  insidious,  and  the  symptoms 
usually  indefinite.     The  cyst  takes  two  or  three  years  before  it  acquires  the 


1876  TEXT-BOOK  OF  MEDICmE 

size  seen  in  my  two  cases.  The  general  health  remains  good,  except  for 
pain,  dyspnoea,  and  dyspepsia,  and  we  are  surprised  to  see  such  an  enormous 
tumour  compatible  with  apparent  health.  A'ery  serious  complications  are, 
however,  to  be  feared  in  the  long  run,  especially  infection  and  suppuration 
of  the  cyst,  with  perforation  of  the  diaphragm  and  invasion  of  the  pleura, 
as  in  the  two  cases  which  I  have  just  quoted. 

Danger  also  arises  from  the  invasion  of  other  organs  by  the  hydatids. 
As  long  as  the  spleen  alone  is  infected,  we  may,  by  a  well-timed  operation, 
remove  the  trouble,  but  if  the  hydatids  afiect  the  liver,  the  kidneys,  the 
lungs,  the  brain,  etc.,  the  situation  is  far  more  formidable. 

My  second  patient  who  recovered  from  the  splenic  hydatid  had  also  a 
cyst  in  his  left  kidney.  Here  the  pain  in  the  left  lumbar  region,  and  the 
colic  produced  by  the  passage  of  the  hydatid  membrane,  revealed  the 
diagnosis. 

I  have  collected  a  fairly  large  number  of  cases  in  which  the  splenic 
cyst  was  complicated  by  cysts  in  other  regions  :  Hydatid  cysts  of  the  spleen 
and  liver ;  hydatid  cysts  of  the  spleen,  Hver,  and  lung  ;  hydatid  cysts  of 
the  spleen,  liver,  and  pehds  ;  hydatid  cysts  of  the  spleen  and  right  pleura  ; 
hydatid  cysts  of  the  spleen,  right  pleura,  and  brain  ;  hydatid  cysts  of  the 
spleen  and  pehds  ;  hydatid  cysts  of  the  spleen,  liver,  gall-bladder,  omentum 
and  of  the  right  FaUopian  tube  ;  hydatid  cysts  of  the  spleen  and  the 
omentum. 

The  multiplicitv  of  hvdatid  cysts,  and  especially  the  localization  of  some 
of  them,  cause  special  complications  as  regards  prognosis.  It  is  always 
necessary  to  think  of  the  possibility  of  general  hydatid  infection. 

Treatment. — Apart,  from  cases  in  which  several  organs  are  attacked, 
we  may  say  that  hydatid  cyst  of  the  spleen,  which  was  formerly  a  most 
formidable  disease,  is  now  curable,  thanks  to  the  marvellous  progress  of 
surgery.  And  yet  it  is  highly  necessary  that  surgical  intervention  should 
not  be  delaved  too  long,  for  here,  as  in  aU  cases,  it  is  not  sufficient  to  operate  : 
the  operation  must  be  performed  in  time.  The  duty  of  making  a  correct 
diagnosis  and  of  deciding  as  to  surgical  intervention  is  incumbent  upon  the 
physician.  The  surgeon's  duty  is  to  perform  the  operation  of  choice.  Intra- 
splenic  cysts  necessitate  splenectomy,  while  the  spleen  may  be  preserved 
in  the  case  of  juxtasplenic  cysts. 


PART  VII 

PATHOLOGY  OF  THE  BLOOD 

I.  CLINICAL  EXAMINATION  OF  THE  BLOOD. 

The  clinical  exaiuiuatioii  of  the  blood  may  afford  valuable  information  in 
diagnosis  and  prognosis.  Physicians  were  formerly  content  with  the  gross 
physical  and  chemical  examination  of  the  blood  withdrawn  from  a  vein. 
This  study  was  rendered  easier  by  the  frequency  of  bleeding  as  a  thera- 
peutic measure.  It  is  sufficient  to-day  to  withdraw  a  few  drops  of  blood  by 
pricking  the  finger  in  order  to  obtain  the  necessary  clinical  information, 
which  depends  upon  the  histological  condition  of  the  blood,  its  chemical 
composition,  and  its  bacteriological  features. 

The  enumeration  of  the  blood-corpuscles  is  made  with  Malassez's  or 
with  Hayem's  instruments,  but  we  cannot  here  enter  into  the  details  of  the 
technique. 

The  percentage  of  haemoglobin  is  estimated  by  the  colorimetric  appa- 
ratus of  Malassez,  Hayem,  or  of  Henocque.  Malassez's  instrument  gives 
the  weight  of  haemoglobin  in  100  c.c.  of  blood.  On  dividing  the  amount 
by  the  nimiber  of  red  blood-corpuscles,  we  easily  obtain  the  weight  of 
haemoglobin  contained  in  a  single  red  blood-corpuscle,  which  is  called  the 
colour  index.  This  information  is  of  the  highest  importance  in  clinical 
medicine. 

Normal  blood  contains  4,500,000  red  blood-corpuscles  per  cubic  milli- 
metre, and  10  to  15  grammes  of  haemoglobin  per  100  c.c.  of  blood,  while 
the  colour  index  is  from  28  to  30.  Malassez's  system  of  cormting  is  the 
best,  but  other  authors  express  the  quantity  of  haemoglobin  in  percentages, 
employing  a  comparative  standard  of  so-called  normal  blood  to  which  they 
assign  a  value  of  100.  Others,  again,  including  Hayem,  estimate  the 
quantity  of  hasmoglobin  (which  they  call  the  globular  richness)  by  the 
number  of  healthy  red  blood-corpuscles. 

Spectroscopic  examination  gives  information  as  to  the  state  of  the 
blood  in  certain  pathological  conditions,  such  as  carbonic  oxide  asph}^sia. 

Bacteriological  examination  of  the  blood  comprises  the  direct  examina- 
tion upon  the  slide  of  fresh  blood,  and  of  fixed  and  stained  blood,  as  well  as 
II.  1877  110 


1878  TEXT-BOOK  OF  MEDICINE 

tlie  cultivation  of  tlie  blood  on  various  culture  media  and  inoculation  in 
animals.  We  have  frequently  had  occasion  to  speak  of  this  method  during 
the  course  of  this  treatise. 

The  histological  examination  of  the  blood  should  be  made  upon  fresh 
preparations,  as  weU  as  upon  fixed  and  stained  films. 

For  the  examination  of  fresh  blood,  it  suffices  to  place  a  drop  of  blood 
upon  a  slide,  to  put  a  cover-glass  over  it,  and  to  seal  the  edge  with  paraffin, 
but  we  may  also  employ  Malassez's  air-chambers  or  Hayem's  hoUow  ceU. 
These  consist  of  thick  glass  slides,  upon  which  a  disc  of  glass  is  isolated  by 
means  of  a  circular  trench.  If  the  preparations  are  examined  under  the 
microscope,  we  find  a  large  number  of  smaU,  yellowish  corpuscles  floating  in 
a  colourless  fluid — the  blood  plasma.  These  are  the  red  bloOd-COrpuscIes, 
which  have  the  shape  of  a  biconcave  disc.  They  often  form  rouleaux,  and 
present  their  edge  to  the  observer.  These  rouleaux  are  united  by  their 
extremities,  and  enclose  spaces  in  which  the  plasma  contains  only  the  white 
corpuscles,  or  leucocytes. 

The  white  corpuscles  are  present  in  much  fewer  numbers.  They  have 
the  appearance  of  colourless,  shining,  mobile  cells.  Lastly,  we  see  small, 
colourless  granulations,  or  Hayem's  hsematoblasts,  united,  as  a  rule,  in 
small  groups.  These  extemporaneous  preparations,  which  should  always 
be  examined,  indicate  approximately  the  richness  of  the  blood  in  red  and 
white  cells.  They  may  reveal  the  presence  of  dark  pigment  grains  and  of 
parasites.  If  the  preparation  is  left  alone,  fibrin  is  precipitated,  and  forms 
a  network  of  fine  fibrillse,  so  that  we  may  estimate  in  an  approximate 
manner  the  richness  of  the  blood  in  fibrin. 

It  is  necessary  to  fix  and  stain  the  blood  if  we  wish  to  obtain  permanent 
preparations.  The  most  widely  employed  method  consists  in  collecting  a 
drop  of  blood  on  the  end  of  a  slide,  spreading  it  out  over  the  slide,  and 
drying  the  thin  layer  of  blood  by  shaking  in  the  air. 

If  the  process  of  drying  lasts  for  some  weeks,  the  blood  is  fixed,  and 
remains  unaltered  by  water.  In  the  contrary  case,  it  is  necessary  to  com- 
plete the  fixation  by  the  action  of  difierent  reagents  (absolute  alcohol, 
mixture  of  absolute  alcohol  and  ether,  or  a  1  per  cent,  solution  of  chromic 
acid),  or  by  dry  heat  at  120°  C,  according  to  Ehrlich's  method. 

In  exceptional  cases,  as  in  myelogenic  leuksemia,  we  may  advantageously 
employ  for  comparison  Jolly's  method,  which  consists  in  employing  the 
fixative  agent  (Fleming's  solution)  to  the  blood,  which  has  been  spread  out, 
but  not  dried. 

Haematoxylin  and  aniline  dyes  are  the  usual  stains  employed  in  staining 
the  blood.  The  aniline  dyes  are  divided  by  Ehrlich  into  acid  and  basic. 
The  former  comprise  eosin,  orange  and  acid  fuchsin,  and  act  upon  the 
eosinophiles,  granules,  and  the  red  corpuscles  ;  while  the  basic  dyes  comprise 


rATHOLOGY  ()F  THE  BLOOD  1870 

thionine,  methyl  violet,  and  methylene  blue.  They  Ktain  the  Ho-caHed 
baaophile  granides,  the  nucleus  of  the  leucocyteH,  and  the  nucleated  red 
blood  cells.  Lastly,  Ehrlich  has  distinguished  in  the  neutral  stains  those 
which  are  ])roduced  by  the  admixture  of  acid  and  basic  dyes,  and  also 
neutrophile  granules.  Jolly  has  shown  that  the  neutrophile  granules  may 
take  the  acid  stains,  though  more  feebly  than  the  eosinophile  granules. 
The  examination  of  fixed  and  stained  preparations  shows  the  nucleus  of 
the  leucocytes,  marks  out  their  various  granulations,  indicates  the  per- 
centage of  the  varieties,  and  distinguishes  the  changes  in  form  and  the 
staining  reactions  of  the  red  corpuscles,  the  presence  of  nucleated  red  cor- 
puscles, and  the  increase  or  the  diminution  in  the  haematoblasts. 

The  histological  lesions  of  the  blood  cannot  be  properly  understood, 
unless  we  know  the  varieties  of  leucocytes  normally  present.  It  is,  there- 
fore, advisable  to  mention  these  points  in  haematology.  Normal  blood 
contains  about  7,000  leucocytes  per  cubic  millimetre,  or  one  white  corpuscle 
to  600  red  corpuscles.     Jolly  has  classified  the  leucocytes  as  follows  : 

The  first  variety  comprises  the  small  mononuclear  leucocytes.  I  would 
prefer  to  call  them  microlymphocytes,  in  order  to  distinguish  them  from 
the  leucocytes  proper.  They  form  the  most  important  element  in  the 
lymphatic  glands,  but  they  are  rare  in  normal  blood,  amoimting  to  2  per 
cent,  of  the  white  corpuscles.  They  are  smaller  than  the  red  corpuscles, 
and  the  nucleus  is  at  times  so  large  that  it  appears  to  fill  the  whole  cell, 
leaving  but  little  room  for  the  protoplasm.  We  shall  see  later  that  the 
accumidation  of  lymphocytes  in  the  blood  is  the  characteristic  feature  of 
one  of  the  varieties  of  leucocythsemia. 

The  second  variety  comprises  the  large  mononuclear  leucocytes.  The 
cell  contains  one  nucleus,  but  the  protoplasm  is  more  abundant  than  in  the 
preceding  variety. 

This  variety  includes  the  so-called  intermediary  leucocjrtes,  in  which 
the  nucleus  is,  as  it  were,  strangulated.  The  nucleus  looks  as  if  it  were 
about  to  divide,  and  the  leucocyte  is,  therefore,  said  to  be  intermediate 
between  the  mononuclear  and  poljTiuclear  leucocytes.  The  large  mono- 
nuclear and  intermediary  leucocytes  form  36  per  cent,  of  the  white  cor- 
puscles. 

The  third  variety  comprises  the  polynuclear  leucocytes.  The  nucleus  is 
sometimes  bent  in  the  form  of  a  rod,  constricted  at  certain  points  ;  at  other 
times  there  are  several  distinct  nuclei,  as  though  the  rod  had  broken  at 
different  points.  These  leucocjrtes  amount  to  60  per  cent,  of  the  total 
number  of  leucocytes  in  normal  blood. 

The  fourth  variety  comprises  the  eosinophile  cells.     In  normal  blood 

they  amount  to  1  or  2  per  cent.     The  protoplasm  contains  granules,  which 

stain  deeply  with  eosin. 

119—2 


1880  TEXT-BOOK  OF  MEDICINE 

Abnormal  Elements. — Certain  rare  or  abnormal  elements  are  found  in 
the  blood.  Their  number  does  not  exceed  1  or  2  per  cent.,  but  it  is 
greater  in  pathological  conditions.  Some  are  about  as  large  as  a  lymphocj^e, 
and  the  protoplasm  stains  deeply  with  the  blue  dyes.  They  are  called 
plasma  cells.  The  nucleus  is  sometimes  clear,  and  scarcely  stained.  The 
cell  is  a  mononuclear  basophile.  Others  are  also  mononuclear,  but  they 
also  contain  neutrophile  or  eosinophile  granulations.  They  have  been 
called  granular  myelocytes,  because  they  originate  from  the  bone-marrow, 
and  appear  to  give  rise  to  the  normal  polynuclear  cells.  Lastly,  we  have  the 
mastzeUen,  in  which  the  nucleus  is  multilobar  or  regular,  and  in  which  the 
protoplasm  contains  basophile  granulations. 

Some  writers,  by  means  of  artificial  haemolysis,  have  found  abnormal 
pigmentary  and  neoplastic  cells  in  the  blood.  The  latter  are  often  difficult 
to  distinguish  from  the  large  mononuclears  of  normal  blood.  In  cases  of 
cancer  their  presence  in  the  blood  indicates  the  generalization  of  the 
disease. 

Variations  in  the  Leucocytes. — The  leucocytes  show  more  or  less  con- 
stant variations  in  the  course  of  the  different  morbid  processes.  In  some 
cases  we  find  an  increase  in  the  number  of  leucocytes  or  leucocytosis ;  in 
others  there  is  a  diminution  or  leucopenia,  Leucocytosis  is  more  common 
than  leucopenia,  and  marked  leucocytosis  often  follows  recovery  from 
transient  leucopenia. 

Leucocytosis  is  most  marked  in  the  inflammatory  affections  :  acute 
rheumatism,  pneumonia,  erysipelas,  suppurative  troubles,  and  scarlatina. 

Leucopenia  occurs  in  typhoid  fever,  in  certain  forms  of  malaria,  in  severe 
and  fatal  infections  or  intoxications,  etc. 

Great  importance  is  attached  at  the  present  day  to  the  qualitative 
variations  in  the  leucocytes  in  the  course  of  disease.  In  most  cases  we  find 
an  increase  in  the  number  of  polynuclears  (polynucleosis) ;  in  some  cases 
the  increase  is  in  the  mononuclears  (lymphocytosis),  and  in  others  it  is  in 
the  eosinophiles  (eosinophilia). 

Polynucleosis  is  met  with  in  inflammatory  and  suppurative  affections  : 
pneumonia,  empysema,  acute  meningitis.  The  percentage  may  be  as  high 
as  85  or  90.  It  is  also  seen  in  scarlatina  (95  per  cent.).  It  may  help  to 
distinguish  between  pneumonia  and  typhoid  fever,  between  acute  tuber- 
cular pleurisy  or  bacillary  meningitis,  and  purulent  pleurisy  or  meningitis, 
between  measles  and  scarlet  fever.  In  certain  affections  —  pneumonia 
(Loeper),  erysipelas  (Chantemesse  and  Widal) — a  polynucleosis  of  more 
than  95  per  cent,  indicates  rapid  death. 

In  polynucleosis  the  presence  of  glycogen  in  the  leucocytes  may  be 
shown  by  the  iodine  test.  Brown  granules  are  seen  in  the  protoplasm  of  the 
leucocytes.     The  reaction  indicates  acute  inflammation. 


TATHOLOGY  OF  T7TE  BLOOD  1881 

Monomicloosis  is  seen  in  the  stationary  stage  of  typhoid  fever,  in  mumps, 
and  in  mahiriu. 

Lymphocviosis,  which  is  always  marked  in  the  infant,  is  almost  constant 
in  the  following  conditions  :  whooping-cough,  measles,  acute  tuberculosis  of 
the  organs  and  serous  membranes,  syphilis,  and  lead-poisoning. 

Eosinophilia  is  common  in  convalescence  from  rheumatism,  tyjjhoid 
fever,  scarlatina,  and  erysipelas.  In  this  case  it  has  been  called  critical 
eosinophilia.  On  the  other  hand,  reactionary  eosinophilia  has  been  described 
in  certain  intoxications  (mercury,  iodine),  in  diseases  of  the  skin  (Diihring's 
dermatitis),  and  in  helminthiasis. 

Plasma  cells  are  common  in  the  critical  stage  of  diseases.  Granular  and 
non-granular  myelocytes  are  foimd  in  the  blood  in  certain  morbid  conditions  : 
purpura,  hsemorrhagic  typhoid  fever,  hereditary  syphilis,  and  variola. 

These  leucocytic  variations  are  not  specific,  because  they  depend  chiefly 
on  the  gravity  of  the  affection,  on  the  anatomical  process  which  charac- 
terizes it,  and  not  upon  the  nature  of  the  micro-organism  or  poison  which 
is  at  work. 

Moreover,  polynucleosis,  mononucleosis,  and  eosinophilia  are  often  mere 
phases  of  a  more  complex  reaction.  On  closer  study,  the  leucocytic  formulae 
appear  to  be  traced  on  the  same  type  :  at  the  onset,  polynucleosis,  primary 
reaction ;  in  the  stationary  stage,  mononucleosis,  more  profound  reaction 
of  immunity  ;  in  the  stage  of  convalescence,  eosinophilia,  stigma  of  recovery. 
Accordingly,  the  early  appearance,  the  persistence,  and  the  abmidance  of 
the  different  forms  of  leucocytes,  rather  than  their  presence,  are  of  use  in 
bsemo-diagnosis  and  hsemo-prognosis. 

II.  AN.EMIA. 

Any  change  in  the  respiratory  function  of  the  blood  is  called  an  anaemia 
(Jolly).  This  change  may  consist  in  the  diminution  of  the  mmiber  of  red 
blood-corpuscles,  in  the  diminution  or  the  alteration  of  the  haemoglobin, 
in  the  lowering  of  the  colour  index,  etc.,  and  these  different  lesions,  which 
are  associated  in  various  ways,  affect  the  chief  function  of  the  blood — 
namely,  its  power  of  distributing  oxygen. 

In  slight  anaemia  we  see,  as  a  rule,  some  diminution  in  the  number  of 
red  blood-corpuscles  ;  in  more  severe  cases  the  lowering  of  the  colour  index 
is  also  present,  in  addition  to  the  diminution  in  the  number  of  the  red 
corpuscles.  In  chlorosis,  the  lowering  of  the  colour  index  predominates.  It 
may  coexist  with  the  normal  number  of  red  corpuscles.  In  pernicious 
anaemia,  the  number  of  red  corpuscles  is  always  diminished  to  a  considerable 
degree,  but  the  colour  index  is,  on  the  contrary,  normal  or  even  increased. 

Anaemia  following  haemorrhage  has  served  as  the  basis  for  the  study  of 


1882  TEXT-BOOK  OF  MEDICINE 

anaemia,  and  for  researches  as  to  the  repair  of  the  blood.  It  has  been 
studied  experimentally,  because  it  can  be  readily  produced  in  animals.  In 
man,  it  is  exceptional  to  meet  with  it  under  such  conditions  that  the  result 
may  not  be  produced  by  the  disease  which  has  caused  the  haemorrhage. 
Nevertheless,  it  is  sometimes  possible. 

In  one  of  my  patients  blanched  by  severe  bsematemesis,  following  exulceratio  simplex 
of  the  stomach,  and  having,  on  his  admission  to  hospital,  only  650,000  red  blood- 
corpuscles  per  cubic  millimetre,  JoUy  was  able  to  follow  the  repair  of  the  blood  under 
the  most  favourable  conditions. 

He  showed  that  this  repair  took  place  in  the  same  manner  as  in  animals 
which  had  been  bled.  After  an  acute  haemorrhage,  we  find  a  first  period, 
in  which  the  number  of  red  corpuscles  and  the  quantity  of  haemoglobin 
continue  to  fall  on  parallel  lines.  The  colour-index,  therefore,  remains 
stationary.  In  the  second  period,  the  number  of  red  corpuscles  increases 
rapidly.  Nucleated  red  corpuscles  appear  in  the  blood,  but  the  haemoglobin 
remains  stationary,  and  rises  again  very  slowly  ;  consequently,  the  colour- 
index  is  lowered.  In  the  third  period,  the  number  of  red  corpuscles  con- 
tinues to  rise,  though  slowly.  The  haemoglobin  count  increases  rapidly, 
and  the  colour-index  rises.  These  results  are  interesting,  because  they  have 
a  general  application,  and  because  the  repair  of  the  blood  takes  place  in 
the  same  manner  in  all  cases  of  symptomatic  anaemia,  as  well  as  in  chlorosis. 

In  the  experimental  anaemias,  just  as  in  the  traumatic  anaemias  in  man, 
we  may  see  in  the  blood  during  the  period  of  repair  nucleated  red  cells, 
which  are  sometimes  present  in  large  numbers  (Jolly). 

The  various  diseases  of  nutrition,  the  acute  and  chronic  infectious  dis- 
orders, and,  in  particular,  acute  rheumatism,  malaria,  variola,  chronic  tuber= 
culosis,  the  intoxications  such  as  lead-poisoning,  intestinal  parasites, 
syphilis,  and  cancer,  most  often  cause  anaemic  conditions,  which  are  grouped 
together  under  the  term  secondary  or  symptomatic.  We  look  on  them  as 
the  opposite  of  the  so-called  essential  anaemias,  in  which  the  blood  lesion 
is  not  a  secondary  symptom,  or  a  simple  consequence,  but  comprises  prac- 
tically the  whole  disease.  Such  are  pernicious  anaemia  and  chlorosis,  which 
will  form  the  subject  of  special  sections. 

III.  PEOGRESSIVB  PERNICIOUS  ANEMIA. 

Biermer  deserves  the  merit  of  having  described  in  1868  and  in  1872 
pernicious  anaemia  as  a  morbid  entity,  but  it  must  not  be  thought  that  the 
clinical  type  was  unknown  before  his  day.  Andral,  Piorry,  Beau,  and 
Addison  had  previously  noticed  it,  and  Trousseau  had  given  a  masterly 
description,  which  has  hardly  been  added  to  by  the  researches  of  haema- 
tology. 


PATHOLOGY  OF  THE  BLOOD  188^ 

While  numerous  authora  have  contributed  to  indix-idualize  pernicious 
anncmia  by  researches  as  to  the  retiology,  pathological  anatomy,  and  haema- 
tology,  others  have  asked  whether  the  anatomy  of  this  morbid  tvi>e  in  real, 
and  whether  it  is  not  always  sjinptomatic  of  cancerous,  tubercular,  or  other 
lesions.  The  tnith  is  that,  in  addition  to  the  extreme  deuteropathic 
anaemias,  there  is  room  for  a  grave  essential  anaemia,  of  which  the  primary 
cause  will  doubtless  be  revealed  to  us  some  day,  just  as  it  has  been  in  miners' 
anaemia. 

The  disease  occurs  chiefly  in  certain  very  poor  districts  of  Switzerland, 
Prussia,  and  Sweden,  and  especially  in  pregnant  and  nursing  women.  It  is 
most  frequently  caused  by  insufficient  nourishment,  physical  or  intellectual 
overwork,  excesses,  or  trouble. 

Pathological  Anatomy. — Post  mortem,  the  tissues  are  extremely  pale. 
The  skin,  the  mucous  membranes,  and  the  parenchyma  are  oedematous.  or 
studded  with  small  hsemorrhages.  The  heart  shows  partial  fatty  degenera- 
tion of  its  muscular  fibres.  The  liver  is  pale,  the  cells  are  atrophied,  and 
the  nuclei  no  longer  stain  (Hanot  and  Segry). 

Certain  authors  have  recently  attempted  to  place  the  initial  lesion  of  the 
disease  either  in  the  stomach  or  in  the  bone-marrow. 

The  glands  of  the  stomach  are  often  afiected  by  fatty  degeneration  and 
by  extreme  atrophy,  and  the  organ  itself  may  be  so  thin  as  to  resemble  a 
serous  membrane  (Gilbert).  Fenwick,  Quincke,  and  Nothnagel  have  insisted 
on  the  presence  of  this  lesion,  but  before  we  can  admit  with  Fenwick  that 
pernicious  anaemia  is  only  a  symptom  of  gastric  atrophy,  we  have  to  prove 
that  this  atrophy  is  not  the  result  of  the  anaemia. 

The  bone-marrow  is  often  red,  rich  in  nucleated  corpuscles,  and  thus 
shows  a  return  to  the  embryonic  condition.  Pepper  would  make  this  change 
in  the  marrow  the  'priynum  movens  of  the  disease.  It  is  possible,  says 
Gilbert,  that  pernicious  anaemia  is  a  myelogenous  lymphadenia ;  but  would 
it  not  be  better  to  reverse  the  proposition,  and  consider  the  return  of  the 
marrow  to  the  embryonic  condition  as  the  consequence  of  the  extreme 
anaemia  ?  In  pernicious  anaemia  we  find  diminution,  not  only  of  the  red 
corpuscles,  but  also  of  the  haematoblasts.  This  anhaematopoiesis,  as  Hayem 
calls  it — that  is  to  say,  the  sterility  of  the  blood — would  cause  a  resurrection 
of  the  foetal  haematopoietic  functions  of  the  liver,  of  the  spleen,  and  especially 
of  the  bone-marrow. 

The  bacteriological  researches  of  recent  years  have  thrown  no  light  upon 
the  pathogenesis  of  the  disease.  Feltz  and  Engel  have  seen  small  rods  in 
the  blood,  and  Henrot  has  noted  little  granulations.  The  elements  with  a 
rounded  body  and  furnished  with  a  tail  described  by  Petrone  and  Franken- 
hauser  are,  perhaps,  only  poikilocytes  which  had  become  mobile  by  reason 
of  the  extreme  anaemia. 


1884  TEXT-BOOK  OF  MEDICINE 

Symptoms. — The  onset  is  insidious.  The  disease  commences  with  pallor, 
breathlessness,  palpitation,  and  digestive  disorder.  Extreme  feebleness 
soon  appears,  and  compels  the  patient  to  take  to  his  bed. 

The  anaemia  is  sometimes  accompanied  by  a  slightly  jaundiced  tint  of 
the  conjunctivae,  oedema  of  the  legs,  and  ascites.  The  skin  and  mucous 
membranes  are  often  covered  with  haemorrhages.  Epistaxis,  stomator- 
rhagia, and  haematemesis  may  occur.  Haemorrhage  into  the  retina  is  one 
of  the  most  important  symptoms. 

The  temperature  may  remain  normal,  or  may  reach  104°  F.  in  the  febrile 
form  of  the  disease.  It  has  been  seen  to  fall  as  low  as  91°  F.  in  the  last  stages 
of  the  malady.  Palpitation  is  frequent,  and  the  cardiac  dullness  is  some- 
times increased.  The  stethoscopic  signs  are  less  frequent  than  in  chlorosis, 
but  we  may  find  a  hruit  de  diable  with  a  thrill  over  the  internal  jugular  vein. 
The  mind  often  becomes  weak  towards  the  end  of  the  disease,  which 
may  end  in  coma. 

As  regards  the  stomach,  we  often  find  very  marked  troubles,  as  the 
anatomical  lesions  would  lead  us  to  suspect.  They  reveal  themselves  by 
anorexia,  distension  of  the  abdomen,  vomiting,  and  diarrhoea.  The  dis- 
appearance of  the  hydrochloric  acid  has  been  recognized  in  one  case  by 
Cahn  and  von  Mering. 

The  blood  undergoes  very  marked  changes.  The  red  corpuscles  faU  to 
a  million,  and  often  as  low  as  some  hundreds  of  thousands.  Their  diameter 
is  increased,  and  the  giant  cells,  measuring  8'5  /i  to  16  yu,,  may  represent  an 
eighth  part  of  the  total  count  (Hayem).  The  colour-index  is  increased,  or, 
in  other  words,  in  opposition  to  what  is  seen  in  chlorosis,  the  number  of  red 
cells  is  more  reduced  than  the  proportion  of  haemoglobin. 

The  red  blood-corpuscles  are  deformed,  and  assume  a  racquet  or  a 
spindle  shape.  These  deformities,  as  well  as  the  mobility  of  the  cells,  result 
from  their  abnormal  contractile  power.  The  altered  cells  may,  indeed, 
present  amoeboid  movements  of  rocking,  oscillation,  and  propulsion,  which 
have  led  writers  to  look  upon  them  as  parasites. 

The  haematoblasts  and  the  leucocytes  are  diminished  in  number.  The 
presence  of  nucleated  red  cells,  and  the  increase  of  their  colour-index,  form 
the  characteristic  features  in  this  anaemia.  These  nucleated  ceUs  are  thrown 
into  the  blood  by  the  spleen  and  by  the  bone-marrow  in  order  to  compensate 
for  the  insufficiency  of  haematopoiesis  by  the  haematoblasts. 

The  course  of  the  disease  is  progressive,  as  its  name  indicates,  and  death 
occurs  in  a  year  or  even  in  a  few  months.  The  disease  in  some  cases  shows 
remissions,  followed  by  relapses  at  more  or  less  short  intervals.  Cases  of 
definite  recovery  have  been  recorded  (Quincke). 

Diagnosis. — The  disease  is  characterized  by  extreme  anaemia,  in  which 
the  patient's  stoutness  is  preserved,  and  in  which  retinal  haemorrhages  and 


PATTTOLOOY  OF  THE  P.LOQD  1885 

Bpecial  corpuscular  changes  are  present ;  but  yet  this  affection  is  so  rare 
that  tlie  clinician  should  always  ask  whether  he  is  not  dealing  with  a  symp- 
tomatic antvmia.     The  question  is  sometimes  in  douht  until  the  autopsy. 

Extreme  anai'inia  of  the  fourth  degree  may  be  met  with  after  severe 
ha'morrhago,  or  in  the  course  of  chlorosis,  tuberculosis,  and  cancer  of  the 
stomach  and  of  the  liver.  The  relations  or  the  general  evolution  of  the 
disease  are  generally  sufficient  to  settle  the  diagnosis.  Miners'  anaemia, 
caused  by  the  duodenal  ankylostoma,  or  the  anaemia  caused  by  the  Bothrio- 
cefhalus  latus,  is  not,  as  a  rule,  extreme,  and  does  not  reach  the  fourth 
degree.  The  eggs  of  the  ankylostoma  or  of  the  bothriocephalus  will  be  found 
in  the  stools,  and  will  remove  all  doubt. 

Treatment. — The  stomach  and  tiie  general  health  furnish  us  with  indica- 
tions for  treatment,  which  should  be  based  upon  a  diet  composed  of  milk, 
eggs,  grilled  meat,  vegetables  en  puree,  stewed  fruits,  bread  in  very  small 
quantities,  light  beer,  white  wine  mixed  with  water,  and  a  change  of  air 
from  the  town  to  the  country.  Iron  may  give  good  results,  but  arsenic,  in 
the  form  of  Fowler's  solution,  in  doses  of  from  10  to  20  drops  daily,  appears 
to  be  the  specific  drug  for  the  disease,  and  Padley's  statistics  attribute  a 
large  number  of  recoveries  to  it.  Opotherapy  with  bone-marrow,  radio- 
therapy, and  injections  of  antidiphtheritic  serum  have  caused  improvement 
(Renon  and  Texier). 

IV.  LEUCOCYTILEMIA. 

Discussion. — When  Bennet  and  Virchow,  in  1845,  described  the  disease  which  forms 
the  subject  of  this  section,  they  were,  without  doubt,  especiaUy  impressed  by  the  colour 
which  the  blood  took  from  the  exaggerated  and  permanent  formation  of  its  white 
corpuscles,  whence  the  name  leucocythaemia,  given  by  Bennet  (AeuKos,  white ;  kvtos, 
cell ;  atixa,  blood),  and  leukaemia,  created  by  Virchow. 

This  change  in  the  blood,  though  important,  represents  only  one  feature  of  the 
disease.  The  changes  iu  the  adenoid  tissue  are  also  of  much  importance.  In  the 
normal  condition  the  adenoid  tissue,  scattered  through  the  economy,  is  formed  of  a 
reticular  connective  tissue,  the  meshes  of  which  are  filled  by  lymphatic  cells  (His)  ; 
and  it  is  sometimes  necessary  to  brush  out  the  lymphatic  cells,  in  order  to  show  the 
deUcate  reticulum.  We  find,  however,  in  leucocythaemia,  such  exuberant  growth  of 
this  adenoid  tissue  that  it  not  only  multiplies  in  the  organs  where  it  is  normally  present 
(hypergenesis) — such  as  the  spleen,  the  lymphatic  glands,  and  the  bone-marrow — but 
the  more  serious  matter  is,  that  it  appears  somewhat  Uke  a  maUgnant  growth  in  organs 
which  are  normally  free  from  it  (heterotopy),  such  as  the  hver  and  kidney,  serous 
membranes,  etc.  These  lymphoid  growths  have  been  called  lymphadenomata  (Virchow), 
whence  the  name  of  lymphadenie,  given  by  Ranvier  to  the  morbid  process. 

In  some  cases  this  overgrowth  of  adenoid  tissue,  or  lymphadenia,  invades  the 
organs,  especially  the  lymphatic  glands  and  the  spleen  (Barfils,  1856 ;  Cossy,  1861), 
without  a  corresponding  increase  of  the  leucocytes  in  the  blood.  Accordingly,  when 
the  question  was  not  clearly  understood,  authorities  attempted  to  separate  these  cases 
of  leucocythremia,  and  described  them  imder  the  name  of  adenie  (Trousseau),  or  pseudo- 
leukaemia.     Jaccoud  rendered  good  service  by  proving  the  unity  of  l^Tiiphadenia, 


1886  TEXT-BOOK  OF  MEDICINE 

but  the  terms  of  "  leukaemic  "  and  "  aleuksemic  "  lymphadenia  have  not  the  former 
signification,  since  the  question  of  leucocythsemia  has  been  recast. 

When  we  see  a  patient  with  enlarged  glands,  with  or  without  an  enlarged  spleen, 
the  question  is  not  solely  to  know  to  what  extent  the  white  corpuscles  have  increased 
in  the  blood ;  we  must  also  learn  what  varieties  are  present.  In  short,  from  a  more  exact 
knowledge  of  the  morphology  of  the  white  corpuscles,  physicians  have  recognized  that 
they  occur  in  very  different  forms,  and  we  know  that  in  leucocythaemia  the  morpho- 
logical changes  in  the  blood  are  certainly  as  important  as  the  numerical  ones.  It  ia 
the  quahty  of  the  leucocytes  and  not  the  quantity  alone  which  matters. 

At  the  present  moment,  however,  we  look  upon  leucocythsemia  as  only  the  reaction 
of  the  organism  which  shows  itself  by  the  changes  in  the  blood  and  by  the  lesions  in 
the  hsematopoietic  organs,  with  sjmptoms  dependent  to  these  lesions.  We  know 
perfectly  well  that  this  reaction  of  the  organism  is  not  always  the  same,  but  it  is  as  yet 
impossible  to  say  whether  the  lesions  and  symptoms  correspond  to  a  single  disease  or 
belong  to  different  maladies. 

etiology. — The  causes  of  leucocythsemia  are  unknown.  It  is  more 
frequent  in  men  than  in  women,  and  develops  chiefly  in  the  middle  period 
of  life.  Splenic  lymphadenia  in  nurslings  has,  however,  been  described 
(Jaksch,  Luzet).  In  the  patient's  previous  history  we  find  malaria,  typhoid 
fever,  syphilis,  and  alcoholism ;  but  this  so-called  aetiology  is  subject  to 
variations.  Privation,  grief,  and  repeated  pregnancies  appear  to  play  some 
part,  and  in  some  cases  the  onset  of  the  affection  seems  to  date  from  an 
injury  in  the  left  hypochondrium,  from  a  chill,  a  local  lesion,  an  osteo- 
myelitis following  on  amputation,  or  from  chronic  otorrhoea  (Virchow). 
"  Possibly  we  may  be  right  in  suspecting  in  these  facts  the  forgotten  exist- 
ence of  some  mucous  or  cutaneous  irritation,  giving  rise  to  primary  adeno- 
pathy which  precedes  the  outburst  of  the  general  disease  "  (Trousseau). 
There  is,  however,  no  proof  on  this  point. 

For  some  years  past  the  infective  origin  of  leucocjrthsemia  has  been 
suggested  by  many  authors  (Bard,  Delbet),  but  contagion  has  not  been  proved 
in  any  case,  and  experimental  reproduction  in  animals  has  failed  (G-ilbert 
and  Cadiat),  As  regards  the  infective  nature  of  the  disease,  the  multiplicity 
of  the  organisms  suspected  shows  that  it  is  not  a  specific  affection,  but  at 
most  a  commonplace  process  of  secondary  infection. 

Pathological  Anatomy. — Let  us  consider  (1)  the  changes  of  the  blood  ; 
(2)  the  changes  in  the  tissues  and  organs. 

1.  Changes  in  the  Blood. — The  blood  in  leucocythaemia  presents 
alterations  appreciable  to  the  naked  eye  only  when  there  is  considerable 
increase  in  the  white  corpuscles.  In  such  a  case  the  blood  is  almost  colour- 
less, and  its  shade  is  sometimes  like  that  of  pus.  Leuksemic  blood,  de- 
fibrinated  and  placed  in  a  test-tube,  separates  into  three  layers  :  the  lowest 
is  formed  of  red  blood-corpuscles ;  the  white  corpuscles  form  the  inter- 
mediary layer  ;  and  the  serum  floats  above.  The  clots  produced  by  bleeding, 
and  those  removed  from  the  cadaver,  are  separated  into  two  layers — a  lower 
red  and  an  upper  greyish  one. 


PATHOLOGY  OF  THE  P.LOOT)  1887 

From  this  point  of  view  we  must  consider  two  chivi  forms  of  leuco- 
cythaemia  :  the  one  is  lymphocythaomia — in  this  case  the  lymphocytes  of 
the  blood  arc  similar  to  those  of  the  lymphoid  tissue  of  the  glands  ;  the  other 
is  myelocyiihaBraia,  and  in  this  case  the  cells  resemble  those  found  in  the 
bone-marrow. 

LymfhocythcBmia. — The  number  of  lymphocytes  may  reach  600,000 
per  cubic  millimetre  ;  the  increase  is,  however,  far  less  in  most  cases.  To 
this  variety  belong  cases  in  which  the  number  of  leucocytes  is  but  little 
increased  or  practically  normal  (Jolly,  Vaquez).  The  increase  chiefly  affects 
the  lymphocytes,  which  may  then  reach  as  high  as  90  per  cent. 

Myclocythceynia. — This  variety  of  lencocythaemia  includes  most  of  the 
cases  in  which  the  number  of  leucoc)rtes  is  considerably  increased.  They 
may  exceed  the  total  of  600,000.  Instead  of  1  leucocyte  to  600  red  cor- 
puscles (normal  condition),  the  relative  proportion  may  be  1  to  20,  1  to  10, 
1  to  9,  and  even  be  1  to  1.  All  the  varieties  of  white  cells  found  in  normal 
blood  are  represented  in  variable  proportions  in  this  variety  of  leucocy- 
thsemia.  The  special  point  is  the  appearance  of  large  numbers  of  cells  not 
present  in  normal  blood,  including  rounded  cells,  with  a  large,  rounded, 
oval,  or  slightly-curved  nucleus.  These  cells  in  their  general  appearance 
resemble  the  large  mononuclear  cells  of  normal  blood,  but  their  protoplasm, 
instead  of  being  clear,  is  filled  either  with  fine  granulations  ("  neutrophiles  ") 
or  with  large  refractile  granulations  ("  eosinophiles  ").  We  may  also  find 
cells  in  which  the  protoplasmic  granulations  stain  with  "  basic  "  dyes,  such 
as  thionin  and  methyl  violet,  and  answer  to  the  "  mastzellen  "  of  Erhlich. 

The  nucleus  of  the  myelocytes  appears  diffuse  in  the  usual  preparations  ; 
these  cells  were  therefore  looked  upon  as  degenerate  or  dead  elements.  Such 
is  not  the  case,  and  JoUy  has  shown  that  the  myelocytes  and  the  lympho- 
cytes are  living  and  mobile  cells.  Relying  on  these  facts,  Ehrlich  has  tried 
to  maintain  that,  in  the  different  varieties  of  leukaemia,  the  various  species 
of  leucocytes  come  from  the  haematopoietic  organs  of  the  blood  by 
diapedesis. 

In  some  cases  the  large  mononuclear  cells  (myelocytes)  predominate  in 
the  blood,  and  the  polynuclear  cells  are  the  exception. 

These  cases  have  sometimes  been  classed  under  the  term  of  splenic 
leukaemia,  or  wrongly  confounded  with  lymphatic  leukaemia.  In  reality 
they  belong  to  myelocythsemia.  In  myelocjrthaemia,  as  in  lymphocy- 
thaemia,  the  red  corpuscles  are  less  nimierous,  and  their  colour-index  is 
lowered.  Lastly,  this  anaemia  is  often  accompanied  by  the  presence  of 
nucleated  red  cells. 

Chemical  Examination. — Chemical  analyses  of  the  blood  in  leukaemia 
show  the  presence  of  glutin,  hypoxanthin,  leucin,  and  tyrosin.  The  peculiar 
crystals  described  by  Charcot  in  the  blood  of  anaemic  patients  are  probably 


1888  TEXT-BOOK  OF  MEDICINE 

due  to  the  latter  substance  or  to  some  closely  allied  substance.  These 
crystals,  known  by  the  name  of  Charcot-Leyden  crystals,  are  only  found 
in  the  blood  after  death. 

2.  Lesions  of  the  Connective  Tissue  and  of  the  Organs.— These 
lesions  consist  in  the  hypertrophy  of  the  lymphoid  tissue  in  the  places  where 
it  exists  normally,  and  in  the  formation  of  lymphoid  tissue  which  is  not 
present  in  health.  Lymphoid  or  adenoid  tissue  is  the  tissue  of  the  lymphatic 
glands.  It  is  formed  by  a  reticular  connective  tissue,  the  meshes  of  which 
are  filled  with  lymphatic  cells.  "  Capillaries  run  through  this  reticular 
tissue,  being  themselves  surrounded  by  a  condensed  layer,  from  which  the 
fibrillse  of  the  reticulum  take  their  origin  "  (Cornil  and  Ranvier). 

In  leucocythaemia  the  normal  adenoid  tissue  may  be  hypertrophied  in 
every  organ. 

The  lymphatic  glands  of  the  neck,  axiUa,  groin,  mesentery,  and  of  the 
bronchi  are  often  invaded,  and  form  tumours  as  large  as  a  hazel-nut,  a  walnut, 
or  an  egg.  They  may  form  considerable  masses  in  such  regions  as  the  neck 
and  the  axilla. 

In  some  cases,  even  apart  from  any  scrofular  or  tubercular  aetiology,  the 
glands  may  become  caseous.  The  predominance  of  the  lesion  in  the  lym- 
phatic glands  has  led  to  the  admission  of  a  variety  of  lymphadenia  known 
as  the  glandular  form. 

The  spleen  may  weigh  over  four  pounds,  but  is  not  altered  in  shape  ; 
it  is  hard,  its  capsule  is  thickened  and  often  adherent  to  the  peritoneum, 
and,  on  section,  we  see  the  corpuscles  of  Malpighi,  which  are  whitish  and 
sometimes  as  large  as  a  lentil,  clearly  marked  against  the  red  ground.  The 
lesions  are  similar  to  those  in  the  lymphatic  glands. 

The  intestinal  mucosa  is  frequently  affected.  Three  chief  lesions  may 
be  present  (Gilly)  :  Folliculo-hypertrophic  form,  which  develops  at  the 
expense  of  closed  follicles  and  Peyer's  patches,  but,  so  to  say,  never  leads 
to  ulceration ;  diffuse  hyperplastic  and  neoplastic  forms,  which  originate  in 
the  submucous  adenoid  layer  and  ulcerate  very  rapidly.  The  neoplastic 
form  is  chiefly  f oimd  in  the  lower  part  of  the  ileum,  without  narrowing  of  the 
lumen  of  the  bowel ;  it  is  nearly  always  aleuksemic. 

The  tonsils,  the  closed  follicles  of  the  tongue,  the  thyroid  body,  and  the 
bone-marrow  participate  m  the  increase  of  lymphoid  tissue.  The  atrophied 
thymus  sometimes  regains  its  ordinary  size. 

When  the  liver  is  affected,  the  hypertrophy  involves  the  whole  of  the 
organ,  and  its  area  of  dullness  blends  with  that  of  the  spleen.  The  capillaries 
are  dilated  with  blood  crammed  with  white  cells.  A  true  apoplexy  of  leuco- 
cytes may  be  seen.     New  formations  are  not  found. 

In  the  connective  tissue  of  the  portal  spaces  we  find  a  neo-formation 
of  lymphoid  tissue.     Strictly  speaking,  this  lymphoid  tissue  most  often 


rATJLUl.UGY   UF  TllK  DLUUl)  1889 

consists  in  an  inliH ration  of  th<^  connective  tissue,  by  colls,  like  tliose  of  the 
glands,  although  this  connective  tissue  may  assume  the  ajjpearance  of  true 
reticular  tissue.  It  is  also  found  in  the  lymphomata  of  the  cortical  sub- 
stance of  the  kidney.  The  bone-marrow  is  sometimes  c-onverted  into  lym- 
phoid tissue.  Finally,  we  may  find  it  in  the  skin  and  in  regions  where  it  is 
not  present  nornmlly. 

The  accumulation  of  white  blood-corpuscles  in  the  vessels  explains  the 
ha'morrhages  which  may  take  place  in  the  liver,  kidney,  brain,  retina, 
meninges,  nasal  mucous  membrane,  gums,  internal  ear,  or  in  the  skin  (pur- 
pura). In  the  intestine  ulceration  of  the  lymphoid  tumours  also  gives 
rise  to  hsemorrhage. 

I  have  just  described  in  general  terms  the  various  lesions  of  leucocy- 
thsemia,  but  for  some  years  past  physicians  have  noticed  the  production  of 
certain  lymphoid  gro\\i;hs,  which  differ  somewhat  in  .structure  from  that  of 
the  lymphatic  glands.  They  form  leukaemic  tumours,  which  are  especially 
frequent  in  the  liver  and  spleen,  and  which  are  composed  of  cells  larger  than 
lymphocytes.  These  cells  'have  a  large  round  nucleus,  and  their  proto- 
plasm often  contains  granulations,  like  those  in  the  cells  of  the  bone-marrow. 
Under  these  conditions  the  tissue  is  not,  properly  speaking,  lymphoid,  but 
rather  myeloid. 

It  has  furthermore  been  noticed  that  these  growths  of  myeloid  tissue 
are  allied  to  the  hsematological  forms  which  we  have  learnt  to  know  under 
the  name  of  "  myelocythsemia."  These  facts,  joined  to  our  knowledge  of 
the  morphology  of  the  blood  and  of  the  structure  of  the  bone -marrow,  con- 
tribute to  new  ideas  as  regards  the  pathological  physiology  of  leucocy- 
thaemia. 

If  myeloc}^;h8emia  and  lymphocythsemia  do  not  exactly  correspond  to 
distinct  clinical  types,  they  yet  form  special  anatomical  types,  in  which  the 
lesions  of  the  blood  are  different.  In  lymphocythsemia  the  lymphocytes 
of  the  blood  come  from  the  glands  and  from  the  new  lymphatic  tissue, 
formed  at  various  points,  and  even  in  the  bone-marrow.  In  myelocythaemia 
the  leucocytes — or,  at  any  rate,  the  majority  of  them — come  from  the  hyper- 
plastic bone-marrow  and  from  the  newly-formed  myeloid  tissue  in  various 
organs,  but  especially  in  the  spleen. 

Such  is  the  new  conception  of  leucocythaemia.  According  to  Ehrlich, 
the  masses  and  the  myeloid  tumours  are  formed  by  metastasis  ;  the  bone- 
marrow  sends  to  the  spleen  its  own  cells,  which  are  grafted  there  (heterotopy), 
in  this  point  resembling  malignant  tumours.  According  to  Dominici,  the 
process  depends,  not  upon  metastases,  but  on  the  revival  of  a  myeloid  tissue 
which  existed  in  the  organ  during  the  foetal  state. 

In  the  cases  which  we  have  just  examined  the  formation  of  the  new 
lymphoid  and  myeloid  tissue  is  accompanied  by  important  changes  in  the 


1890  TEXT-BOOK  OF  MEDICmE 

blood.  These  changes,  however,  appear  to  be  non-existent  in  some  cases 
which  answer  to  the  names  of  adenia,  aleuksemic  lymphadenia,  pseudo- 
leuksemia,  Hodgkin's  disease,  etc.  It  is  practically  certain  that  these 
descriptions  have  been  applied  in  error  to  varieties  distinct  from  leucocy- 
thsemia.  According  to  Jolly,  these  varieties  are  as  follows  :  "  (1)  Chronic 
adenitis,  with  or  without  polynuclear  leucocytosis,  adenopathies  of  undeter- 
mined nature,  infective  and  especially  tubercular ;  (2)  glandular  tumours, 
primary  or  secondary,  and  running  their  course  with  or  without  polynuclear 
leucocytosis ;  (3)  true  cases  of  lymphocythsemia,  in  which  the  absolute 
number  of  white  corpuscles  is  not  increased,  or  increased  only  to  a  slight 
extent ;  (4)  cases  of  cutaneous  lymphadenia  and  of  mycosis  fungoides  which 
belong  to  the  category  of  lymphocythaemia ;  (5)  lymphadenic  lesions  analo- 
gous to  those  of  lymphocythaemia,  without  other  change  in  the  blood  except 
a  polynuclear  leucocytosis.  Certain  facts  tend  to  show,  moreover,  that 
these  cases  may  represent  only  a  passing  stage  in  the  evolution  of  lympho- 
cythaemia." 

Often,  too,  we  include  wrongly  in  the  category  of  lymphadenia  various 
kinds  of  splenomegalia  without  blood  changes. 

As  regards  the  infantile  pseudo-leuksemic  anaemia  of  Jaksch  and  Luzet, 
We  do  not  know  whether  it  is  an  infantile  form  of  leukasmia  or  an  anaemia 
due  to  different  varieties  of  hypertrophy  of  the  spleen  with  leucocytosis. 

Symptoms. — The  onset  of  leucocythsemia  is  often  insidious.  The 
patient  suffers  from  increasing  feebleness,  fatigue,  pallor,  and  breathlessness. 
In  some  cases  no  enlargement  of  the  glands  is  as  yet  visible  externally,  the 
spleen  is  not  increased  in  size,  and  yet,  if  the  blood  is  examined,  diminution 
of  the  red  cells  and  considerable  increase  in  the  leucocjrfces  or  lymphocytes 
wiU  be  found.  In  some  circumstances  the  contrary  obtains.  One  or  several 
lymphatic  glands  undergo  an  enlargement  which  appears  at  first  immaterial, 
but  the  hypertrophy  soon  becomes  general,  although  the  blood  does  not 
show  any  excess  of  leucocytes. 

In  glandular  leukaemia  the  hypertrophied  lymphatic  glands  are  painless 
and  distinct  from  one  another.  In  the  lateral  regions  of  the  neck  they  form 
by  their  agglomeration  enormous  tumours,  on  which  the  head  seems  to  rest. 
When  the  chain  of  the  tracheal  and  bronchial  glands  is  invaded,  we  may  note 
the  onset  of  compression  symptoms,  such  as  dyspnoea,  spasm  of  the  glottis, 
tubular  breathing,  stridor,  dysphagia,  and  oedema  of  the  face  and  arms, 
described  under  Mediastinal  Tumours.  The  lymphatic  tumours  of  the  axilla 
and  of  the  groin  hamper  the  movements  of  the  arms  and  legs.  The  hyper- 
trophy of  the  mesenteric  glands  causes  compression  of  the  veins,  ascites,  and 
oedema  of  the  legs.  The  glandular  tumours  of  lymphadenia  have  no  ten- 
dency to  become  inflamed  and  to  suppurate. 

In  splenic  leukaemia  the  spleen  finally  attains  a  considerable  size.     It 


PATHOLOGY  OF  THP:  BLOOD  1891 

causes  an  enormous  projection  in  the  abdomen.  It  may  participate  alone 
in  the  process,  or  else  the  process  may  affect  both  the  spleen  and  the  glands. 

The  general  symptoms  become  more  marked  as  the  disease  progresses : 
the  feebleness  increases,  the  appetite  is  lost,  and  anaemic  murmurs  are  heard 
in  the  heart  and  in  the  vessels.  The  patient  complains  of  headache,  vertigo, 
nausea,  visual  troubles  (leukaemic  retinitis),  and  dysphagia  (ulcerative, 
leukajmic  phar^-ngitis) ;  he  is  liable  to  haemorrhage,  epistascis,  purpura,  and 
bleeding  from  the  gums. 

The  wasting  of  the  face  and  of  the  limbs  contrasts  with  the  mass  of  the 
glandular  tumours  and  with  the  abnormal  size  of  the  abdomen.  After  a 
duration  which  varies  from  some  months  to  two  years  the  period  of  pachexia 
commences,  the  tendency  to  haemorrhage  becomes  far  more  marked,  the 
cedema  becomes  general,  the  diarrhoea  is  continuous,  the  wasting  progresses, 
the  hands  are  the  seat  of  erythematous  eruptions,  and  fever  often  appears. 

The  patient  is  carried  off  by  the  incessant  progress  of  the  cachexia  or  by 
some  intercurrent  trouble,  excessive  enlargement  of  the  bronchial  glands 
or  cerebral  haemorrhage,  which  may  supervene  long  before  the  period  of 
cachexia. 

Acute  Leucocythsemia. — The  first  cases  were  reported  by  Ebstein  in 
1889.  Since  that  time  numerous  researches  have  been  published.  At  the 
last  Congress  of  Internal  Medicine  in  Berlin  Fraenkel  and  other  authors 
brought  forward  cases  which  established  the  existence  of  super-acute 
leucoc}i;haeniia,  and  they  called  it  acute  leukaemia  or  lymphocythaemia, 
for  the  very  reason  that  it  is  characterized,  as  regards  haematology,  by  the 
superabundance  of  lymphocytes  or  small  mononuclear  cells.  Their  almost 
exclusive  presence  in  the  blood  makes  the  prognosis  grave  and  the  rapid 
course  of  the  disease  foreseen. 

This  variety  of  leukaemia  is  perhaps  not  yet  established  with  certainty. 
I  have,  however,  been  able  to  verify  its  extreme  gravity  in  one  of  my  cases. 

The  patient  was  admitted  to  hospital  in  a  condition  of  advanced  cachexia.  His 
colour  resembled  that  of  a  patient  with  cancer  :  earthy  pallor,  colourless  mucous  mem- 
branes, oedema  of  the  legs  and  purpura.  He  experienced  no  sufEering,  but  complained 
of  great  weakness.  His  health  had  always  been  excellent,  and  in  his  past  history  we 
found  no  disease  worthy  of  note.     The  present  condition  was  of  a  few  weeks'  duration. 

On  examination  we  found  an  enormous  tumour  in  the  belly.  This  swelling  was 
hard  and  painless,  and  deformed  the  left  flank  and  hypochondrium.  It  descended 
almost  to  the  umbUicus,  and  was  wedged  above  under  the  ribs,  where  the  dullness 
reached  as  high  as  the  fifth  intercostal  space. 

The  diagnosis  of  an  enlarged  spleen  was  evident,  but  the  nature  of  the  lesion 
remained  to  be  proved.  There  could  be  no  question  of  malaria,  because  the  patient 
had  never  suffered  from  that  disease.  Hydatid  cyst  of  the  spleen  was  also  eliminated, 
because  it  never  causes  such  marked  cachexia  in  a  few  weeks.  If  a  patient  is  cachectic, 
with  an  enlarged  spleen  and  glandular  tumours  in  the  neck,  the  groin,  or  in  the  axilla, 
we  must  first  think  of  leucocythsemia ;  but  this  patient  had  no  apparent  hypertrophy 
of  the  glands. 


1892  TEXT-BOOK  OF  MEDICINE 

And  yet  this  was  not  a  reason  for  abandoning  the  diagnosis  of  leucocythgemi*» 
spleen,  because  splenic  lymphadenia  may  exist  without  obvious  enlargement  of  the 
glands. 

In  order  to  decide  the  question,  Apert  examined  the  blood,  and  the  diagnosis  of  an 
enlarged  leucocythsemic  spleen  was  confirmed.  The  patient  had  50,000  white  corpuscles 
to  1,900,000  red  ones — i.e.,  a  proportion  of  1  to  40,  instead  of  1  to  60,  as  in  the  normal 
condition. 

In  leucocythaemia,  however,  it  is  not  sufficient  to  find  a  considerable  excess  of  the 
white  corpuscles ;  we  must  also  know  to  which  variety  they  belong.  Preparations  of 
the  blood  showed  that  the  leukaemia  was  in  this  case  due  to  small  mononuclear  leuco- 
cytes.    It  was  therefore  a  case  of  lymphocythaemia. 

Kg.  87  shows  a  film  dried  and  stained  with  eosin  and  methylene  blue.  We  see 
numbers  of  small  leucocytes,  stained  blue  and  smaller  than  the  red  corpuscles,  as  well 
as  two  large  mononuclear  leucocytes  and  a  polynuclear  leucocyte. 

A  fortnight  after  the  patient  came  under  my  care  the  number  of  lymphocytes 
increased  from  50,000  to  90,000,  and  the  proportion  of  the  lymphocytes  to  the  red 
corpuscles  varied  between  1  to  40  and  1  to  20.  The  glands  of  the  neck,  which  were 
scarcely  perceptible  on  the  patient's  admission,  formed,  in  a  fortnight,  swellings  similar 
to  a  bag  of  nuts.     A  httle  later  the  axillary  glands  hypertrophied,  and  we  also  found 


glands  (where  they  are  not  found  normally)  in  a  continuous  chain  along  the  inner  edge 
of  the  biceps.  A  hard,  subcutaneous  nodule  appeared  on  the  anterior  surface  of  the 
right  thigh.  It  was  adherent  to  the  skin,  and  was  rightly  considered  to  be  a  cutaneous 
lymphoma.  At  the  same  time  the  spleen  became  more  enlarged,  the  strength  diminished 
progressively,  the  cachexia  increased,  and  the  patient  finally  died  five  weeks  after 
his  admission.  A  few  days  before  death  the  lymphocytes  had  reached  150,000,  and 
their  relation  to  the  red  corpuscles  was  an  1  to  10. 

The  autopsy  showed  the  lesions  of  leucocythaemia.  The  spleen  was  enormous. 
It  weighed  nearly  5  pounds  instead  of  6  ounces.  It  had  therefore  increased  in  size 
tenfold.  The  hypertrophy  affected  all  its  diameters.  The  length  was  10  inches  instead 
of  5  inches,  the  breadth  was  doubled,  being  6  inches  instead  of  3  inches,  and  the  thick- 
ness was  trebled,  being  3-|-  inches  instead  of  1 J  inches. 

In  spite  of  this  marked  hypertrophy,  the  organ  had  preserved  its  normal  shape, 
although  the  tipper  end  was  curved  inwards,  forming  a  kind  of  hook,  with  its  concavity 
internal  and  below.  It  seemed  to  have  been  hindered  in  its  growth  by  the  resistance 
of  the  diaphragm,  and  consequently  it  had  continued  to  grow  towards  the  middle  line  ; 
while  the  rest  of  the  organ,  finding  only  the  viscera,  which  were  easily  displaced,  grew 
in  situ,  and  without  modification  of  its  general  shape.  On  longitudinal  section  of  the 
organ  the  parenchjTna  appeared  normal.  It  was  of  violet  colour,  with  some  whitish 
streaks ;  it  was  perhaps  a  Kttle  more  firm  than  usual,  but  really  differed  from  the 


rATUOr.OGY  OF  THE  liLODI)  1893 

uormal  appearance  only  to  a  slight  extent.  The  only  abnormal  condition  in  the  spleen, 
apart  from  its  size,  was  the  marked  tliickoning  of  the  capsule,  winch  was  whitish,  Imrd, 
and  bound  do\m  to  tho  neighbouring  organs  by  librous  adhosiuns. 

Basidos  this  enormous  spleen,  wo  found  everywhere  enlarged  glands  :  the  mosentoric 
glands,  the  glands  of  the  hilum,  of  tho  liver,  and  of  the  spleen.  The  prevertebral  and 
the  mediastinal  glands  formed  large  masses.  Some  of  the  glands  were  as  largo  as  an 
apple,  being  white  and  firm  on  section,  wliile  others  showed,  in  their  centre,  violet 
spots,  due  to  interstitial  hiomorrhago.  The  viscera,  liver,  kidneys,  lungs,  and  heart 
presented  notliing  worthy  of  note  ;  the  follicles  of  the  intestine  and  tho  tonsils  were  not 
hypertropliied.  It  was  important  to  take  count  of  the  lesions  of  the  bone-marrow, 
where  changes  are  usual  in  leucocythaemia.  The  right  humerus  was  sawn  through 
at  two  different  levels,  and  a  tube  of  marrow  extracted.  It  had  lost  its  usual  fatty 
apixvarance,  and  presented  the  same  aspect  as  the  substance  of  the  glands,  with  violet; 
spots  in  the  middle  of  a  dull  white  parenchyma. 

Histological  examination  of  the  diseased  organs  showed  a  very  interesting  pecuharity. 
In  the  histological  sections  made  by  Apert,  we  found  lymphocytes  almost  exclusively — 
not  only  in  the  glands,  where  the  lymphocyte  is  the  normal  white  corpuscle,  but  also  in 
the  pulp  of  the  spleen  and  in  the  bone -marrow,  where  the  lymphocytes,  by  reason  of 
their  abundance,  masked  the  polymorphous  cells,  wliich  are  normally  the  most  numerous. 
As  in  cancer,  whatever  the  situation  in  which  the  secondary  growths  are  formed,  we 
always  find  the  same  kind  of  cell.  So  here,  whatever  organs  are  infected  by  the 
l^onphoid  infiitration,  the  lesions,  both  in  the  organs  and  in  the  blood,  are  characterized 
by  the  presence  of  lymphocythsemia.  This  resemblance  to  cancer  has  led  writers  to 
call  leucocji:h;vmia  cancer  of  the  blood. 

Such,  then,  are  the  anatomical  and  clinical  varieties  of  leucocythaemia. 
We  cannot  say  whether  acute  leucocythaemia  is  only  a  clinical  variety  or  a 
distinct  disease,  but  it  is  certain  that  the  increase  in  number  of  the  white 
blood-corpuscles  chiefly  concerns  the  l}Tnphocytes.  The  s}Tnptom- complex 
resembles  that  of  chronic  leukaemia,  but  the  rapid  course,  sometimes  accom- 
panied by  fever,  gives  the  disease  a  special  appearance. 

Death  is  the  constant  end  of  acute  and  of  chronic  leukaemia  ;  the  acute 
form  lasts  only  a  few  weeks,  the  chronic  form  some  months  or  years.  The 
streptococcus  appear  to  be  fatal  in  leukaemic  patients. 

Diagnosis. — The  diagnosis  of  leucocythaemia  is  often  difficult,  and 
sometimes  the  disease  remains  undiscovered.  Accordingly,  we  must  always 
examine  the  blood  in  patients  with  enlargement  of  the  spleen,  of  the  liver, 
or  of  the  lymphatic  glands,  as  weU  as  in  patients  suffering  from  purpura,  and 
in  any  case  of  abnormal  leukaemia,  or  of  cachexia  of  unknown  origin. 

Examination  of  the  blood  will  remove  all  doubt,  and  will  prevent  con- 
fusion between  leukaemia  and  other  leucocytoses.  Physicians,  however, 
have  recently  discovered  in  the  leucocytosis  of  variola  a  type  which  recalls 
in  an  attenuated  manner  the  changes  of  the  blood  in  myelocythaemia.  This 
fact  is  a  link  between  the  leucocytoses  and  leucocythaemia. 

The  diagnosis  is  sometimes  difficult  in  patients  who  have  chains  of 
enlarged  glands,  without  specific  changes  in  the  blood  and  without  myelo- 
c}i;haemia  or  lymphocythaemia.  In  such  a  case  we  must  think  of  adenitis,  due 
CO  tuberculosis,  cancer,  syphilis,  etc.     We  must  bear  in  mind  malignant 

u.  120 


1894  TEXT-BOOK  OF  MEDICINE 

lymphadenoma  if  we  find  clironic  adenopathy  whicli  runs  a  progressive 
course,  especially  if  it  commence  in  tlie  cervical  region. 

Treatment. — No  benefit  lias  resulted  from  surgical  measures,  such  as 
removal  of  the  spleen  and  of  the  glandular  tumours.  It  is  therefore  prefer- 
able to  abstain  from  operations  of  this  nature  in  patients  suffering  from 
leuksemia.     There  is  no  medical  treatment  for  the  disease. 

Extracts  of  spleen  tissue  and  of  bone-marrow,  preparations  of  arsenic, 
and  injections  of  cacodylate  of  soda  have  produced  some  transient  improve- 
ment. 


V.  CHLOROSIS— CHLORO-BRIGHTISM. 

Chlorosis  and  ansemia  should  not  be  included  in  a  single  description, 
because  the  two  terms  are  not  synonymous.  Anaemia  is  only  a  symptom  of 
many  and  complex  origins  and  varieties.  It  is  caused  by  haemorrhage,  by 
various  losses  undergone  by  the  organism,  and  by  many  infectious  or  clironic 
diseases.  The  study  of  ansemia,  or,  rather,  the  study  of  the  anaemias,  is, 
therefore,  a  question  of  semeiology,  and  cannot  find  a  place  here.  Chlorosis, 
on  the  other  hand,  is  a  more  definite  morbid  entity,  being  related,  on  the 
one  hand,  to  the  anaemias,  and,  on  the  other,  to  the  neuroses  ;  not  that  the 
dyscrasic  and  nervous  elements  are  forcibly  subordinated  one  to  the  other, 
but  their  association  and  their  origin  give  rise  to  a  morbid  type  which  has  its 
own  autonomy. 

^Etiology. — Chlorosis  owes  its  name  to  the  colour  of  the  skin.  It  is 
seen  in  young  girls  about  the  age  of  puberty  {cachexia  virginum),  and  its 
appearance  seems  to  be  intimately  bound  up  with  the  evolution  of  the 
genital  organs.  It  exists,  however,  before  puberty — doubtless  when  the 
physical  growth  of  the  child  is  not  in  relation  with  its  means  of  repair  (See). 
Chlorosis  may  be  present  in  yoimg  boys,  just  as  hysteria,  though  a  disease 
special  to  the  female,  is  seen  in  men. 

Heredity  plays  an  important  part  in  the  development  of  chlorosis,  and 
as  occasional  causes  we  may  mention  menstrual  troubles,  disturbances  of  the 
nervous  system,  emotion,  grief,  weakness,  and  dwellings  which  are  dark  and 
wanting  in  sunlight. 

Pathogenesis — Pathological  Anatomy.  —  The  pathogenesis  and  the 
pathological  anatomy  of  chlorosis  have  for  some  years  been  the  subject  of 
numerous  researches,  and  it  has  been  asked  whether  the  blood-changes  seen 
in  chlorotic  patients  do  not  suffice  to  differentiate  chlorosis  from  the 
anaemias. 

The  number  of  red  corpuscles  in  chlorotic  blood  shows  nothing  charac- 
teristic, as  it  is  normal,  increased,  or  decreased,  according  to  the  case. 

The  exaggerated  size  of  the  red  corpuscle  has  no  importance,  for  in  every 


TATHOLOGY  OF  THE  KLOOD  1895 

anaemia  the  disturbance  occasioned  in  the  formation  and  development  of 
the  cells  gives  rise  to  abnormal  forms  of  red  corpuscles,  which  recall  more  or 
less  clearly  the  foetal  condition  of  the  elements. 

Is  it,  then,  the  composition  of  the  blood  or  the  diminution  of  the  haemo- 
globin which  produces  a  change  special  to  chlorosis  ?  Tliis  change  in  the 
ha?moglobin  is  not  absolutely  special  to  chlorosis,  since  it  exists  in  other 
anoDuiias,  and  especially  in  the  anaemia  of  cancer  (Hayem).  The  nature  of 
the  changes  in  the  blood  cannot,  therefore,  establish  a  distinction  between 
the  anaemias  and  chlorosis.  The  diminution  of  the  haemoglobin  in  chlorotic 
patients  is,  no  doubt,  an  important  element  of  which  we  must  take  count, 
but  it  is  the  symptom- complex,  and  especially  the  aetiology  of  the  affection, 
which  gives  to  chlorosis  its  distinctive  place.  The  opinion,  formerly  ex- 
pressed by  See,  that  the  distinguishing-point  between  chlorosis  and  the 
anaemias  is  its  origin,  has  thus  been  realized. 

The  lesions  in  the  blood  are  not  the  only  ones  seen  in  chlorosis.  We  owe 
our  knowledge  of  the  cardio- vascular  and  genital  lesions  to  the  works  of 
Rokitansky,  Bamberger,  and  especially  of  Virchow.  These  changes  have 
allowed  the  German  school  to  enunciate  an  organic  theory  of  chlorosis. 

The  most  frequent  anomaly  is  a  want  of  development  in  the  vascular 
system. 

The  aorta  is  sometimes  so  narrowed  that  its  lumen  scarcely  admits  the 
Uttle  finger ;  its  calibre  is  only  as  large  as  the  carotid  or  the  iliac  artery. 
The  coats  are  thinned  and  the  vessel  allows  itself  to  be  stretched  like  india- 
rubber.  The  intercostal  and  the  lumbar  arteries  arise  in  an  asymmetrical 
fashion  from  the  descending  aorta.  The  internal  coat  is  studded  with 
reticulated  blotches  ;  it  often  shows  fatty  degeneration  which  is  quite 
superficial,  in  contradistinction  to  the  lesions  of  atheroma. 

The  malformations  of  the  heart  are  variable  in  chlorosis.  The  organ  is 
sometimes  remarkably  small,  or,  at  other  times,  larger  than  normal.  Accord- 
ing to  Virchow,  who  bases  his  opinion  on  a  large  number  of  autopsies,  the 
heart  in  chlorosis  is  originally  small,  and  remains  so  in  case  of  permanent 
oligaemia.  If  the  volume  of  blood  become  too  large,  the  heart  becomes 
hvpertrophied  and  dilated,  because  it  has  to  struggle  against  the  narrowing 
of  the  aoi-ta. 

Changes  of  the  genital  organs  are  relatively  frequent  in  chlorosis.  These 
organs  are  sometimes  hypertrophied,  but  more  often  atrophied.  The  infantile 
character  of  the  uterus  and  of  the  ovaries  is  frequently  mentioned  in  Virchow's 
cases.  This  author  considers  the  genital  anomaUes  as  secondary  and  the 
vascular  hypoplasia  as  the  primary  lesion  causing  chlorosis. 

If  these  lesions,  though  rarely  seen  in  France,  are  frequently  noted  in 
the  protocol  of  German  autopsies,  we  must  remember  that  in  Germany, 
without  troubling  about  the  sj-mptoms  present  during  life,  they  apply  the 

12U— 2 


1896  TEXT-BOOK  OF  MEDICINE 

name  aortis  cMoroticcB  to  any  aorta  which  is  small  and  pale  and  which 
shows  abnormal  origin  of  its  branches. 

Moreover,  this  theory  of  chlorosis  is  applicable  only  to  some  cases,  and 
has  been  invalidated  by  other  autopsies,  so  that  it  merely  deserves  to  be 
retained  as  an  exception. 

Description. — The  chlorotic  woman  is,  as  a  rule,  not  wasted ;  her  face 
and  hands  have  a  sallow  and  yellowish  look,  like  old  wax,  while  a  greenish 
colour  is  sometimes  added.  The  lips  and  the  conjunctivae  are  bloodless  and 
pale,  the  look  is  sad  and  languid,  the  conjunctiva  is  bluish,  the  face  is  pufiy, 
and  the  eyelids  are  sometimes  oedematous.  This  oedema,  which  is  not  solely 
of  anaemic  origin,  is  also  seen  in  the  legs  and  feet.  The  cheeks  sometimes 
assume  a  sudden  and  passing  redness,  which  in  some  cases  may  be  very 
marked  {cMorosis  fortiorum). 

The  nervous  troubles  somewhat  resemble  those  of  hysteria.  The  chlorotic 
patient  is  melancholy,  irritable,  and  strange ;  she  complains  of  headache, 
vertigo,  fainting,  insomnia,  disturbed  dreams,  and  facial  or  intercostal 
neuralgia.  She  is  always  tired,  and  often  feels  ready  to  drop  ;  her  respiration 
rate  is  increased ;  and  palpitation  is  brought  on  by  the  least  exercise  or  by 
the  slighest  emotion.  The  palpitation  is  sometimes  violent,  and  comes  on 
in  the  form  of  attacks.  Epistaxis,  haemoptysis,  and  metrorrhagia  may  be 
present.  Anaesthesia  and  hyperaesthesia  are  both  seen.  The  muscular 
weakness  may  end  in  paralysis. 

In  the  chlorotic  woman  the  appetite  is  sometimes  exaggerated  (boulimia) 
or  at  other  times  suppressed  (anorexia) ;  it  is  often  depraved  (pica,  malacia). 
Dyspeptic  troubles,  such  as  flatulence,  gastralgia,  pyrosis,  vomiting,  dis- 
tension of  the  abdomen,  and  constipation,  are  sometimes  associated  with  this 
perversion  of  the  appetite. 

Hypopepsia,  hyperpepsia,  and  hyperchlorhydria  have  also  been  noted 
(Hayem). 

Functional  troubles  of  the  genital  organs  are  constant.  It  has  been 
asked  whether  they  are  the  cause  or  the  effect  of  the  chlorotic  state. 
Amenorrhoea  and  dysmenorrhoea  are  common,  but  monorrhagia  is  more 
rare  (Trousseau).  Leucorrhoea  is  very  frequent,  and  the  menstrual  blood  is 
serous  and  colourless.  Chlorosis  does  not  necessarily  cause  sterility,  and 
pregnancy  sometimes  has  a  beneficial  influence. 

The  urine  is  pale,  poor  in  urea  and  phosphates,  and  contains  uro- 
haematin. 

The  examination  of  a  chlorotic  patient  gives  the  following  results  :  On 
auscultation  we  often  find  a  systolic  murmur,  situated  at  the  aortic,  at  the 
tricuspid  orifice,  and  at  the  other  orifices.  If  the  finger  is  lightly  placed  over 
the  great  vessels  in  the  neck,  above  the  clavicle,  the  "  fremissement  cataire  " 
may  be  felt,  and  auscultation  of  these  vessels,  especially  on  the  right  side, 


rATIIOLOriY  OF  TTIK  r.LOnn  1897 

ro veals  an  intermittent,  systolif^  murmur  of  arterial  orif^in  and  a  continuous 
murmur  of  a  venous  origin,  which  is  more  or  less  musical  in  tone,  and  has 
been  compared  to  the  purring  of  a  cat,  to  the  sound  of  a  .sj)inning-wheel  or  of 
a  humming-top  (diaUe),  whence  the  terra  bruit  de  diahlc  given  by  Bouillaud. 

Tiiese  murmurs  are  not  confined  to  chlorosis,  and  have  not  the  diagnostic 
RJgnilicance  formerly  attributed  to  them.  The  intermittent  arterial  murmur 
is  explained,  but  the  explanation  of  the  continuous  murmur  is  more  diffictdt. 
Writers  have  suggested  the  vibrations  of  the  walls  of  the  vessel,  the  spas- 
modic condition  of  the  walls,  and  the  vibrations  of  the  valves  in  the  veins 
(Ohauveau).  The  veins  of  the  neck  sometimes  show  pulsation.  Hyper- 
trophy of  the  th\Toid  body  is  also  found  in  some  cases,  in  addition  to  the 
cardio-vascular  troubles  (Hayem). 

The  temperature  may  be  normal  or  lowered.  In  some  cases  a  notable 
elevation  of  the  central  temperature  has  been  observed  {fehris'  alba 
virgimim). 

Examination  of  the  blood,  which  only  requires  a  prick  of  the  finger, 
serves  to  complete  the  clinical  picture  in  chlorosis.  The  blood,  though 
rery  fluid,  coagulates  normally,  because  the  fibrin  is  present  in  the  proper 
quantity.  The  blood-serum  appears  chemically  normal,  and  yet  it  must 
exercise  a  deleterious  globulicidal  action  on  the  red  blood-corpuscles. 

The  number  of  red  corpuscles  is  not  much  diminished,  and  it  is  rare 
to  find  the  count  below  3,000,000 — indeed,  the  number  may  be  almost 
normal.  The  important  and  characteristic  lesion  of  the  blood  concerns 
the  haemoglobin.  The  size  of  the  red  corpuscles  is  very  variable.  In  the 
normal  condition  the  diameter  is  about  7  /jl,  but  in  the  chlorotic  patient  a 
number  of  dwarf  corpuscles  with  a  diameter  of  from  3  to  4  yu,  are  seen,  as  well 
as  giant  cells  with  a  diameter  of  from  12  to  14  /j,. 

The  normal  corpuscle  is  discoid.  In  the  chlorotic  patient  we  find  the 
most  varied  forms,  especially  among  the  dwarf  corpuscles,  which  may  be 
fusiform  or  piriform  or  racquet-shaped.  These  changes  in  shape  are  due  to 
the  morbid  contractility  of  the  protoplasm. 

The  red  blood-corpuscles  are  much  paler  than  normal,  because  they 
contain  less  haemoglobin.  We  know  that  the  red  corpuscle  is  composed  of  a 
stroma  or  of  a  felting  called  globulin,  and  of  a  colouring  matter  rich  in  iron 
and  essential  to  the  respiratory  function.  Tliis  colouring  matter,  which  im- 
pregnates the  globidin  and  is  of  an  albuminoid  nature,  is  called  haemoglobin. 
The  globidin  is  normal  in  the  chlorotic  patient,  but  the  haemoglobin  is  altered  : 
the  individual  red  corpuscle  is  diseased,  its  haemoglobin  is  diminished,  and 
the  saturation  of  the  blood  with  oxygen  is  notably  lowered.  The  researches 
of  Duncan  and  Mantegazza,  as  well  as  more  recent  studies  (Hayem,  Quin- 
quaud,  Malassez),  have  elucidated  these  changes. 

The  corpuscular  change  in  the  chlorotic  woman  is  so  great  that  the  blood, 


1898  TEXT-BOOK  OF  MEDICINE 

which,  normally  contains  12  to  15  parts  of  haemoglobin  per  100  c.c, 
contains  only  5  to  8  parts,  and  as  the  number  of  red  blood-corpuscles 
is  often  very  slightly  diminished,  the  colour-index — that  is  to  say,  the 
quantity  of  haemoglobin  contained  in  a  single  corpuscle — is  always  very 
low;  it  may  fall  to  18  or  20  parts,  as  compared  with  28  to  30  parts 
in  the  normal  condition.  This  change  explains  the  pale  colour  of  the  sldn 
and  of  the  mucous  membranes,  and  perhaps  has  some  bearing  on  the  greenish 
tint  seen  by  reflected  light  in  women  suffering  from  chlorosis,  if  we  admit 
that  their  diluted  haemoglobin  allows  the  green  rays  to  pass.  The  loss  of 
respiratory  power  in  the  corpuscle  is  ia  part  responsible  for  the  poverty 
of  the  organic  combustion,  for  the  feebleness  of  the  muscular  contrac- 
tions, and  for  the  respiratory  troubles. 

The  hsematoblasts,  which  must  not  be  confounded  with  the  dwarf 
corpuscles,  are  often  increased  in  chlorosis  (Hayem).  They  are  considered 
by  Hayem  as  elements  destined  to  be  changed  into  red  blood-corpuscles,  and 
are  therefore  charged  with  the  function  of  renewing  the  blood.  Most 
authors,  however,  reject  this  view.  The  signification  of  these  elements  is 
as  yet  unknown. 

Course — Diagnosis — Treatment.  —  Chlorosis  may  develop  suddenly 
(acute  emotion,  suppression  of  the  menses)  or  slowly.  The  nervous  symp- 
toms sometimes  precede  those  of  anaemia,  a  proof  that  they  are  not  subor- 
dinate to  them.  The  duration  of  the  disease  is  indefinite,  and  recovery 
takes  place  after  a  lapse  of  several  months  or  of  several  years.  Nevertheless, 
"  it  leaves  an  almost  indehble  impression,  so  that  a  young  girl  who  has 
suffered  from  severe  chlorosis  feels  the  effects  for  almost  the  rest  of  her  life, 
even  though  the  blood  has  long  since  become  normal,  furnishing  a  further 
proof  that  chlorosis  should  be  considered  as  a  nervous  disease,  causing  a 
change  in  the  blood,  rather  than  as  a  cachexia  producing  nervous  disorders  " 
(Trousseau). 

The  prognosis  in  chlorosis  is  not  grave  ;  the  possibility  of  Brightism, 
epistaxis,  and  metrorrhagia,  to  which  some  patients  with  chlorosis  are 
subject,  should,  however,  be  taken  into  serious  consideration. 

Phlegmasia  alba  dolens  is  not  a  very  rare  complication.  The  phlebitis 
obliterans  usually  affects  the  veins  of  the  legs,  and  disappears  after  lasting 
some  weeks,  but  it  may  cause  embolism,  followed  by  death.  Thrombosis  of 
the  sinuses  (Bollinger)  and  of  the  pulmonary  artery  (Rendu)  have  several 
times  been  noted. 

Certain  authors  consider  chlorosis  as  bemg  favourable  to  pulmonary 
phthisis.  Although  this  assertion  may  be  true  in  some  cases,  there  is  stiU 
a  source  of  error  which  must  be  avoided.  Tuberculosis  at  its  onset  may 
simulate  chlorosis,  and  is  the  false  chlorosis  on  which  Trousseau  has  dwelt 
at  length.     The  diagnosis  is  not  always  easy,  but  the  following  considerations. 


TATHOLOGY  OF  THE  BLOOD  1899 

in  tlio  absence  of  Koch's  bacilli,  will  aid  in  the  diar^nosia  :  "  When  i)hthisi8 
assumes  the  appearance  of  chloro-anainiia,  we  can  put  the  matter  in  a  nut- 
shell. There  is  a  general  dystrophy,  while  true  chloro-anfcmia  principally, 
and  perhaps  sololy,  affects  the  blood.  On  comparing  phthisis  and  chlorosis 
from  the  only  common  point  of  view — that  is  to  say,  from  the  change  in 
the  blood  and  from  the  phenomena  which  result — we  can  assure  ourselves 
of  their  predominance  in  primary  chloro-anaemia  and  of  their  less  signification 
in  organic  anaemia  :  (1)  The  vascular  murmurs,  which  are  so  marked  and  so 
characteristic  of  the  diminution  in  the  number  of  corpuscles,  are  almost 
always  al)scnt  in  organic  chlorosis  ;  (2)  the  cardiac  murmur  at  the  arterial 
and  auriculo- ventricular  orifices  are  never  present  in  the  anaemia  of  phthisis 
as  a  true  murmur :  there  is  rather  an  exaggerated  hruit  de  claquement  vcd- 
vulaire ;  (3)  the  circulation  is  constantly  quickened  in  tuberculosis  with 
anaemia,  and  the  palpitation  is  permanent,  whether  it  is  or  is  not  perceived 
by  the  patient.  In  the  chlorotic  patient,  on  the  other  hand,  the  circu- 
lation preserves  its  special  type  and  rhythm  ;  (4)  the  dyspnoea  in  the 
chlorotic  patient  occurs  later,  but  is  more  complete  because  of  the  hypo- 
globulia. 

Here  is  the  positive  proof  of  the  malnutrition,  which  at  once  strikes  the 
phthisical  patient  and  spares  the  chlorotic  one  :  (1)  Muscular  fatigue  is  early 
and  complete,  hindering  walking,  especially  up-hill.  Moreover,  it  is  this 
fatigue,  due  to  the  malnutrition,  which  produces  dyspnoea,  so  that  the 
phthisical  patient  at  length  cannot  make  the  least  movement  without 
breathlessness.  (2)  The  skin,  instead  of  being  colourless  and  pale  (on 
account  of  the  diminution  in  the  haemoglobin),  presents,  'in  the  phthisical 
patient,  a  dull  greyish  tint,  as  in  cachexia.  (3)  The  menstruation,  after 
certain  irregularities,  is  suppressed,  although  later  than  in  chlorosis,  but 
then  the  menstrual  troubles  are  totally  and  definitely  compromised. 
(4)  Chlorosis  is  apyretic,  or,  rather,  it  never  presents  the  same  degree  of  fever 
as  does  tuberculosis.  (5)  Wasting  appears  from  the  first,  while  in  chlorosis 
the  embonpoint  is  usually  preserved.  In  short,  the  condition  of  the  muscles 
and  of  the  skin,  the  oxidation  and  the  general  nutrition,  indicate  an  immediate 
failing  which,  in  the  case  of  the  chlorotic  patient,  affects  only  the  blood 
(See). 

The  disease,  described  under  the  name  of  progressive  pernicious 
ansemia  (Biermer),  does  not  appear  to  have,  as  yet,  an  indisputable  noso- 
logical value.  It  closely  resembles  chlorotic  cachexia,  and  it  may  possibly 
be  an  exceptionally  grave  chlorosis  (Jaccoud).  The  anaemic  symptoms  are 
excessive  :  retinal  haemorrhages,  epistaxis,  petechias,  and  fever  are  seen  ; 
diarrhoea  and  oedema  appear  later.  The  disease  is  not  absolutely  fatal,  but 
it  is  extremely  grave. 

Iron  occupies  the  first  place  in  the  treatment  of  chlorosis.     It  may  be 


1900  TEXT-BOOK  OF  MEDICINE 

given  in  the  form  of  pills  or  of  syrup,  but  it  should  always  be  taken  at 
meals.  Syrup  of  iodide  of  iron  and  the  syrup  of  the  ammoniacal  citrate  are 
usually  the  best  tolerated.  The  iron  waters  of  Saint  Moritz,  Spa,  etc.,  are 
useful.  Preparations  of  iron  must  be  continued  for  several  weeks,  and 
repeated  at  intervals.  Inhalations  of  oxygen,  hydrotherapy,  and  sea-baths 
are  indicated  in  some  cases.  I  cannot  recommend  too  strongly  preparations 
of  arsenic,  and  especially  injections  of  cacodylate  of  soda,  as  described  in 
the  Appendix.  The  chlorotic  patient  should  live  in  the  open  air,  where  it 
is  bright  and  sunny.  Chlorosis  often  improves,  and  may  be  cured  ;  but  it  is, 
I  repeat,  subject  to  relapses. 

Ovarian  extract  has  been  suggested  in  the  treatment  of  chlorosis,  but 
the  number  of  cases  is  still  too  restricted  to  form  any  definite  opinion  as  to 
this  method,  which,  a  'priori,  would  appear  to  be  useful. 

Chloro-Brightism. 

I  shall  discuss  here  the  association  and  relations  between  chlorosis  and 
Brightism  which  I  pointed  out  in  my  communication  to  the  Academie  de 
Medecine.*  I  have  given  the  name  of  chloro-Brightism  to  this  association, 
to  which  my  attention  was  called  many  years  ago.  In  order  to  avoid  mis- 
understanding, let  me  state  the  question  clearly. 

Under  the  denomination  of  "  chloro-Brightism  "  I  do  not  allude  to 
patients  in  whom  Brightism,  especially  when  associated  with  syphilis,  is 
accompanied  by  more  or  less  marked  anaemia.  Chloro-Brightism,  in  my 
opinion,  should  ]be  confined  to  patients,  either  women  or  girls,  "w-ho  show 
the  symptoms,  the  attributes,  and  the  mask  of  chlorosis,  the  characteristic 
tint  of  the  face,  the  decoloration  of  the  skin  and  of  the  mucous  membranes, 
the  varied  uterine  troubles,  dysmenorrhoea,  amenorrhoea,  leucorrhoea,  menor- 
rhagia,  breathlessness  and  palpitations,  as  well  as  dyspepsia  with  or  without 
anorexia,  cardiac  and  vascular  murmurs,  considerable  diminution  in  the 
number  of  red  blood-corpuscles,  and  more  or  less  marked  lowering  of  the 
colour-index. 

I  think  that  in  this  case  there  is  no  possible  error  as  to  the  interpretation 
of  the  facts,  and,  whatever  be  the  theoretical  idea  adopted  as  to  the  patho- 
genesis of  chlorosis,  we  can  aflfirm  that  every  young  woman  presenting  the 
above  symptoms  is  either  chlorotic  or  chloro-ansemic. 

Many  of  these  patients  also  suffer  from  Bright's  disease.  I  shall  attempt 
to  show  the  truth  of  this  opinion  by  applying  these  considerations  to  some 
forty  cases,  mostly  taken  from  my  clinique  at  the  Necker  Hospital  and  at 
the  Hotel-Dieu,  but  I  shall  first  show  by  an  example  the  nature  of  the 
association  in  chloro-Brightism. 

*  Dieulafoy,  Academie  de  Medecine,  Seance  du  20  Juin,  1895. 


rATTiOLony  of  the  blood  looi 

A  physician  is  rallod  to  spo  a,  ^irl  from  fiftoon  to  twenty  years  of  age, 
who  has,  for  some  time  past,  attracted  the  attention  of  her  parents  by  symp- 
toms of  chloro-anfpmia,  and  the  following  dialogue  takes  place  between  the 
mother  and  the  physician  : 

"  Soe,  doctor,  liow  p.ilo  and  colonrloss  the  child  is !  She  looks  like  old  wax  ;  anri 
if  you  look  at  her  hands,  lip.s,  and  gums,  you  would  say  that  she  is  bloodlesH." — 
"  Certainly,  madam,  she  has  the  appearance  of  chlorosis." — "  She  has  not  been  regular 
for  the  p;ist  four  months,"  continues  the  girl's  mother,  "  but  she  suffered  from  a  loss 
of  blood  several  months  ago,  and  since  then  the  menses  have  not  reappeared.  However, 
she  has  leucorrhoea,  which  quite  wears  her  out." — "  Yes,  madam,  such  is  the  case  in 
chlorosis." — "  And  her  appetite,  doctor  !  She  eats  nothing,  and  prefers  only  salad 
and  acid  food.  Just  see  how  she  has  wasted  !  A  trifle  fatigues  her.  She  cannot 
walk  quickly,  or  go  upstairs  without  experiencing  breathlessness  and  palpitation  of  the 
heart." — "  It  is  chlorosis." — "  She  has  incessant  headache,  vertigo,  and  neuralgia." 
— "  It  is  chlorosis." — "  She  was  examined,  and  the  doctor  said  that  she  has  murmurs." 
— *'  It  is  chlorosis." — "  The  blood  has  been  examined,  and  the  number  of  the  red  blood- 
corpuscles  was  found  to  be  diminished  by  half." — "  It  is  chlorosis." — "  Often,  too,  her 
eyes  are  puffy  and  her  hmbs  are  swollen." — "  It  is  chlorosis." 

And  this  dialogue,  which  recalls  somewhat  that  between  Toinette  and  Argan  in 
the  "  Malade  Imaginaire,"  ends  with  the  following  question  on  the  part  of  the  mother  : 
"  But,  doctor,  what  treatment  are  you  going  to  prescribe,  in  order  to  cure  the  chlorosis  ?" 
— "  Your  daughter  has  need  of  underdone  meat,  strong  soups,  meat -juice,  jellies,  generous 
wines,  extract  of  quinine,  preparations  of  iron  or  of  arsenic,  and  we  shall  succeed  in 
overcoming  the  chlorosis." 

Before  the  end  of  his  reply  the  physician  has,  however,  been  interrupted.  "It  is 
no  use  to  advise  that  diet,  because  it  has  been  prescribed  ten  times  already,  and 
each  time  it  has  had  to  be  abandoned.  My  daughter  gets  worse  as  soon  as  she 
commences  it." 

The  treatment,  indeed,  had  been  of  no  use,  and  had  been  badly  borne, 
because  the  patient  in  question  was  suffering  from  chloro-Brightism.  If  we 
make  careful  inquiry  as  to  Brightism,  we  shall  find  that  for  several  months 
she  has  been  compelled  to  get  up  two  or  three  times  at  night  to  pass  water, 
has  cramp  in  the  calves  and  in  the  legs,  sensation  of  dead  fingers,  and  ex- 
periences electric  shocks  on  lying  down.  The  crysesthesia  is  of  long  duration, 
and  she  cannot  keep  her  legs  and  feet  warm  ;  she  has  slight  morning  epis- 
taxis  ;  the  urine  is  of  feeble  toxicity,  and  sometimes  shows  a  cloud  of  albumin. 
In  short,  the  girl  is  suffering  both  from  chlorosis  and  Brightism.  The 
headache,  set  down  to  chloro- anaemia,  may  be  due  to  Bright's  disease  ;  the 
oedema  of  the  eyelids,  face,  and  legs,  which  has  been  put  down  to  chloro- 
ahpemia,  is  really  due  to  the  kidney  mischief.  Brightism  is  the  chief  feature 
in  this  case. 

My  conclusions  on  chloro-Brightism  are  confirmed  by  the  fact  that,  in 
thirty  cases  mentioned  by  me  at  the  Academic,  as  well  as  in  those  which  I 
have  since  collected  at  the  Hotel-Dieu,  I  found  chloro-Brightism  in  all  its 
forms,  often  without  albuminuria,  but  sometimes  with  it — chloro-Brightism 


1902  TEXT-BOOK  OF  MEDICINE 

against  which  the  tonic  and  strengthening  treatment  of  simple  chlorosis 
completely  fails  and  in  which  nulk  diet  nearly  always  succeeds.  For  it  is 
a  fact  worthy  of  remark  that  most  of  these  women  and  girls  suffering  from 
chloro-Brightism,  in  which  the  symptoms  are  aggravated  by  a  meat  diet, 
improve  rapidly,  and  in  some  cases  completely,  under  the  influence  of  a 
milk  regime. 

As  a  result  of  this  diet  the  colour  returns,  the  red  blood-corpuscles 
increase  in  number,  the  colour-index  rises,  the  oedema  disappears,  the 
breathlessness  and  the  palpitation  diminish  in  severity,  the  strength  comes 
back,  and  menstruation  is  re-established.  I  therefore  feel  convinced  that, 
of  the  two  factors  which  enter  in  the  association  of  chloro-Brightism,  the 
greater  part  is  often  played  by  the  Brightism. 

At  the  Hotel-Dieu  I  had  an  opportunity  of  giving  a  lecture  on  a  case  of 
chloro-Brightism,  and  I  give  here  the  resume  of  it : 

A  woman,  twenty-two  years  of  age,  came  under  my  care  for  chlorosis.  She  was 
as  pale  as  old  wax,  the  gums  and  conjunctivse  were  colourless,  and  the  hands  as  white 
as  ivory.  She  could  scarcely  walk  up  to  the  ward  without  feeling  palpitation  and  such 
severe  breathlessness  that  she  was  compelled  to  sink  into  an  arm-chair.  She  complained 
of  headache,  palpitation  of  the  heart,  and  continual  oppression.  The  picture  of  chlorosis 
was  completed  by  auscultation  of  the  vessels  of  the  neck,  revealing  bruit  de  diable  and 
fremissement  cataire.  And  yet  the  case  was  clearly  one  of  chloro-Brightism  and  not 
of  pure  chlorosis,  by  reason  of  the  puflfiness  of  the  face,  the  oedema  of  the  legs,  the  clearly 
marked  sensation  of  dead  fingers,  the  frequent  epistaxis,  the  itching,  the  buzzing  in 
the  ears,  the  electric  shocks,  and  the  cramps  in  the  calves. 

This  history  was  as  foUows  :  The  breathlessness  and  palpitation  had  appeared  before 
the  age  of  fourteen,  so  that  the  patient  could  not  play  with  her  friends.  She  men- 
struated at  fourteen,  but  she  soon  became  pale.  Amenorrhcea  appeared,  and  lasted 
for  some  months.  The  chlorosis  was  treated  most  successfully  for  six  years  by  tonics 
and  strengthening  medicines.  At  this  time  Brightism  appeared  with  oedema  of  the 
face  and  legs.  A  physician  found  a  marked  quantity  of  albumin  in  the  urine,  and 
prescribed  milk  diet.  As  the  result  of  this  diet  the  improvement  was  so  marked  that 
the  physician,  in  order  to  make  it  complete,  considered  it  advisable  to  order  a  return 
to  underdone  or  to  raw  meat,  and  so-called  generous  wines.  The  new  diet,  however, 
failed,  the  dyspnoea  and  the  palpitation  returned,  and  the  patient  felt  herself  becoming 
weaker  daily.  Then  everybody  gave  her  advice,  and  the  paler  and  weaker  she  became 
the  more  was  she  compelled  to  take  kola  and  coca  wines,  quinine  with  iron  preparations 
and  confection  of  Saint  Vincent  de  Paul.  The  situation  became  worse,  and  the  girl 
was  admitted  to  the  Hotel-Dieu  in  the  condition  above  described.  I  therefore 
prescribed  milk  diet,  because  the  Brightism  was  of  more  importance  than  the 
chlorosis. 

In  about  a  week  the  colour  began  to  come  back  to  the  skin,  the  dyspnoea  improved, 
the  headache  disappeared,  and  the  patient  gained  4  pounds  in  weight.  After  a  fort- 
night of  milk  diet  the  improvement  was  even  more  manifest.  The  patient  suffered  no 
longer  from  breathlessness  or  palpitation,  and  she  took  6  pints  of  milk  with  bread. 
In  a  month  she  had  put  on  12  pounds,  her  strength  had  returned,  and  as  she  was  con- 
sidered cured,  I  allowed  her  to  leave  the  hospital,  on  the  understanding  that  she  con- 
tinued the  milk  diet  for  several  months. 

The  following  table,  compiled  by  Jolly,  shows  clearly  the  progressive  increase  in 


rATlI()I.Or;V  DF  THE  P.LOOD 


1903 


tho  red  corpusclos,  in  tho  li{Binogiol)in,  and  in  tho  colour-index.     This  oano  formf  an 
excollont  demonstration  of  tho  importanoo  of  milk  diot  in  chloro-Britrh(ism. 

March  23.  before  tho  [;;«dcorpns,.lo3 
milk  diet  jhajmoglobm 

l^oolour-indox 


April  3,  milk  di(it 


April  15,  milk  diot 


April  28,  milk  diot 


(red  corpiiHclos 
}  haimoglobin 
l^colour-indox 
[rod  corpuscles 
•J  h.iemoglobin 
I  colour -index 
Tred  corpuscles 
-I  hfemoglobin 
[colour -index 


.     3,150,000 

4-3 

130 

.     4,200,000 

8 

19 

.     4,700,000 

9 

189 

.     4,400,000 

8-5 

19 

It  may  be  asked  wliat  becomes  of  these  patients  in  the  long  run,  and  what 
future  is  reserved  for  them  as  regards  the  evolution  of  Bright's  disease. 
Gubler,  who  had  considered  the  matter,  and  had  noted  albuminuria  in 
chlorotic  patients,  asked  whether  this  condition,  composed  of  chlorosis  and 
of  albuminuria,  might  not  at  some  time  end  in  Bright's  disease. 

I  think  I  can  answer  both  these  questions.  In  the  great  majority  of 
cases  chloro-Brightism  does  not  end  in  confirmed  Bright's  disease.  The 
morbid  condition  only  shows  itself  by  the  minor  symptoms  of  Brightism 
with  or  without  albuminuria.  In  some  cases,  however,  as  I  have  myself 
reported,  chloro-Brightism  finally  ends  in  severe  uraemia,  and  even  in  death. 

A  young  girl  had  been  under  treatment  for  two  months  for  chloro -anaemia.  The 
symptoms  of  this  so-called  chlorosis  increased,  her  sight  became  aflFected,  and  Gale- 
zowski  found  albuminuric  retinitis.  I  also  saw  the  patient  and  found  uraemia,  following 
the  troubles  of  chlorosis  and  Bright's  disease,  which  had  run  a  slow  course.  Death 
was  the  result. 

In  consultation  I  saw  a  patient  whose  case  has  been  reported  by  Hays.  This 
young  girl  was  attacked  by  fatal  symptoms  of  uraemia,  with  multiple  haemorrhages. 
The  disease  in  this  case  had  begun  about  sis  years  before  with  symptoms  of  chloro- 
Brightism  ;  the  albuminuria  did  not  appear  imtil  four  years  later. 

These  cases  prove  that  cliIoro-Brightism,  although  benign  in  general,  may  in  some 
cases  result  in  uraemia  and  end  fatally. 

In  a  case  of  chloro-Brightism  published  by  Hanot,  a  young  girl  was  seized  with 
urjemic  convulsions,  which  yielded  to  bleeding  and  milk  diet.  Labadie-Lagrave's 
case  deals  with  a  young  girl,  who  in  the  course  of  chloro-Brightism,  was  seized  with  an 
acute  uraemia  during  influenza.  The  uraemia  ended  in  recovery.  A  case  of  chloro- 
Brightism,  reported  by  Boudet,  ended  fatally. 

Pregnancy  and  Chloro-Brightism.— The  relations  between  the  puer- 
peral condition  and  chloro-Brightism  are  highly  important. 

I  had  under  my  care  a  woman,  twenty  years  of  age,  suffering  from  chloro-Brightism 
without  albumin.  She  married  shortly  afterwards  ;  the  pregnancy  was  uneventful ;  there 
was  no  albuminuria,  but  three  days  after  her  confinement  acute  attacks  of  eclampsia 
supervened,  with  total  anuria  for  twenty-four  hours,  and  some  days  afterwards  albu- 
minuria.    The  patient  recovered. 


1904  TEXT-BOOK  OF  MEDICINE 

With  Got,  I  SciTv  a  young  woman  "who  had  had  chloro-Brightism  when  a  young  girl. 
During  her  first  pregnancy  she  suffered  from  albuminuria,  and  a  miscarriage  took  place 
at  the  third  month.  During  her  second  pregnancy  she  suffered  from  anasarca,  and 
was  prematurely  confined  at  the  seventh  month. 

The  question  of  Briglitism  and  pregnancy  has  been  well  put  by  Pinard. 
A  woman  suffering  from  Bright's  disease  may  become  pregnant,  as  occurs 
daily.  Wliile  impregnation  does  not  appear  to  be  influenced  by  the  renal 
lesion,  it  is  quite  otherwise  as  regards  the  pregnancy.  We  may  say  that 
every  pregnancy  in  a  woman  with  Bright's  disease  or  with  chloro-Brightism 
will  be  disturbed  by  the  appearance  of  complications  afEecting  the  mother 
or  the  child. 

In  the  Mother. — The  complications  will  depend  on  the  severity  of  the 
renal  lesion  on  the  one  hand,  and  on  the  duration  of  the  pregnancy  on  the 
other.  Although  they  are  more  frequent  and  more  serious  in  the  later 
months  of  pregnancy,  we  must  stiU  remember  that  formidable  complications 
may  appear  from  the  commencement  of  gestation. 

With  Pinard  I  saw  a  young  woman  suffering  from  Bright's  disease,  in  whom  com- 
plications showed  themselves  as  early  as  the  second  month  of  the  pregnancy,  and  were 
so  severe  that  it  was  necessary  to  empty  the  uterus  at  the  third  month.  Pinard  per- 
formed the  operation,  which  was  completely  successful.  The  young  woman  recovered, 
but  the  albuminuria  did  not  disappear.  Pinard  has  informed  me  of  several  similar 
cases. 

In  the  Child. — Apart  from  cases  in  which  therapeutic  abortion  is  neces- 
sary, the  development  of  the  foetus  is  hindered  or  interrupted  by  the  appear- 
ance of  placental  lesions  in  women  sufiering  from  Bright's  disease  or  from 
chloro-Brightism.  This  fact  has  been  absolutely  proved  by  the  researches 
of  Pinard  and  his  pupils.  Moir  (Edinhurgh  Medical  Times)  in  1864,  Simpson 
in  1874,  and  Chanteuil  in  1879  {Lemons  Cliniques),  suspected  the  relations 
between  the  renal  lesion  in  the  mother  and  the  placental  lesion  of  the  child ; 
they  were  definitely  established  in  1885  by  Pinard  and  Fehling. 

The  lesion  is  characterized  by  the  appearance  of  haemorrhages,  which  are 
converted  into  white  infarcts.  The  primary  lesion  is  hsemorrhagic  in  nature  ; 
the  white  infarct  is  secondary.  Furthermore,  it  is  always  intraplacental  and 
most  often  intracotyledonous.  The  number  of  foci  is  extremely  variable '; 
sometimes  one  cotyledon,  or,  at  other  times,  the  whole  placenta  may  be 
invaded.  The  recent  infarct  containing  fluid  blood,  or  having  a  gelatinous 
consistency,  is  almost  of  a  black  colour,  and  clearly  marked  from  the  paler 
tint  of  the  surrounding  tissue.  It  resembles  a  truffle  let  into  the  cotyledon  ; 
hence  the  name  of  placenta  truffe,  given  by  Pinard  to  the  placenta  in  cases 
of  albuminuria.  When  the  infarct  is  older,  it  becomes  pale,  the  colouring 
matter  of  the  blood  disappears  gradually,  and  the  residue  of  the  haemorrhage 
presents  a  tint  which  is  at  first  chocolate  coloured,  then  reddish-yellow,  and 
finally  reaches  the  tint  of  the  white  infarct. 


PATHOLOGY  OF  THE   I'-LOOD  1905 

If  the  infarct  is  incised,  it  appears  formed  of  fibrin  more  or  less  dense 
and  homogeneous  in  appearance,  and  sometimes  disposed  in  a  series  of 
concentric  layers.  In  the  centre  we  oft<;n  find  a  small  collection  of  more 
Or  less  coloured  fluid,  forming  the  residue  of  the  blood-serum.  Nevertheless, 
it  is  not,  properly  speaking,  a  focus,  but  rather  an  infiltration.  The  size 
of  these  hemorrhagic  foci  or  infiltrations  is  also  extremely  variable  ;  they  may 
vary  from  the  size  of  a  millet-seed  to  that  of  a  pigeon's  egg.  The  haemor- 
rhage in  some  cases  may  extend  beyond  the  limits  of  the  placenta,  and  give 
rise  to  retroplacental  haemorrhage  (Pinard),  which  may  prove  fatal  to  the 
mother.  It  seems  needless  to  add  that  in  the  same  placenta  we  may  find 
recent  and  old  foci,  and  thus  very  easily  follow  the  difierent  degrees  in  the 
evolution  of  the  placental  hasmatoma  described  above. 

In  spite  of  the  works  of  Wiedow  (1887),  Cohn,  and  especially  of  Rossier 
(Leipzig,  1888),  the  pathological  histology  of  the  albuminuric  placenta  has 
been  hardly  more  than  outlined.  Are  the  intraplacental  haemorrhages 
related  to  the  lesions  of  the  vessels  of  the  decidua,  or  to  lesions  of  the  foetal 
vessels  ?  Rossier  does  not  venture  on  any  conclusion.  Pinard  says  there 
is  no  doubt  that  the  lesion  is  of  maternal  origin,  and  this  opinion  is  supported 
by  the  recent  histological  studies  of  Schaefier. 

From  what  has  gone  before,  it  is  easy  to  understand  how  and  why  the 
development  of  the  foetus  may  be  interrupted  in  a  woman  suffering  from 
Bright's  disease  or  from  chlcro-Brightism.  As  soon  as  a  focus  occurs  the 
field  of  hsematosis  is  restricted.  As  the  child  lives  solely  upon  the  maternal 
blood,  it  is  evident  that  anything  which  hinders  the  exchange  of  matter 
in  the  placenta  diminishes  the  nourishment  of  the  foetus,  and  hence  we  find 
the  wasted  and  spider-like  fcetus  (according  to  Pinard's  expression).  If  the 
lesions  become  general,  the  foetus  dies  of  inanition,  whence  the  frequent 
expulsion  of  a  dead  and  macerated  foetus. 

The  recognition  of  these  facts  is  of  extreme  importance  from  the  point 
of  view  of  diagnosis  and  of  treatment. 

As  regards  the  diagnosis  of  Bright's  disease,  examination  of  the  placenta 
is  of  the  highest  interest.  Pinard  possesses  a  number  of  records  in  which 
the  placental  lesion  alone  pointed  the  way  to  the  diagnosis,  the  other  symp- 
toms of  Brightism  being  unnoticed  until  the  expulsion  of  the  products  ot 
conception. 

Numerous  cases  show  that  rigorous  treatment  during  the  whole  duration 
of  pregnancy  will,  in  a  more  or  less  complete  fashion,  prevent  the  production 
of  placental  lesions  in  women  suffering  from  Bright's  disease  and  chlorosis, 
and  in  the  same  way  prolong  the  Life  of  the  child  to  full  term,  or,  at  any  rate, 
until  it  is  viable.  It  is  superfluous  to  say  that  this  treatment  should  be 
an  absolute  milk  diet. 

Li  short,  when  examining  a  chlorotic  patient  we  must  always  think  cf 


1906  TEXT-BOOK  OF  MEDICINE 

the  possibility  of  Brightism,  and  look  carefully  for  the  "  minor  symptoms." 
We  also  have  to  decide  the  question  of  prognosis,  especially  as  regards  the 
pregnancy  and  the  puerperium.  A  woman  sufiering  from  Bright's  disease 
and  chlorosis  wiU  be  more  liable  to  albmninm-ia  gravidarum  and  to  attacks 
of  eclampsia. 

Hygienic  measures,  preparations  of  iron  and  arsenic,  or  injections  of 
cacodylate  of  soda,  which  have  been  advised  in  chlorosis,  are  also  applicable 
in  chloro-Brightism,  but  in  the  latter  ease  milk  diet  forms  the  basis  of 
the  treatment. 

The  pathogenesis  of  chloro-Brightism  may  be  interpreted  in  various 
ways.  If  I  have  personally  abstained  from  hypotheses,  I  have  done  so 
because  none  of  them  are  quite  satisfactory.  I  have  been  content  to  observe 
the  facts  without  proposing  an  explanation.  Hanot  has  suggested  the 
following  theory  :  "  In  chlorosis  the  work  of  internal  nutrition  is  disturbed, 
and  the  incompletely  oxidized  products  of  disassimilation  accumulate  in 
the  organism,  are  eliminated  by  the  kidneys,  and  may  finally  produce  an 
epithelial  nephritis.  The  noxious  action  is  often  facilitated  by  the  coiaci- 
dence  of  arterial  aplasia  in  the  kidneys,  as  has  been  noted  by  Lancereaux, 
and  in  this  way  the  kidney  becomes  an  organ  of  least  resistance." 

Chatin  has  attempted  to  verify  the  question  of  diminished  oxidation  in 
chlorosis.  We  should  suppose,  says  he  (if  the  theory  previously  presented 
be  true),  that  the  toxicity  of  the  urine  would  become  increased  in  the 
chlorotic  patient  by  reason  of  the  elimination  of  insufficiently  oxidized 
products,  and  that  this  urinary  toxicity  would,  on  the  other  hand,  faU  below 
normal  when  once  nephritis  has  declared  itself— that  is  to  say,  in  the  case  of 
chloro-Brightism.  Experimental  facts  have  not  confirmed  this  hypothesis. 
The  toxicity  is  always  diminished  in  chlorosis,  and  this  diminution  of 
toxicity  "  does  not  appear  due  to  a  diminution  in  the  causes  of  auto -intoxica- 
tion. The  state  of  latent  renal  iasufficiency,  which  manifests  itseK  by  the 
slight  signs  of  Brightism,  may  play  a  large  part  in  the  matter  "  (Chatin). 

In  short,  whatever  be  the  theory  invoked,  it  is  certain  that  chlorosis 
has  a  tendency  to  cause  renal  iasufficiency.  We  may  say  of  every  chlorotic 
woman  that  her  urinary  depuration  will  become  insufficient  at  some  time  or 
other.  Chloro-Brightism  is  made  up  clinically  of  the  symptoms  of  chlorosis, 
to  which  are  added,  at  some  time,  the  minor  troubles  of  Brightism,  with  or 
without  albuminuria.  The  albuminuria  is  not  constant ;  it  may  be  transi- 
tory, and  does  not  constitute  an  absolute  sign  as  regards  diagnosis,  consider- 
ing the  possible  dissociation  of  the  morbid  processes  in  the  kidney,  but  its 
importance  is  of  the  first  order. 

Chlorosis  may  precede  the  appearance  of  Brightism  by  several  months 
or  even  by  several  years.  Chloro-Brightism  rarely  ends  in  severe  uraemia. 
Every  patient  should,  however,  be  under  careful  supervision,  because  she 


PATHOLOGY  OF  THE  BLOOD  1007 

is  threatened  with  iiraemia.  Any  infectious  disease,  such  as  influenza, 
tonsillitis,  pneumonia,  syphilis,  etc.,  may  give  rise  to  urtcraia  in  those 
patients,  and  in  their  case  pregnancy,  deserves  special  attention.  The 
therapeutic  indications  are  merely  formal,  and  milk  diet  sums  up  the 
treatment. 

VL  PURPURA— SCUKVY— INFANTILE  SCURVY. 

1.  Purpura. 

The  word  purpura  (purple),  taken  in  its  truest  sense,  signifies  "  eruption 
of  blood  spots  " — that  is  to  say,  haemorrhage  into  the  skin.  The  red  and 
purple  spots  are  of  various  sizes,  and  are  situated  in  various  regions.  They 
are  rounded,  prominent,  discrete,  or  confluent.  More  or  less  diffuse  and 
extensive  ecchymoses  are  often  found,  in  addition  to  the  petechise. 

The  purpuric  spots  differ  from  congestive  spots,  in  that  they  do  not  fade 
on  digital  pressure  or  on  distension  of  the  skin.  Histological  examination 
shows  that  they  are  formed  by  an  extravasation  of  red  blood- corpuscles  in 
the  dermis  and  hypodermis.  This  extravasation  may  be  the  only  lesion. 
We  sometimes  find  enormous  dilatation  of  the  capillaries  in  the  papillae  and 
in  the  dermis,  with  an  accumulation  of  blood-corpuscles  in  their  interior.  The 
extra vasated  red  blood-corpuscles  show  the  same  changes  as  the  traumatic 
ecchymoses  ;  the  haemoglobin  is  converted  into  hsematoidin,  which  becomes 
gradually  reabsorbed.  The  tint  of  the  petechise  indicates  this  conversion. 
It  changes  from  a  reddish-\dolet  to  dark  brown,  faded  green,  greyish-green, 
and  chamois-yellow ;  it  disappears  completely  at  the  end  of  from  six  to 
ten  days.     Desquamation  of  the  epidermis  is  often  seen. 

Such  is  a  concise  description  of  the  cutaneous  haemorrhage  called  pur- 
pura. Purpura  is  called  simplex  when  it  is  limited  to  the  skin,  but  another 
idea  is  attached  to  this  term  purpura.  It  is  that  the  patient  sufiering  from 
this  disease  has  a  more  or  less  marked  predisposition  to  other  haemorrhages 
(nasal,  buccal,  intestinal  haemorrhages),  and  this  idea  is  clearly  formulated 
in  the  term  purpura  JKBmorrhagica,  which  mdicates  the  tendency  of  the 
disease  to  multiple  haemorrhages. 

There  is,  however,  no  clearly  defined  line  between  purpura  simplex  and 
purpura  hcemorrhagica.  No  one  can  say  whether  a  case  which  begins  with 
the  symptoms  of  purpura  simplex  will  not  become  one  of  purpura  hasmor- 
rhagica. 

The  pathogenic  processes  put  forward  to  explain  purpura  comprise 
fragile  character  of  the  capillaries,  capillary  embolisms,  changes  in  the 
blood,  and  the  action  of  toxi-infectious  agents. 

Purpura  is  sometimes  present  as  a  symptom  in  the  course  of  various 
diseases ;  at  other  times  it  becomes  a  morbid  entity.     Classifications  are 


1908  TEXT-BOOK  OF  MEDICINE 

not  lacking  as  regards  the  different  varieties  of  purpura  (Rayer),  but  I 
cannot  reproduce  tkem  here,  for  it  is  rather  a  question  of  semeiology,  and 
I  shall  content  myself  with  enumerating  the  chief  varieties  of  symptomatic 
purpura,  relying  on  their  apparent  setiology.  I  say  "  apparent,"  for  many 
factors  are  often  united  in  this  rough-and-ready  setiology. 

Purpura  is  frequent  in  the  infectious  diseases.  It  is  at  times  limited 
to  the  skin  in  the  form  of  petechias  and  ecchymoses,  with  or  without  exan- 
themata, and  at  other  times  it  is  the  prelude  of  multiple  haemorrhages, 
which  are  of  the  worst  augury. 

In  most  of  the  cachectic  conditions,  such  as  Bright's  disease  and  lymph- 
adenia,  purpura  is  not  always  limited  to  petechiae  on  the  skin.  The  purpura 
of  tuberculosis  deserves  special  mention.  It  is  more  frequent  in  acute 
tuberculosis  than  in  chronic  phthisis,  and  it  also  betrays  itself  by  general 
haemorrhages. 

Purpura  may  supervene  in.  nervous  troubles,  which  vary  exceedingly 
both  in  origin  and  nature.  In  some  cases  it  is  associated  with  lesions  of 
the  spinal  cord :  tabes,  myelitis,  or  cancer  of  the  spine.  The  purpuric  spots 
are  usually  symmetrical,  and  accompanied  by  anaesthesia,  hyperaesthesia, 
or  by  multiple  and  fugitive  arthralgias. 

Certain  drugs,  such  as  mercury,  copaiba,  belladonna,  and  iodine,  give 
rise  to  eruptions  of  purpuric  spots,  preceded  or  accompanied  by  exan- 
thematous  eruptions.  Purpura  due  to  iodine  almost  always  attacks  the 
anterior  surface  of  the  limbs  in  the  neighbourhood  of  the  hair-follicles. 

We  must  now-  consider  two  other  varieties  of  purpura  with  fairly  well- 
defined  characters. 

Exanthematic  Purpura. — This  term  includes  a  group  of  cases  in  which 
purpura  appears  as  a  congestive  exanthema  of  the  skin  (polymorphous, 
infective,  or  seasonal  erythemata).  Sometimes,  also,  this  form  of  purpura 
is  in  reality  an  erythema  rendered  haemorrhagic  by  the  severity  of  the 
cutaneous  congestion  or  by  a  special  predisposition  of  the  organism  to 
hemorrhage.  This  feature  is  evident  when  both  eruptions  are  associated 
in  the  same  attack. 

Exanthematic  purpura  is  most  often  seen  in  children,  and  especially  in 
those  who  have  a  fine  white  skin,  and  come  of  an  arthritic  stock.  In  adults, 
the  female  sex  is  more  often  attacked.  The  purpura  reappears  at  the 
menstrual  periods,  and  may  return  every  month.  I  have  seen  a  case  of 
this  periodic  purpura  in  one  of  my  patients,  who  for  four  years  suffered 
almost  every  month  from  an  attack  of  purpura  and  a  haemorrhoidal  flux. 

Rheumatoid  Purpura. — Rheumatoid  purpura,  or  peliosis  rheumatica 
(7reXio9,  livid),  is  rarely  associated  with  acute  articular  rheumatism.  In 
the  majority  of  cases  it  is  an  association  of  purpura  with  pseudo-rheumatism 
rather  than  of  rheumatism  with  purpura  (Besnier). 


PATHOrXJOY  OF  THE   HLOOD  1900 

This  form,  which  is  more  frequent  in  children  than  in  adults,  is  especially 
prevalent  in  s])ring  and  summer,  just  like  the  polynif»r})hou8  erythomata 
or  erj'thoma  nodosum  with  which  rheumatoid  purpura  has  many  points  in 
comnuin.  Pain,  oedema,  and  gastro-intestinal  troubles  are  associated  with 
the  purpuric  exanthem,  as  in  the  following  example  :  A  youth,  after 
fatiguing  exercise,  or  without  apparent  cause,  is  seized  with  pains  in  the 
joints  and  in  the  muscles,  in  the  knees,  insteps,  calves,  thighs,  and  arms. 
The  pains  are  reawakened  by  pressure,  and  are  sometimes  accompanied  by 
slight  effusion  in  the  joints.  At  the  same  time,  gastro-intestinal  troubles, 
with  vomiting  of  bile  and  food,  pains  in  the  stomach,  colic,  and  diarrhoea, 
which  is  sometimes  streaked  with  blood,  supervene.  We  may  see  associated 
with  these  symptoms  white  oedema,  which  is  more  or  less  limited  aroimd 
the  joints,  and  more  or  less  extensive  over  the  rest  of  the  body,  sometimes 
attacking  the  face,  and  simulating  the  oedema  of  Bright' s  disease  or  of 
cardiac  lesions. 

The  purpuric  eruption  appears  during  these  symptoms,  which  are  more 
or  less  marked  according  to  the  particular  case.  The  purpuric  spots  are 
chiefly  seated  on  the  lower  limbs.  They  are  sometimes  symmetrical,  and 
are  usually  petechial,  but  rarely  ecchymotic.  The  disease  is  sometimes 
accompanied  by  slight  fever,  which  may  occur  in  successive  attacks,  and  last 
several  weeks  or  several  months.  It  is  rarely  followed  by  other  haemorrhages. 
If  it  is  accompanied  by  itching  it  takes  the  name  of  purpura  urticans. 

We  may  find,  in  addition  to  the  purpuric  eruption,  an  eruption  of 
erythema  papulosum  or  of  erythema  nodosum,  which  shows  the  affimty 
existing  between  rheumatic  purpura  and  the  polymorphous  and  urticarial 
erythemata. 

Infectious  Purpura. — This  variety  of  purpura  sometimes  supervenes  in 
the  course  of  well-defined  infectious  diseases.  Variola,  scarlatina,  varicella, 
erysipelas,  and  typhoid  fever  may  be  complicated  by  purpura.  Septicsemic 
conditions  of  surgical  or  of  obstetrical  origin,  infective  endocarditis,  pyaemia, 
and  various  suppurative  infections  often  give  rise  to  purpuric  eruptions. 
In  some  cases  this  purpura  is  limited  to  the  skin  in  the  form  of  petechias 
and  of  ,ecch}Tnoses,  with  or  without  rashes  ;  at  other  times  it  is  the  prelude 
of  multiple  haemorrhages,  which  are  very  serious  as  regards  prognosis. 

Apart  from  these  cases  of  secondary  infectious  purpura,  we  may  also 
see  purpura  hcemorrltagica  in  the  course  of  ill-defined  infectious  conditions 
of  unknown  origin.  These  cases  constitute  the  most  perfect  type  of  the 
so-called  primary  infectious  purpura. 

The  following  example  is  quoted  by  Hutinel : 

A  boy  thirteen  and  a  half  years  old,  hitherto  in  good  health,  was  seized  with  re- 
peated epistaxis,  which  required  plugging.  The  child  was  brought  to  the  hospital. 
On  examination  the  skin  was  pale,  an  eruption  of  petechiae  was  present  over  the  front 

n.  121 


1910  TEXT-BOOK  OF  MEDICINE 

of  the  tibiae,  and,  furthermore,  there  were  deep  ecchymoses.  The  temperattire  and  the 
urine  were  normal.  CoHc  suddenly  appeared,  and  was  accompanied  by  blood  in  the 
stools,  shght  delirium  and  incoherence,  but  no  fever.  The  melsena  continued,  and 
hsematuria  now  declared  itself.  A  few  hours  later  death  supervened.  The  absence 
of  fever  proves  that  we  cannot  judge  the  severity  of  the  disease  by  the  height  of  the 
temperature.  The  autopsy  revealed  ecchymoses  and  hsemorrhagic  foci  in  the  lungs, 
Uver,  spleen,  kidneys,  stomach,  cerebellum,  bulb,  and  testis.  It  was  indeed  a  ful- 
minant case  of  primary  infectious  purpura. 

In  these  forms  of  'purpura  hcemorrJiagica,  wlietlier  febrile  or  apyretic, 
hsemorrhage  occurs  on  every  side  (stomatorrhagia,  epistaxis,  h.Eematuria, 
haemoptysis,  metrorrhagia).  Ecchjonoses  appear  on  the  surface  of  the  body, 
and  the  trunk  and  the  face  are  not  spared,  which  is  not  the  case  in  exanthe- 
matic  purpura.  Visceral  haemorrhages  are  common,  especially  into  the 
meninges.     I  have  seen  several  cases  at  the  Necker  Hospital. 

One  of  my  patients  had  been  attacked  by  severe  infectious  pixrpura.  AU  danger 
appeared  at  an  end,  when  she  was  found  dead  in  her  bed.  The  autopsy  revealed 
meningeal  hsemorrhage.  Another  patient  with  infectious  purpura  was  seized  with 
vomiting.  She  raised  herself  up  to  get  the  spittoon,  and  fell  unconscious,  with  her 
head  over  the  bedside.  She  was  raised  up  and  died  some  hours  afterwards.  The  autopsy 
revealed  meningeal  hsemorrhage. 

Infectious  purpura  may  be  complicated  by  gangrene.  In  some  cases 
the  purpuric  spots  necrose  (necrotic  purpura) ;  in  others  the  gangrene  is 
diffuse,  and  attacks  extensive  areas.  Let  us  also  note  the  appearance  of 
suppuration  in  the  purpuric  spots  (ecthymatous  purpura)  or  in  the  form  of 
diffuse  phlegmon. 

In  addition  to  the  rapid  forms  just  described,  we  also  find  cases  of 
primary  infectious  purpura  in  which  the  course  is  less  rapid  and  the  symp- 
toms are  less  severe.  They  correspond  to  the  old  description  of  Verlhoff's 
disease  {morhus  mamilosus  Verlhoffii),  and  may  last  for  months  and  years. 

In  some  cases  purpura  assumes  a  typhoid  character,  with  an  insidious 
onset — fever,  rise  of  temperature,  prostration,  and  haemorrhages  into  the 
skin  and  mucous  membranes. 

Pathogenesis. — It  is  probable  that  the  different  varieties  of  purpura- 
purpura  simplex,  purpura  hsemorrhagica,  rheumatoid  purpura,  fulminant 
purpura,  and  typhoid  purpura — have  not  clearly  defined  limits,  They 
depend  for  the  most  part  on  infectious  causes.  Attempts  to  discover  the 
pathogenic  agent  have  not  been  successful.  Micrococci  (Petrone)  and  a 
bacillus  (Letyerich)  have  been  found,  but  they  have  not  any  specific  char- 
acter.    Hanot  and  Luzet  have  published  a  very  interesting  case  : 

A  woman  sufEering  from  meningitis  and  purpura  gave  birth  at  term  to  a  dead  foetus. 
She  died  herself  two  days  afterwards.  At  the  autopsy  on  the  mother  streptococci 
were  found  in  the  meninges,  in  the  spleen,  and  in  a  bleb  which  had  developed  in  a  pur- 
puric spot.  At  the  autopsy  on  the  foetus  there  was  no  trace  of  purpiu'a  in  the  skin, 
but  ecchymoses  containing  streptococci  were  found  in  the  pleura,  peritoneum,  and 
pericardiuia. 


PA'PlloLfKIY  OF  THE   I'.LOOI)  lOlL 

Nervous  lesions  influence  the  localization  of  the  orujition.  In  Hallian'a 
case  the  purpura  was  confined  to  a  limb  atrophied  by  infantile  paralysis  ; 
in  Crilbcrt's  case  it  had  spared  the  healthy  half  of  the  body  in  a  person 
sulTcriug  from  hemiplegia. 

The  visceral  changes  favour  the  production  of  purpura,  and  in  the  grave 
hiemorrhugic  forms  we  find  hepatic  lesions,  first  noted  })y  Aj)ort,  and  con- 
firmed by  later  researches.  Purpura  is  often  seen  bi  afTections  which 
accompany  changes  in  the  blood — leukocythasmia,  chronic  malaria,  and 
pernicious  an;emia.  Lastly,  in  the  hemorrhagic  forms  of  purpura  we  may 
meet  with  a  curious  lesion  of  the  blood.  The  clot  does  not  retract,  and  the 
blood-serum  does  not  separate  from  the  clot.  This  lesion,  however,  is 
neither  constant  in  hfiemorrhagic  purpura  nor  special  to  this  affection.  It 
may  be  met  with  in  the  absence  of  purpura,  especially  in  typhoid  fever 
(Widal,  Apert). 

The  prognosis  of  exanthematic  purpura  is  good.  It  recovers,  but  it  is 
prone  to  relapse  when  the  convalescent  begins  to  get  up.  Verlhoff's  disease 
may  recover  in  a  few  days,  but  infectious  purpui'a  is,  on  the  other  hand,  a 
severe  affection,  both  on  its  own  account,  as  well  as  on  that  of  possible 
complications. 

The  treatment  is  as  follows  :  abundant  nourishment,  composed  of  meat, 
fruit,  and  fresh  vegetables,  and  beverages  containing  a  large  amoimt  of 
orange- juice.  Perchloride  of  iron,  ergot,  extract  of  rhatany,  and  Rabel 
water  may  be  given  for  the  haemorrhage. 

Chloride  of  calcium,  introduced  by  Wright,  gives  good  results  in  the 
hsemorrhagic  forms  and  in  the  chronic  form  of  VerlhofE's  disease.  Injections 
of  artificial  serum  are  indicated  in  grave  cases,  but  should  be  given  with  the 
greatest  care. 

In  the  following  severe  case  of  hsemorrhagic  purpura  I  employed 
adrenaline  with  success  : 

A  woman,  thirty-two  years  of  age,  came  into  the  Hotel-Dieu  on  June  22,  1903. 
Saliva,  mixed  \vith  blood,  flowed  incessantly  from  the  mouth.  This  stomatorrhagia 
had  appeared  twenty-four  hours  before  her  admission  to  hospital,  commencing  suddenly 
without  any  prodromata.  Uterine,  cutaneous,  and  possibly  also  intestinal  haemorrhages 
were  present.  Although  the  flow  of  blood  from  these  various  channels  had  been  present 
only  since  the  previous  evening,  the  haemorrhage  from  the  gums  was  so  incessant  and 
copious  that  the  patient  was  very  anaemic,  and  had  already  the  classical  facias  of  severe 
haemorrhage.     The  usual  mecUcation  was  ordered. 

Next  day  the  lower  hmbs,  the  elbow,  and  the  face  showed  very  extensive  ecchymoses, 
but  there  was  no  injury  which  could  have  given  rise  to  them.  The  hmbs  were  mottled 
with  red  blotches.  The  temperature  was  shghtly  above  normal,  and  the  pulse  was  but 
little  accelerated.  The  arterial  tension  appeared  to  be  lowered.  A  diagnosis  of  giavo 
hiemorrhagic  piu-pura  was  made. 

I  painted  the  gums  with  a  solution  of  adrenalin,  1  to  1,000,  and  gave  chloride  of 
calcium  and  sulphate  of  quinine  without  obtaining  any  improvement.     The  anaemia 

121—2 


1912  TEXT-BOOK   OF  MEDICINE 

became  worse.  Fresh  hasmorrhages,  including  haematuria,  appeared  from  the  mucous 
membranes,  and  the  situation  became  threatening. 

The  examination  of  blood  showed  intense  ansemia  (1,800,000  red  corpuscles)  and 
very  shght  leucocytosis  with  a  normal  formula.  The  coagulation  of  the  blood  took 
place  as  usual,  but  the  clot  retracted  badly,  and  the  serum  was  laky.  I  then  pre- 
scribed daily  1  miUigramme  of  rencdine  franpaise,  which  is  the  same  as  adrenalin.  Next 
day  the  bleeding  from  the  mouth  was  much  less.  A  day  later  there  were  no  more 
haemorrhages.     Some  vesicles  of  herpes  appeared  on  the  lower  hp. 

From  this  time  the  situation  improved  rapidly,  and  the  patient  might  be  considered 
as  cured,  eleven  days  after  the  onset  of  the  affection  and  six  days  after  the  administra- 
tion of  the  renaUne  (4J  miUigrammes  in  five  days).  On  July  20  the  patient  left  the 
hospital.  One  of  the  most  remarkable  points  in  this  case  was  the  marked  blood  reaction 
which  the  adrenalin  caused.  The  number  of  leucocytes  rose  in  forty-eight  hours 
from  18,000  to  26,000.  The  number  of  polynuclears  increased,  and  nucleated  red 
cells,  as  well  as  myelocytes,  appeared  in  the  blood.  The  red  cells  gradually  regained 
their  normal  count.  These  various  phenomena  in  hsematology  are,  without  doubt, 
the  index  of  a  reparative  action  on  the  part  of  the  adrenaUn  in  the  blood  of  a  patient 
suffering  from  purpura. 

Experiments  undertaken  in  my  laboratory  by  Loeper  and  Crouzon  have 
also  proved  the  existence  of  variations  in  the  red  and  white  corpuscles  in 
animals  following  injections  of  adrenalin  in  non-toxic  doses. 

2.  Scurvy. 

Scurvy  is  usually  an  epidemic  disease,  which  for  centuries  has  developed 
under  absolutely  identical  conditions.  As  a  matter  of  fact,  in  the  aetiology 
of  scurvy  it  is  always  a  question  of  besieged  towns,  crowded  populations, 
armies  on  short  rations,  overcrowded  gaols,  and  passenger  ships  in  which 
the  hygienic  conditions  are  bad.  The  prime  cause  of  scurvy  has  not  been 
discovered.  Damp  cold,  bad  water,  deprivation  of  fruit  and  fresh  vegetables 
(insufficiency  of  potash),  and  the  abuse  of  salt  meats  (too  much  chloride  of 
sodium)  have  been  suggested.  It  is  certain  that  in  a  besieged  town  scurvy 
ceases  after  revictuaUing. 

Pathological  Anatomy. — The  changes  in  the  blood  are  not  well  under- 
stood. The  fibrine  has  been  increased  in  some  cases,  and  diminished  in 
others.  The  red  blood-corpuscles  are  less  numerous,  and  the  salts  of  sodium 
appear  to  be  in  excess,  while  the  quantity  of  potash  salts  is  lowered.  The 
blood  is  dark  and  very  fluid.  Infiltrations  of  blood  may  be  found  in  aU  the 
tissues — in  the  cellular  tissue,  in  the  muscles,  under  the  periosteum,  in  the 
space  between  the  diaphyses  and  the  epiphyses,  in  the  serous  cavities,  in 
the  joints,  etc.  Bacteriological  examinations  (Murri,  Babes)  have  not  given 
exact  results. 

Description. — Apart  from  the  exceptional  cases  in  which  scurvy  com- 
mences with  local  changes  in  the  mouth,  there  is  a  period  of  weakness 
characterized  by  progressive  loss  of  strength.  During  this  period  pains 
are  felt  in  the  legs,  in  the  joints,  and  in  the  base  of  the. chest.     The  face 


rATnOLOriY  of  the  blood  1913 

becomes  pale  and  the  skin  dry,  but  the  patient  has  no  fever.  The  changes 
in  the  mouth  tlien  supervene.  The  swollen  and  softened  gums  l)<'C(»riie 
ulcerated  and  bleed,  the  breath  is  Untid,  the  bui^cal  mucous  membraiif  is 
swollen  and  covered  with  ecchymoses  and  blebs  contiiining  hlood,  uiid 
mastication  becomes  extremely  painful. 

Petechiio  appear,  especially  around  the  hair-follicles.  The  lower  limbs 
are  covc^red  with  purpuric  spots  and  ecchymoses,  but  the  upper  limbs  are 
not  so  much  affected.  The  skin  becomes  of  a  dark  livid  or  greenish-yellow 
tint,  according  to  the  age  of  the  ecchymoses.  The  cellular  tissue  is  some- 
times invaded  by  hard  oedema.  Blood  tumours  develop,  and  form  sanious 
ulcers  (scorbutic  ulcers).  Haemorrhages  also  occur  in  the  cellular  tissue, 
in  the  popliteal  space,  in  the  groin,  and  in  the  interior  of  the  muscles.  The 
infiltration  of  CBdema  and  of  blood  cause  extreme  hardness  in  certain  parts 
of  the  calf  and  thigh. 

The  pains  are  increased  by  the  slightest  movement.  Muscular  efforts 
readily  cause  rupture  of  the  muscles  and  haemorrhage.  The  patient  experi- 
ences a  feeling  of  constriction  at  the  base  of  the  chest,  and  dyspncea, 
independent  of  any  lesion,  in  the  respiratory  organs.  The  pulse  is  small, 
constipation  is  usually  present,  but  the  urine  does  not  contain  albumin. 

If  the  disease  reaches  its  final  stage,  the  symptoms  increase  in  severity, 
the  teeth  become  loose,  and  may  fall  out,  giving  rise  to  alarming  haemorrhage. 
In  young  patients  the  epiphyses  of  the  long  bones  become  detached,  and 
the  ribs  are  separated  from  their  cartilages.  The  sphincters  are  relaxed,  con- 
stipation gives  place  to  bloody  diarrhoea,  fever  appears,  the  skin  is  covered 
with  cold  sweat,  and  the  patient  dies  from  adynamia  or  from  syncope. 

Other  and  more  rare  forms  are  seen,  in  addition  to  these  classical  ones. 
Scurvy  may  be  characterized  only  by  the  changes  in  the  gums,  haemorrhage 
being  absent.  In  other  conditions — as  in  the  Crimea,  for  example — the 
swelling  of  the  gums  was  often  absent,  and  the  scurvy  revealed  itself  by 
muscular  pains,  with  oedema  of  the  lower  limbs,  and  by  the  formation  of 
tumours  in  the  popliteal  spaces  (Laveran).  Scurvy  is  often  associated  with 
typhus  or  with  dysentery  in  armies  in  the  field.  Pneumonia,  pleurisy,  and 
haemorrhagic  pericarditis  are  frequent  complications. 

Scurvy  lasts  the  longer  in  proportion  as  its  causes  are  the  more  lasting, 
and  its  gravity  varies  in  different  epidemics  and  according  to  the  aetiological 
conditions.  Even  after  recovery  the  patient  remains  feeble  for  a  long  time, 
suffers  from  pain,  and  shows  a  notable  tendency  to  relapse.  Sporadic 
scurvy  is  much  less  grave. 

We  must  not  confound  scurvy  with  purpura,  which  usually  arises  with- 
out prodromata.  The  usual  causes  of  scurvy  are  absent,  and  we  do  not 
find  fungous  stomatitis,  ulcerated  haematomata,  or  the  infiltrations  of  the 
muscles  proper  to  scurvy. 


1914  TEXT-BOOK  OF  MEDICINE 

The  presence  of  lymphatic  tumours  and  the  leukaemia  will  distinguish 
the  lymphogenous  diathesis  from  scurvy,  although  lymphadenia  may  some- 
times be  accompanied  by  swelling  and  haemorrhage  of  the  gums. 

Treatment. — Prophylactic  measures  consist  in  giving  fruits,  fresh 
vegetables,  and  lemon- juice.  Persons  must  avoid  as  far  as  possible  damp 
and  gloomy  dwellings. 

The  same  measures  should  be  employed  when  the  disease  is  persistent — 
namely,  fresh  fruit  and  vegetables,  watercress,  lemon  or  orange  juice,  wine, 
and  alcoholic  beverages.  The  gums  may  be  touched  with  a  mixture  of 
citron- juice  and  alcohol,  or  with  diluted  hydrochloric  acid.  The  haemor- 
rhages should  be  treated  by  rhatany,  Rabel  water,  perchloride  of  iron,  and 
ergot. 

Injections  of  artificial  serum  may  give  good  results. 

3.  Infantile  Scurvy. 

Scurvy  may  occur  in  very  young  children.  It  differs  notably  from  the 
disease  in  the  adult,  but  yet  the  two  affections  are  identical  in  nature. 
The  divergences  depend  only  upon  the  differences  of  the  soil  in  which  the 
disease  arises. 

The  disease  was  first  described  in  Germany  in  1859  by  UroUer  under  the 
name  of  acute  or  heemorrhagic  rickets.  In  1883  Barlow  showed  that  this 
so-called  rickets  was  really  scurvy  occurring  in  children  fed  on  tinned  foods, 
and  cured  by  antiscorbutic  treatment  with  fresh  food.  The  name  of 
Barlow's  disease  has  been  given  to  infantile  scurvy. 

Description. — InfantUe  scurvy  hardly  ever  appears  before  the  age  of 
five  months  or  after  the  age  of  eighteen.  It  usually  appears  in  infants 
apparently  healthy,  in  the  sense  that  they  are  large,  fat,  and  well  developed  ; 
but  they  are  pale,  the  flesh  is  soft,  and  there  is  more  fat  than  muscle  under 
the  skin.  The  first  symptoms  consist  in  an  increased  pallor  of  the  skin. 
The  lips  become  colourless ;  the  little  patient  cries  out  when  his  legs  are 
touched,  and  if  he  is  on  his  feet,  walking  and  standing  become  diflS.cult, 
and  he  lies  in  bed  with  his  legs  semiflexed.  The  pains  are  more  acute  in 
the  neighbourhood  of  the  joints  than  in  the  legs.  Later,  similar  symptoms 
appear  in  the  arms. 

Bony  sweUings  are  seen  on  the  femur,  tibia,  or  fibula — sometimes  at  the 
upper  apophysis,  and  at  other  times  at  the  lower  epiphysis.  Similar 
swellings  may  also  appear  at  the  anterior  extremity  of  the  ribs.  Radio- 
graphy reveals  in  these  sweUings  simple  rarefaction  of  the  bony  tissues, 
an  epiphyseal  separation,  or  a  fracture  in  the  continuity  of  the  bone 
(Renault). 

The  periosteum  is  stripped  off  by  an  effusion  of  blood,  which  gives  the 
sensation  of  blood  crepitus. 


PATHOLOGY  OK  Till':   \\\JK)\)  1915 

The  orbit  may  bo  tlio  snat  of  a  siinibir  swullin;^'.  llccbyraoHis  is  soon  in 
the  lower  eyelid.  The  gums  are  not  aflected  unleas  the  patient  has  tooth. 
The  root  of  the  tooth  shows  littlo  fungous  growths,  which  bleed  easily. 
In  severe  cases  petechia)  may  bn  seen  on  the  mucous  membranes  and  on 
the  skin.  The  temperatirre  rarely  exceeds  100°  F.  The  disease,  when  loft 
to  itself,  is  progressive  and  fatal.  Tlie  pallor  increases,  the  feebleness 
becomes  more  and  morn  marked,  and  the  child  dies. 

i^tiology.— Infantile  scurvy  is  never  seen  in  a  breast-fed  child.  The 
disease  is  also  quite  exceptional  in  children  fed  on  fresh  cow's  milk  or  on 
milk  sterilized  in  the  water-bath  at  212°  F.  according  to  Budin's  method. 
Cases  have  been  seen  in  infants  fed  on  factory  milk  sterilized  at  120°  C, 
and  preserved  for  a  more  or  less  lengthy  period.  The  great  majority  of 
these  cases  of  infantile  scurvy  have  been  seen  in  children  fed  upon  con- 
densed milk  or  on  farinaceous  foods  sterilized  at  high  temperatures.  The 
disease  is  caused  by  skimmed  or  by  diluted  milk,  by  milk  containing  lactose, 
by  centrifugal i zed  or  dried  milk,  sold  commercially  as  humanized  milk,  the 
concentrated  milk  so  frequently  used  in  England  and  Germany,  and  the 
special  foods  prepared  for  young  infants.  This  fact  has  been  clearly  brought 
to  light  in  the  recent  discussions  at  the  Societe  de  Pediatric  de  Paris. 

Diagnosis. — We  must  always  think  of  infantile  scurvy  if  a  bottle-fed 
infant  becomes  pale,  gradually  loses  strength,  and  suffers  from  pain  in  the 
legs.  Rickets  never  begins  so  suddenly.  The  syphilitic  pseudo-paralysis 
of  Parrot  (epiphyseal  separation  by  syphilitic  changes  in  the  bone)  is  not 
likely  to  be  confounded  with  scurvy.  The  former  is  seen  during  the  first 
months  of  life,  and  is  almost  always  accompanied  by  stigmata  of  syphilis, 
especially  purulent  coryza. 

Treatment. — The  use  of  fresh  and  "  living  foods,"  to  use  Barlow's  tenn, 
brings  about  recovery  with  marvellous  rapidity.  Raw  milk  in  the  case  of  very 
young  infants,  and  furee  of  boiled  potatoes,  as  well  as  a  little  raw  meat,  in 
children  of  more  than  a  year,  should  be  substituted  for  the  farinaceous 
foods  and  tinned  milks.  We  may  also  give  a  few  teaspoonfuls  of  lemon- 
juice,  or  the  juice  of  green  vegetables,  after  each  meal.  It  is  remarkable 
to  see  how  quickly  the  bony  swellings  disappear  and  the  child  regains  its 
usual  health. 


PART  VIII 

RHEUMATIC  AND  DYSTROPHIC  DISEASES 

CHAPTEE  I 
RHEUMATISM 

Whatever  place  we  assign  to  rheumatism  in  our  list  of  diseases,  it  must  be  admitted 
that  its  limits  are  somewhat  ill-determined  and  its  nature  ill-defined.  And  yet  rheu- 
matism lends  itself  to  methodical  description,  and  its  importance  in  pathology  is  con- 
siderable. 

As  I  am  compelled  to  divide  the  subject  for  purposes  of  description,  I  shall  describe : 
1.  Acute  articular  rheumatism,  a  disease  most  probably  due  to  microbes  ;  it  is  the 
most  typical  manifestation  of  the  rheumatic  affection,  and  is  often  accompanied  by 
changes  in  the  viscera. 

2. .  Chronic  rheumatism,  which  comprises  several  varieties,  according  as  there  is 
a  tendency  to  become  general  (progressive  polyarticular  rheumatism),  or  to  be  hmited 
to  a  small  number  of  joints  (partial  chronic  rheumatism). 

3.  Visceral  and  muscular  rheumatism. 

4.  Pseu  do -rheumatism,  or  infective  rheumatism,  which  occurs  in  blennorrhagia, 
scarlatina,  puerperal  conditions,  erysipelas,  mumps,  pneumonia,  etc. 

I  hasten  to  say,  however,  that  this  classification  is  in  part  artificial,  and  that,  except 
for  infective  rheumatism  or  pseudo-rheumatism,  of  which  the  origin  and  nature  are 
known  to  us,  the  varieties  of  acute  and  chronic  rheumatism  which  appear  sometimes 
distinct,  when  present  as  extreme  typos,  have  such  close  relationship  that  it  is  necessary 
to  place  them  in  the  same  family. 

I.  ACUTE  ARTICULAE  RHEUMATISM. 

Tlie  acute  manifestations  of  rheumatism  show  a  special  liking  for  the 
joints,  and  although  they  often  attack  a  number  of  organs  at  the  same  time, 
it  is  usual  to  describe  all  these  manifestations  under  the  name  of  acute 
articular  rheumatism.  As  .  a  rule,  the  morbid  series  commences  in  the 
joints,  and  only  afiects  the  organs  secondarily ;  but  there  are  exceptions, 
and  we  shall  see  in  the  course  of  this  article  that  the  so-called  articular 
rheumatism  may  afiect  the  pleura,  the  lung,  and  the  heart  before  attacking 
the  joints. 

etiology. — Although  acute  rheumatism  occurs  in  all  countries  and  at  all 
seasons,  it  shows  a  marked  predilection  for  temperate  climates  and  for  the 
summer  season  (Besnier).     Stoll  has  described  summer  epidemics  of  rheu- 

1916 


niKUMATIC  AND  DYSTROPirrc  DISEASES  1917 

matism.  Kelsch.  whilo  studying  rlKniinatisin  in  tho  French  army,  saw 
rocnidescences  often  coincide  witli  the  end  of  winter  and  the  conimoncernent 
of  spring.  The  most  common  occasional  cause  is  cold,  and  especially  damp 
cold.  Sometimes  the  chill  acts  violently  upon  the  perspiring  body,  and 
rhenmatism  appears  at  once  ;  at  other  times  the  economy  becomes  gradually 
impregnated,  as  may  happen  to  persons  who  live  in  damp  places,  in  a  freshly 
plastered  room,  or  in  a  new  house.  Fatigue  and  excesses  are  predisposing 
causes,  and  a  sprain  or  a  dislocation  has  several  times  been  tlie  cause  of  an 
attack  of  rheumatism  (Verneuil,  Potain). 

Must  we  admit  an  hereditary  or  an  acquired  predisposition  in  patients 
who  suffer  from  rheumatism;  ?  The  answer  to  this  question  would  pre- 
suppose the  pathogenesis  of  the  rheumatic  diseases.  The  pathological 
affinity  which  rheumatism  bears  to  gout,  gravel,  obesity,  and  diabetes  make 
it  fairly  clear  that  nutritive  troubles  of  similar  kind  play  a  great  part  in 
the  evolution  of  these  morbid  conditions  ;  but  while  admitting  that  rheu- 
matism results  from  the  uric  acid  diathesis,  it  does  not  help  the  question 
much,  and  the  intimate  nature  of  the  disease  is  still  unknown. 

Acute  rheumatism  has,  however,  all  the  attributes  of  an  infective 
microbic  disease.  Its  local  manifestations  in  the  endocardium  and  in  the 
serous  membranes  bring  it  into  close  relation  with  the  so-called  infective 
rheumatism,  in  which  the  microbic  or  toxi-infectious  origin  is  known  ;  but 
although  some  authors  have  classed  rheimiatism  with  the  microbic  diseases, 
its  pathogenic  agent  has  yet  to  be  found,  and  the  microbes  so  far  discovered, 
though  including  staphylococci  and  streptococci,  the  anaerobic  bacillus  ol 
Achalme  and  Thiroloix,  or  the  diplococcus  of  Triboulet  and  Coyon,  are  not 
specific.  They  are  only  factors  in  the  secondary  complications.  The  first 
attack  of  rheumatism  appears  between  fifteen  and  thirty  years  of  age. 
Relapses  are  frequent. 

Symptoms. — Acute  articular  rheumatism,  or  rheumatic  fever  of  English 
authors,  rarely  has  a  sudden  and  violent  invasion.  The  patient  often 
experiences  wandering  pains,  with  or  without  rigors.  Fever  appears,  and 
the  articular  troubles  declare  themselves.  In  about  a  third  of  the  cases  at 
least  rh'inmatism  begins  with  a  sore  throat,  accompanied  by  fever,  and 
perhaps  by  albuminuria.  The  angina,  which  is  more  or  less  painful,  and 
accompanied  by  redness  of  the  throat  and  swelling  of  the  tonsils,  may 
precede  the  appearance  of  pains  in  the  joints  by  several  days.  The  instep 
and  the  knees  are  usuaDy  first  attacked  ;  the  elbows,  shoulders,  and  wrists 
are  involved  later.  When  the  small  joints — i.e.,  those  of  the  hand,,  of  the 
feet,  or  of  the  spine — are  invaded,  the  attack  of  rheumatism  is  generally 
long  and  severe. 

Pain  is  the  chief  symptom,  even  from  the  onset.  It  soon  becomes 
severe.     It  disappears  with  the  effusion,  passes  from  one  joint  to  another, 


1918  TEXT-BOOK  OF  MEDICINE 

reappears  in  a  joint  thought  to  be  well,  and  sometimes  becomes  general  in 
the  smaU  joints  of  the  spine,  of  the  ribs,  and  of  the  jaw,  inflicting  acute 
sufEering  upon  the  patient.  The  pain  is  brought  on  by  the  slightest  move- 
ment of  the  diseased  joint,  even  by  the  pressure  of  the  bed-clothes  or  by 
shaking  of  the  bed. 

The  joints  affected  by  rheumatism  are  swollen.  In  the  large  joints — as 
in  the  knee,  for  example — ^the  superficial  tissues  are  the  seat  of  fluxion 
hlanche  (Trousseau),  while  in  the  wrists  and  instep  the  skin  is  rosy,  and 
shows  a  tracing  of  reddish  tracks,  which  indicate  the  course  of  the  tendon- 
sheaths  invaded  by  the  rheumatic  effusion.  As  regards  the  hands,  the 
dorsal  surface  is  oedematous  and  romided,  the  fingers  are  spread  out,  im- 
mobile, and  swollen  like  a  spindle.  The  local  temperature  is  higher  by 
two  or  three  tenths  of  a  degree  in  the  diseased  joint.  The  effusion  is  very 
abundant  in  some  joints,  and  in  the  knee  the  amount  may  exceed  2  or  3 
ounces.  When  it  reaches  these  large  proportions  it  causes  acute  pain,  which 
disappears  on  aspiration  of  the  fluid.* 

If  articular  rheumatism  is  closely  studied,  we  see  in  most  cases  that  the 
bursse,  the  tendon-sheaths,  and  the  tendons  of  the  muscles  are  invaded  in 
the  same  manner  as  the  joint  itself.  Accordingly,  in  the  knee  we  find 
painful  foci  around  the  joint,  which  are  rendered  evident  by  the  slightest 
pressure  on  the  inner  side  of  the  articulation.  The  tendons  of  the  sartorius, 
gracilis,  and  semitendinosus  unite  on  the  crest  of  the  tibia,  after  having 
passed  over  the  internal  tuberosity  of  this  bone.  At  this  point  two  tendon- 
sheaths  are  present — ^the  one  beneath  the  sartorius,  and  the  other  below 
the  tendon  of  the  ham-strings.  We  also  find  on  the  inner  surface  of  the 
knee  a  painful  point  on  the  head  of  the  fibula,  where  the  tendon  of  the 
biceps  muscle  is  inserted  with  an  intervening  bursa.  Painful  points  are 
very  common  in  the  popliteal  space,  and  we  may  also  find  a  painful  centre 
at  the  insertion  of  the  tendon  of  the  triceps  into  the  pateUa,  where  there 
are  two  serous  bursas — ^the  one  between  the  superficial  and  the  deep  fibres 
of  the  tendon,  and  the  other  between  the  tendon  and  the  capsular 
membrane.  These  painful  points  form  a  kind  of  crown  around  the 
knee-joint,  so  as  to  give  rise  to  the  belief  that  the  articulation  itself  is 
diseased,  when  it  is  free  or  only  slightly  invaded.  Similar  remarks  apply 
to  the  instep.  The  tendons  of  the  lateral  peronei  pass  behind  the  malleolus, 
and  the  common  synovial  membrane  bifurcates  in  order  to  accompany 
them.  We  may  sometimes  foUow  the  painful  track  as  far  as  the  base  of 
the  fifth  metatarsal  bone,  into  which  the  peroneus  brevis  is  inserted, 
and  to  the  base  of  the  first  metatarsal,  where  the  peroneus  longus  is 
inserted. 

In  some  cases  the  periarticular  pain  affects  the  insertion  of  a  muscle, 

*  Dieulafoy,  "  Traite  de  I' Aspiration,"  p.  354. 


RHEUMATIC  A:^D  DVSTROrTTTr'  PTF^KAF^KS  1919 

although  noithor  a  tendon  nor  a  l)ursa  is  prosont — for  instance,  at  the 
insertion  of  tht*  deltoid  into  the  hunuTiis.  Further,  th*;  muscles  themselves 
are  often  painful  above  and  below  the  diseased  joint. 

In  short,  articular  rheumatism  not  only  attacks  the  synovial  membrane 
and  the  intra-articular  ligaments,  but  also  the  tendons,  bursae,  tendon- 
sheaths,  muscular  insertions,  and  cellular  tissue. 

The  face  of  a  patient  suffering  from  rheumatism  is  of  a  dull  white, 
which  is  explained  by  the  rapid  and  great  diminution  of  the  red  corpuscles. 
This  rhemnatic  ana?mia  is  also  revealed  by  a  cardiac  murmur.  The  sweat 
is,  as  a  rule,  very  profuse,  and  characterized  by  a  sour  smell,  due  to  the  high 
acidity.  (Edema  of  the  hands  and  feet  is  common.  It  may  be  general. 
The  fever  varies  in  intensity.  The  pulse  is  full  and  hard,  and  the  rate  is 
from  90  to  100.  In  severe  cases  the  evening  temperature  may  rise  to 
104°  F.,  and  the  morning  remission  is  slight.  In  less  severe  cases  the 
evening  temperature  is  not  quite  so  high,  and  the  morning  remissions  are 
more  marked  ;  but  the  cycle  has  no  regular  course.  The  urine  is  scanty,  of 
a  dark  colour,  sometimes  albuminous,  and  rich  in  urea  and  urates.  The 
digestive  fimctions  are  but  shghtly  disturbed.  The  tongue  remains  moist, 
and  the  appetite  is  often  good.  One  patient  may  suffer  from  constipation, 
and  another  from  serous  diarrhoea,  resembling  a  "  true  intestinal  perspira- 
tion "  (Peter).  The  cerebral  functions  are  normal,  and  the  patient  does 
not  suffer  from  headache  or  from  delirium,  but  retains  the  full  control  of 
his  senses.  Epistaxis  is  frequent,  either  at  the  onset  or  during  the  course 
of  the  attack. 

The  duration  of  the  attack  depends  on  the  severity  of  the  disease,  and 
varies  from  two  to  several  weeks.  Each  joint  affected  remains  so  for  only 
a  few  days,  but  it  is  by  no  means  rare  for  the  same  joint  to  be  alternately 
deserted  and  revisited  by  the  rheumatic  inflammation.  S}Tnmetrical  joints 
are  usually  invaded  simultaneously  or  in  succession.  When  the  fever  has 
fallen  and  the  pain  has  disappeared,  the  patient  still  experiences  marked 
discomfort  in  mo%'ing  his  joints,  which  depends  partly  upon  the  muscular 
weakness  caused  by  the  disease. 

Visceral  Localizations  of  Acute  Rheumatism. — In  addition  to  cases  in 
which  the  attack  of  rheumatism  remains  limited  to  the  joints,  we  see  others 
in  which  the  disease  also  affects  the  viscera,  and  gives  rise  to  the  most 
diverse  clinical  forms.  As  a  rule,  the  joints  are  first  attacked,  and  some 
days  later  endocarditis,  pericarditis,  and  pleurisy  appear.  Rheumatism  of 
the  nervous  centres,  of  the  digestive  and  urinary  tracts,  are  also  seen. 
Some  of  these  forms  are  common,  others  are  rare. 

In  some  cases,  however,  the  usual  course  of  the  disease  is  reversed,  and 
the  patient  first  suffers  from  sore  throat,  pleurisy,  or  from  endocarditis,  and 
the  joint  troubles  do  not  appear  for  some  days. 


1920  TEXT-BOOK  OF  MEDICINE 

Rheumatism  of  the  Heart. — The  heart  is  the  organ  most  afiected  by 
rheumatism,  and  it  is  remarkable  that  rheumatism,  usually  so  transient  in 
its  nature,  tends  to  fix  upon  the  heart  with  an  obstinacy  which  causes  most 
of  the  diseases  of  this  organ.  The  history  of  cardiac  rheumatism  was  only 
in  its  infancy  prior  to  Bouillaud,  In  1832  he  described  rheumatic  endo- 
carditis, and  showed  that  it  passes  into  the  chronic  state,  and  becomes  the 
origin  of  organic  lesions  in  the  heart.  He  also  stated  the  laws  of  coincidence, 
according  to  which  changes  in  the  endocardium  or  in  the  pericardium 
are  almost  constant  when  the  articular  rheumatism  is  severe  and  general, 
and  are  exceptional  when  the  disease  is  partial  and  slight.  According  to 
difEerent  statistics,  endopericarditis  has  been  stated  to  be  present  in  the 
proportion  of  30,  40,  or  50  per  cent.  Amid  these  different  opinions,  that  of 
BouUlaud  remains  true,  and  when  articular  rheumatism  is  severe  and 
general,  there  is  the  greatest  likelihood  of  endopericarditis  supervening. 
In  children  cardiac  lesions  are  to  be  feared,  even  in  slight  attacks. 

Endocarditis  is  more  frequent  than  pericarditis.  The  inflammation  of 
the  heart  usually  supervenes  about  the  second  week  of  the  articular  disease, 
though  it  is  sometimes  later,  and  in  exceptional  cases  it  may  precede  the 
joint  troubles. 

There  is  no  need  for  me  to  describe  endocarditis,  for  I  have  treated 
the  question  elsewhere.  I  only  mention  the  fact  that  rheumatic  endo- 
carditis usually  spares  the  aortic  valves,  and  especially  affects  the  mitral 
valve.  Its  onset  is  insidious,  and  it  is  revealed  by  a  systolic  murmur,  most 
marked  at  the  apex.  We  must,  however,  be  on  our  guard  against  mis- 
taking the  ansemic  murmurs  so  common  in  the  course  of  rheumatism  for 
the  murmur  of  endocarditis.  Endocarditis  may  recover  after  a  period 
which  does  not  exceed  two  weeks,  but  the  disappearance  of  the  murmur 
is  not  always  a  sure  sign  of  recovery.  In  such  a  case,  where  recovery  is 
apparent,  the  patient  is  liable  to  chronic  endocarditis,  which  is  slow  and 
latent  in  its  course,  and  the  mitral  lesions  may  not  reveal  themselves  for 
years. 

In  rare  cases  the  endocarditis  may  be  infective,  and  may  then  give  rise 
to  immediate  danger. 

Rheumatic  pericarditis  is  rarely  accompanied  by  effusion.  It  is  revealed 
by  friction  sounds,  which  often  have  a  gaUop  rhythm.  Severe  pericarditis 
is  often  associated  with  left  pleurisy,  which  is  followed  by  right  pleurisy, 
with  or  without  effusion.  Slight  pericarditis  is  not  serious,  but  severe  peri- 
carditis, accompanied  by  effusion  or  by  pleurisy,  is  formidable. 

Rheumatic  phlebitis  is  well  known.  Ti>ousseau  has  quoted  some  remark- 
able examples.  It  appears  in  mild  as  well  as  in  severe  rheumatism.  It 
may  be  localized  to  one  vein  or  may  affect  several,  and  may  simulate 
phlegmasia  alba  dolens,  with  its  train  of  symptom^i.     More  frequently,  says 


IMIKUMATIC  AND  DYSTROPHrC  DISEASES  1921 

Vaquez,  rheumatism  "  choos«'s  a  superficial  venous  segment  without 
obliterating  it,  and  strikes  the  inside  of  it."  Periphlebitis  is  more  common 
than  endophlebitis. 

Rheumatism  of  the  Respiratory  Organs.  Pleurisy  usually  ajipeare 
about  the  second  week  of  the  articular  disease.  It  may  precede  the  joint 
troubles.  Rheumatic  pleurisy  is  at  times  insidious,  and  at  other  times 
severe  and  painful.  It  may  be  single  or  double,  and  is  often  associated  with 
endocarditis  or  with  pericarditis.  Effusion  is  the  rule.  The  fluid  increases 
rapidly,  and  ofton  disappears  just  as  suddenly. 

Congestion  of  the  lung  of  rheumatic  origin  may  occur  in  the  condition 
of  simple  hyperaemia  or  of  inflammatory  hyperaemia.  The  latter  form  is 
often  described  under  the  name  of  rheumatic  pueumonia,  although  it  is 
not  a  pneumonia  in  the  true  sense  of  the  word.  As  a  matter  of  fact,  the 
pneumonia  has  but  little  tendency  to  pass  into  hepatization,  and  the  con- 
gestive element  always  gains  the  day  over  the  inflammatory  one.  Con- 
gestion of  the  lung  is  more  or  less  severe  and  more  or  less  general.  Although 
it  is  usually  transient  and  benign,  and  is  often  associated  with  pleurodynia 
or  with  pleurisy,  it  may  develop  into  suffocative  catarrh,  invading  both 
lungs,  and  proving  fatal  in  a  few  days  or  even  in  a  few  hours. 

Rheumatic  pneumonia  may  appear  and  disappear  several  titnes  in  the 
course  of  the  articular  disease.  It  sometimes  alternates  with  pains  in  the 
joints. 

Cerebral  Rheumatism. — Articular  rheumatism,  whatever  may  be  the 
severity  of  the  pain  and  of  the  fever,  does  not  as  a  rule  cause  mental  troubles. 
When  cerebral  troubles  appear  in  a  rheumatic  patient,  we  must  look  out  for 
some  complication. 

Cerebral  rheumatism  assumes  many  forms.  In  some  rare  cases  (five 
times  out  of  seventy-nine  cases  in  Ball's  statistics)  the  cerebral  troubles  are 
fulminant,  and  supervene  without  prodromata.  This  variety  is  known  as 
apoplectic  rheumatism,  and  I  quote  here  an  example  from  Trousseau  : 

A  strong  man  who  had  been  a  heavy  drinker  was  attacked  by  cerebral  rheumatism 
on  the  eighteenth  day  of  the  joint  disease.  He  complained  suddenly  of  not  being  able 
to  see  clearly,  shouted  and  cried  for  help,  threw  himself  from  his  bed,  struggled  with 
two  attendants,  was  put  back  to  bed,  grew  weak  and  died.  The  whole  affair  lasted 
less  than  a  quarter  of  an  hour. 

Cerebral  rheumatism  is  more  often  ushered  in  by  prodromata — head- 
ache, haDucinations,  and  incoherence  of  ideas.  The  prodromata  may  last 
for  a  few  hours  or  for  a  few  days,  and  the  cerebral  troubles  then  appear. 
The  patient  is  no  longer  conscious  of  articular  pains,  which  in  some  cases 
absolutely  disappear.  The  temperature  may  exceed  106°  F.  The  delirimn, 
which  is  more  or  less  violent,  resembles  that  of  confluent  smallpox  or  of 
severe  t^'phoid  fever.     It  lasts  two  or  three  days.     It  is  sometimes  inter- 


1922  TEXT-BOOK  OF  MEDICINE 

rupted  by  remissions,  and  may  be  accompanied  by  convulsions,  which 
indicate  danger.     In  unfavourable  cases  it  ends  in  coma. 

The  delirium,  however,  may  follow  a  chronic  course,  and  last  several 
weeks.  The  patient  becomes  taciturn,  melancholy,  and  Ijrpemaniacal,  but 
finally  recovers,  as  a  rule. 

The  way  for  cerebral  troubles  is  sometimes  paved  by  the  previous  con- 
dition of  the  patient.  Brain-fag,  grief,  and  depressing  emotions,  alcoholism, 
or  hereditary  predisposition,  appear  to  be  favourable  to  the  outburst  of 
cerebral  rheumatism.  In  afJecting  the  brain,  rheumatism  brings  about  its 
usual  disorders — sometimes  simple  congestion,  which  leaves  no  trace  at  the 
autopsy,  and  at  other  times  persistent  hypersemia,  revealed  by  vascular 
injection  of  the  meninges  and  of  the  brain  substance,  with  effusion  in  the 
ventricles  and  in  the  subarachnoidal  space. 

We  must  not  confound  with  cerebral  rheumatism  the  cerebral  complica- 
tions (embolism,  hemiplegia,  aphasia)  which  are  caused  by  acute  or  chronic 
rheumatic  endocarditis. 

Rheumatism  may  also  affect  the  spinal  cord  and  its  coverings.  It  is 
revealed  by  lumbar  pains,  spreading  to  the  lower  limbs,  with  symptoms  of 
paraplegia  and  of  contracture  (opisthotonos).  The  sphincters  are  intact, 
and  we  find  neither  anaesthesia  nor  trophic  troubles.  Spinal  rheumatism 
presents  this  peculiarity — ^that  it  may  precede  the  articular  manifestations 
by  several  days.  It  is  evident  that  the  pathogenic  diagnosis  may  be  diflficult 
in  the  absence  of  joint  pains.     Spinal  rheumatism  ends  in  recovery. 

Chorea,  disseminated  sclerosis,  and  neuritis  are  also  to  be  numbered 
among  the  nervous  manifestations  of  rheumatism. 

Rheumatism  of  the  Digestive  Tract. — Tonsillitis  is  a  common  mani- 
festation of  rheumatism,  and  often  precedes  the  joint  troubles  (Lasegue). 
Rheumatic  affections  of  the  stomach  and  of  the  intestine  are  very  rare. 
They  occur  in  the  form  of  gastric  catarrh,  colic,  serous  diarrhoea,  or  dysen- 
teriform  stools  (Stoll).  Congestion  of  the  liver,  with  or  without  jaundice, 
is  also  very  rare. 

Rheumatism  of  the  Genito-Urinary  Tract.— Albuminuria  in  the  course 
of  acute  rheumatism  indicates  slight  nephritis.  In  some  cases,  however, 
severe  nephritis  has  been  noticed,  but  this  is  exceptional.  Speaking 
generally,  we  may  say  that  rheumatism,  which,  like  the  infectious  diseases, 
is  so  prone  to  attack  other  viscera,  as  a  rule  spares  the  kidneys.  Rheumatic 
hsemoglobinuria  has  been  noted  (Hayem  and  Robin),  and  after  the  following 
case,  which  I  had  in  the  Necker  Hospital,  I  am  tempted  to  think  that  haema- 
turia  may  occur  in  rheumatism  : 

A  man  came  under  my  care  with  acute  articular  rheumatism  and  hsematuria.  They 
had  both  appeared  at  the  same  time,  and  were  of  a  fortnight's  duration.  The  rheu- 
matism was  acute,  general,  and  accompanied  by  fever.     The  hsematuria  was  rather 


RITEUMATIC  AND  DYSTKOl'lI  in  HISEASES  1923 

striking,  for  the  urino  was  highly  coloured,  and  throw  down  a  fairly  copious  deposit 
of  bluud.  Tho  putiont  tuld  us  Hint  during  liis  first  Httnck  uf  articular  rhouniutiMUi, 
ton  yoara  before,  lio  also  sufforod  fioiu  lucmaturiii,  which  histod  for  sovorul  weeks — 
in  fact,  as  lon^  as  tho  rheumatism.  Some  years  later  he  sudered  from  a  iMjvore  attack 
of  sul)acute  rlKnimatism,  which  brought  him  under  Rigal's  care,  and  for  nine  months 
tho  hivmaturia  {H'rsisted  and  disappeared  witli  tho  rheumatic  pains.  The  patient  had 
hiematuria  in  the  true  sense  of  tiie  word,  and  not  nephritis  witli  hamaluria  ;  for  as  long 
as  the  attack  of  rheumatism  and  tlie  haMuaturia  lasted,  there  was  no  symptom  of 
nephritis,  and  as  soon  as  tho  hannaturia  came  to  an  end,  wo  could  find  no  traces  of  in- 
flammation of  tho  kidney  or  of  Brightism.  Tho  kidney  bled  during  the  attack  of  rheu- 
matism, but  showed  no  after-effects. 

liheiimatism  may  also  afEect  the  bladder  (tenesmus,  dysuria)  and  the 
testis. 

Cutaneous  Manifestations  of  Rheumatism.— Er}i;hema,  puq)ura,  and 
urticaria  are  the  commonest  dermatoses  in  acute  articular  rheumatism,  but 
they  are  especially  prevalent  in  pseudo -rheumatism. 

The  erythema  may  be  papular,  nodular,  or  polymorphous.  It  some- 
times precedes  the  joint  troubles.  The  urticaria  exists  alone,  or  may 
coincide  with  erythema.  The  purpura  is  simple,  and  does  not  fall  under 
the  category  of  haemorrhagic  and  cachectic  purpura.  Its  seats  of  election 
are  the  forearm,  the  legs,  and  the  inner  surface  of  the  thighs.  The  purpuric 
eruption  is  often  called  peliosis  rheumatica. 

In  the  cutaneous  cellular  tissue  the  rheumatic  congestion  reveals  itself 
by  more  or  less  local  oedema.  It  forms  patches  or  nodules  (Jaccoud), 
which  disappear  as  rapidly  as  they  appear.  Sometimes,  however,  these 
rheumatic  nodules  are  of  long  duration.  In  some  cases  of  rheumatism  the 
oedema  may  invade  the  eyelids,  the  cheek,  the  scrotum  (Ferrand),  and  a 
portion  of  the  limbs. 

In  young  children  rheumatism  presents  some  peculiarities  (Roger).  The 
general  symptoms  are  less  severe.  The  fever  is  slight,  the  sweats  are  not 
so  profuse,  cerebral  troubles  are  extremely  rare,  and  but  few  joints  are 
mvaded  ;  and  yet,  in  spite  of  this  apparent  benignity,  the  heart  is  often 
affected.  Cardiac  troubles  may  appear,  even  though  only  one  joint  has 
been  affected. 

Course — Prognosis. — In  the  slight  forms  acute  articular  rheumatism 
lasts  from  two  to  three  weeks.  In  certain  very  mild  cases  the  disease 
merely  touches  a  few  joints,  and  ends  in  a  week.  It  may  be  prolonged  for 
more  than  five  weeks  in  the  severe  forms,  which  are  characterized  by  high 
fever  and  invasion  of  the  smaD  joints.  The  disease  often  shows  successive 
attacks.  After  a  momentary  improvement,  the  fever  increases  and  other 
joints  are  invaded.  Defervescence  is  slow,  and  during  the  first  period  of 
convalescence  fever  sometimes  reappears  at  night.  After  the  disappear- 
ance of  the  pain  and  of  the  fever  the  patient  remains  weak  and  anaemic. 

In  some  cases  we  find  not  only  muscular  weakness,  but  acute  amyo- 


1924  TEXT-BOOK  OF  MEDICmE 

trophy  (Gubler),  which,  may  last  for  two  or  three  months.  Creaking  and 
grating  in  the  joints  are  fairly  frequent  after  an  attack  of  acute  rheumatism. 
Relapses  are  common,  and  may  supervene  in  spite  of  every  hygienic  pre- 
caution. 

The  convalescent  patient  is  not  absolutely  free  from  the  risk  of  visceral 
complications,  and  chorea  may  appear  in  young  subjects  at  a  more  or  less 
distant  date  (See,  Roger). 

The  visceral  troubles  considerably  increase  the  gravity  of  rheumatism. 
In  some  cases  they  lead  to  immediate  danger  (ulcerative  endocarditis, 
cerebral  embolism,  cerebral  rheumatism,  endopericardo-pleuritis,  conges- 
tion of  the  lungs),  but  as  a  rule  the  danger  is  more  remote,  and  the  cardiac 
troubles  only  appear  after  some  months  of  apparent  immunity.  The  lesions 
of  the  heart,  at  more  or  less  remote  intervals,  form  a  most  formidable 
danger  in  an  attack  of  rheumatism. 

In  some  cases  the  rheumatic  affection  does  not  follow  the  classical  forms 
which  I  have  just  described.  The  acuteness  of  the  fever,  the  rise  of  the 
temperature,  and  the  simultaneous  appearance  of  endopericarditis,  of 
pleurisy,  or  of  congestion  of  the  lungs,  may  give  rise  to  a  grave  condition, 
but  this  is  not  an  anomaly.  As  a  matter  of  fact,  an  attack  of  rheumatism 
in  which  the  general  symptoms  rapidly  become  ataxic  and  adynamic,  as 
in  severe  cases  of  typhoid  fever,  is  an  anomaly.  The  attack,  which  scarcely 
affects  the  joints,  but  acts  with  redoubled  violence  upon  the  viscera,  or 
which  ends  in  suppuration  of  the  joints,  is  an  anomaly.  These  various 
anomalies,  which  are  generally  the  indication  of  extreme  gravity,  must  be 
included  under  infective  pseudo-rheumatism,  whether  the  infection  be 
absent  or  whether  the  rheumatic  patient  have  the  germs  of  this  auto- 
infection  previously  present  in  his  economy. 

Pathological  Anatomy. — The  changes  in  the  blood  are  of  great  im- 
portance. The  fibrin  may  be  as  high  as  10  parts  per  1,000  (Andral  and 
Gravarret),  as  in  true  inflammation,  and  therefore  the  blood-clot  is  much 
retracted  (Bouillaud).  The  solid  elements  of  the  serum  may  fall  to  60  per 
1,000  (Quinquaud).  The  haemoglobin,  and  consequently  the  oxidizing 
power  of  the  blood,  are  much  diminished.  The  number  of  red  corpuscles 
may  fall  to  3,000,000  per  cubic  millimetre. 

The  following  lesions  are  found  in  rheumatic  arthritis  :  Both  the  intra- 
and  extra-articular  parts  of  the  joints  are  more  or  less  afEected.  The  effusion 
is  clear,  and  holds  in  suspension  flakes  of  mucus  or  of  fibrin.  Very  few 
leucocytes  are  present.  The  synovial  membrane  is  red,  thickened,  and 
sometimes  velvety.  The  synovial  fringes  are  injected,  and  their  cells  show 
abundant  proliferation  (Cornil  and  Ranvier).  The  cartilages  show  signs 
of  nutritive  irritation,  and  proliferation  of  the  cartilage  cells  is  found. 
The  periosteum  and  the  bones  may,  according  to  some  authors,  present 


IIHEUMATIC  AND  DYSTROrHlC  DISEASES  1925 

changes  which  arc  at  present  ill  understood.  The  lesions  in  the  various 
or<;aiis  affected  by  rheumatism  do  not  require  deHcri[)tion  in  this  se(;tion. 

Treatment.  —In  a  person  suffering  from  severe  acute  articular  rheu- 
niutisni  the  folh)whig  treatment  should  be  employed  :  Salicylate  of  soda  is 
of  considerable  service  (See),  and  the  patient  takes  from  60  to  120  grains 
in  the  twenty-four  hours,  the  dose  being  continued  for  several  days,  and 
progressively  diminished  as  soon  as  improvement  becomes  manifest. 
Another  method  which  has  given  good  results  consists  in  administering 
antipvrin  in  daily  doses  of  30  grains,  together  with  the  salicylate. 

Aspirin  (ucetyl-salicylic  acid)  has  been  employed  with  some  success  in 
acute  articular  rheumatism.  It  is  a  useful  substitute  for  the  salicylate,  as  it 
duos  not  cause  gastric  disturbance,  buzzing  in  the  ears,  etc.  (Growitz,  Ilenon). 

Methyl  salicylate  may  be  of  benefit.  It  is  used  in  the  form  of  an  oint- 
ment, composed  of  10  parts  of  vaseline  with  1  of  the  salicylate. 

The  patient  should  drink  lemonade,  milk,  and  Vichy  water.  The 
articular  pains  are  relieved  by  subcutaneous  injections  of  pure  water  in  the 
neighbourhood  of  the  diseased  joints,  and  very  small  injections  of  morphia 
may  also  be  given  morning  and  evening. 

The  joints  may  be  painted  with  a  liniment  of  the  following  composition  : 

Oil  of  camomile         . .         . .         . .         . .         . .   21  parts. 

Chloroform  . .  . .  . .  . .  . .     8      „ 

Laudanum  . .  . .  . .  . .  . .     2      „ 

When  hyperpyrexia  appears,  with  threatening  cerebral  troubles,  we  must 
employ  cold  baths  (Raynaud).  The  patient  is  placed  in  a  bath  at  a  tem- 
perature of  from  68°  to  72°  F.  for  ten  to  twenty  minutes,  unless  the  chills 
are  so  severe  as  to  necessitate  a  shorter  immersion.  As  a  residt  of  the  bath, 
the  cerebral  symptoms  diminish  in  severity,  and  the  temperature  falls. 
The  treatment  may  be  repeated  three,  four,  or  five  times  in  the  twenty-four 
hours,  and  for  several  days  follo"\\4ng  if  necessary.  This  method  has  cer- 
tainly saved  the  Ufe  of  patients  suffering  from  cerebral  rheumatism. 

II.  CHEONIC  EHEUMATISM. 

It  is  customary  to  describe  the  following  affections  under  the  heading  of 
chronic  rheumatism : 

1.  Simple  chronic  rheumatism. 

2.  Nodular  rheumatism. 

3.  Partial  chronic  rheumatism. 

4.  Fibrous  rheumatism. 

1.  Simple  Chronic  Rheumatism. 
This  variety  may  be  chronic  from  the  lirst,  or  may  follow  attacks  of 
acute  and  subacute  rheumatism,  so  that  the  description  of  chronic  rheuma- 
•li.  l:^:^ 


1926  TEXT-BOOK  OF  MEDICINE 

tism  in  part  concerns  that  of  the  subacute  disease.  We  do  not  see  here,  as 
in  the  acute  forms,  severe  pain  and  high  fever,  but  the  joints  are  painful 
on  pressure,  movement  is  difficult  or  painful,  and  often  accompanied  by 
intra-articular  creaking.  The  patient  also  complains  of  muscular  pain  and 
of  neuralgia,  which  alternate  or  coincide  with  the  joint  manifestations. 
The  painful  points  are  often  seated  in  the  palms  of  the  hands  or  in  the  soles 
of  the  feet  (fascia),  in  the  heel  (bursa),  and  in  the  tibial  and  peroneal  muscles 
(tendon-sheaths).  When  subacute  rheumatism  fixes  itself  upon  a  joint,  it 
is  not  rare  to  see  muscular  atrophy  ia  the  neighbouring  regions,  but  the 
atrophy  shows  no  invading  tendency,  and  yields  in  a  few  weeks  to  the 
iaduced  current. 

Chronic  rheumatism  sometimes  recovers  after  a  duration  of  several 
months.  In  some  cases  it  is  interrupted  by  subacute  attacks  with  fever ;  the 
remissions  are  incomplete,  the  movements  become  more  difficult,  the  muscles 
waste,  the  joints  show  deformity,  and  the  patient  at  length  becomes  helpless. 

The  sufierer  from  chronic  rheumatism  is  extremely  sensitive  to  atmo- 
spheric changes,  and  the  least  change  in  temperature  or  barometric  pressure 
brings  on  the  pain.  The  integrity  of  the  other  functions  is  not  incompatible 
with  chronic  rheumatism.  Cardiac  troubles  are,  however,  by  no  means 
rare,  even  though  the  patient  has  never  suffered  from  acute  rheumatism. 

In  every  variety  of  subacute  or  chronic  rheumatism,  we  may  employ 
with  advantage  applications  of  superheated  air.  ( Vide  Appendix  for  fuU 
details.) 

2.  Nodular  Rheumatism. 

Nodular  rheumatism  is  also  described  under  the  name  of  primary  chronic 
rheumatism,  polyarthritis  deformans  (Jaccoud),  multi-articular  osseous 
chronic  rheumatism  (Besnier).  The  term  "gouty  rheumatism"  (Fuller) 
should  be  abandoned,  for  the  disease  is  not  a  hybrid  between  rheumatism 
and  gout.  Some  authors  would  hold  it  to  be  independent  of  rheumatism, 
and  would  include  it  under  the  group  of  pseudo-rheumatism  pending  definite 
classification. 

Nodular  rheumatism  is  chiefly  seen  between  forty  and  fifty  years  of  age  ; 
it  is  more  frequent  in  women,  especially  at  the  menopause  period,  and  is  more 
common  in  the  poorer  classes.  The  slow  and  progressive  action  of  damp 
cold  favours  its  development. 

Description. — Nodular  rheumatism  is  chronic  from  the  first,  though  there 
are  exceptions,  especially  in  young  children,  who  may  suffer  from  an  acute 
form.  The  disease  presents  a  progressive  mode  of  invasion — ^that  is  to  say, 
when  once  it  has  appeared  it  shows  the  greatest  tendency  to  pursue  its 
invading  course.     It  usually  commences  in  the  small  joints  of  the  hands 


RHEUMATIC  AND  DYSTROPinC  DISEASES  1927 

and  feet,  and  then  proceeds  towarda  the  trunk,  affecting  the  lar^'er  joints  of 
the  limbs.*  It  is  often  symmetrical,  and  causes  considerable  deformities, 
which  are  due  to  a  process  to  be  described  later. 

The  disease  is  sometimes  preceded  by  fugitive  and  wandering  pains, 
which  follow  the  course  of  a  nerve  trunk  or  which  attack  the  muscles  and 
the  joints.  As  a  rule,  the  pain  invades  some  joints,  especially  those  of  the 
hands,  lasts  for  a  more  or  less  lengthy  period,  and  is  accompanied  by  transient 
swelling  of  the  joints.  Later,  fresh  attacks  supervene,  the  crises  of  pain 
become  longer,  the  remissions  arc  less  complete,  and  the  deformities  of  the 
joints,  at  first  transient,  become  marked  and  persistent. 

The  most  marked  deformities  are  seen  in  the  fingers  and  in  the  hand. 
The  disease  attacks  the  index  and  middle  fingers  ;  the  thumb  is  fairly  often 
spared,  in  opposition  to  the  course  of  events  in  the  foot,  where  the  big  toe  is 
frequently  invaded. 

Several  causes  contribute  to  the  marked  deformities  seen.  From  its 
onset  the  disease  causes  in  the  neighbourhood  of  the  invaded  joints  muscular 
contractures,  which  play  a  great  part  in  the  production  of  the  deformities. 
These  contractures,  at  first  transient  and  later  permanent,  are  usually  very 
painful.  Some  authors  suppose  they  are  allied  to  rheumatoid  arthritis, 
while  in  the  opinion  of  others  (Trousseau)  they  are  independent  of  the 
articiUar  lesions,  run  a  parallel  course  with,  and  may,  indeed,  be  antecedent 
to,  them.  In  any  case,  the  muscular  contractures  are  soon  followed  by 
persistent  contraction,  and  fix  the  phalanges  and  the  hand  in  faulty 
positions,  which  are  very  varied,  but  which  usually  take  the  form  of  flexion 
and  of  extension. 

In  the  type  known  as  flexion  the  phalanx  and  the  terminal  phalanx  are 
in  forced  flexion  and  the  second  phalanx  is  extended.  The  articular  surfaces 
stand  out  in  marked  relief  ;  in  some  cases  they  may  be  dislocated.  Accord- 
ingly the  fingers  represent  broken  lines,  the  metacarpo-phalangeal  articula- 
tion projecting  on  the  back  of  the  hand,  while  the  joint  between  the  first  and 
second  phalanges  projects  towards  the  palmar  surface  ;  the  hand  is  semi- 
flexed and  deflected  towards  the  ulnar  side.  In  the  type  known  as  extension 
the  second  phalanx  is  flexed,  while  the  phalanx  and  the  terminal  phalanx  are 
extended. 

Other  causes  play  a  part  in  these  deformities.  We  may  note  the  re- 
traction of  the  fibrous  tissue,  tendons,  and  aponeuroses,  and  in  many  cases, 

*   Statistics  of  forty-five  patients  in  whom  the  joints  were  primarily  invaded 
(Charcot,  "  Maladies  des  Vieillards  ") : 

Small  joints  of  the  feet  and  hands      . .  . .  . .  25  times. 

Big  toe       . .         . .         . .         . .         . .  . .  . .  4     „ 

Hands  and  feet  invaded  at  the  same  time  as  a  large 

joint       . .  . .  . .  7     „ 

Laige  joint  invaded  before  the  fingers  . .  . .  d     „ 

122 2 


1928  TEXT-BOOK   OF  MEDIOHSTE 

especially  when  nodular  rheumatism  has  run  a  slow  course,  the  swelling  of 
the  articular  ends  of  the  bones,  which  are  covered  with  osteophjrtes.  The 
bony  lesion  then  becomes  the  chief  cause  of  the  nodules. 

The  muscles  gradually  become  atrophied  (simple  atrophy),  and  their 
prominences  disappear,  as  in  progressive  muscular  atrophy  (Vidal).  In 
some  cases  the  skin  becomes  thin,  colourless,  and  indurated,  somewhat  as 
in  sclerodermia.  The  functional  troubles  increase  with  the  severity  of  the 
lesions,  and  extreme  diflB.culty  of  movement,  or  even  complete  impotence, 
follows  the  early  stiffness.  The  other  joints  of  the  upper  limb  are  progres- 
sively invaded  in  nodular  rheumatism  :  the  wrist  is  flexed,  the  forearm  is 
pronated,  the  elbow  is  more  or  less  bent,  the  shoulder  is  rigid,  and  the  upper 
limb  is,  as  it  were,  fixed  to  the  thorax. 

The  lower  limbs  are  sometimes  free.  The  lesions  are  symmetrical,  the 
big  toe  is  displaced  outwards  so  as  to  lie  over  the  others  (Charcot),  the  foot 
is  displaced  into  the  position  of  valgus  or  of  equino-varus,  the  knee  is  much 
deformed,  and  the  lower  extremity  of  the  femur  is  in  front  of  the  head  of 
the  tibia.  As  a  rule  the  hip-joint  is  free,  and  this  fact  is  the  more  remarkable, 
as  this  joint  is  the  seat  of  election  of  the  partial  rheumatism,  known  under 
the  name  of  morbus  coxcb  senilis.  Nodular  rheumatism  may  also  affect 
the  spinal  and  temporo-maxillary  joints.  The  functional  troubles  depend 
upon  the  joint  invaded. 

Apart  from  a  few  exceptions,  the  disease  runs  a  very  slow  course.  From 
the  clinical  point  of  view  we  may  distinguish  an  essentially  chronic  form 
which  is  progressive  and  apyretio ;  it  is  the  nodular  rheumatism  of  elderly 
persons.  We  also  see  a  more  acute  form,  which  runs  a  more  rapid  course 
(puerperal  fever,  suckling)  ;  it  has  not  the  same  invading  tendency,  and  may 
end  in  recovery.  Numerous  intermediary  forms  exist  between  the  extreme 
cases. 

Nodular  rheumatism  does  not  immediately  threaten  life  if  complications 
do  not  supervene.  The  blood  does  not  contain  an  excess  of  uric  acid,  the 
nutrition  is  fairly  maintained,  and  bedsores  are  extremely  rare,  in  spite  of 
the  fact  that  the  patient  cannot  move.  We  may  note  among  the  possible 
complications  cardiac  lesions,  especially  pericarditis,  albuminuria,  interstitial 
nephritis,  and  pulmonary  phthisis. 

The  diagnosis  of  nodular  rheumatism  sometimes  presents  serious 
difficulties.  Congenital  atrophy  of  the  brain  and  atrophy  of  the  inter- 
osseous muscles  are  followed  by  deformities  of  the  fingers  and  of  the  hand, 
which  very  closely  resemble  those  of  nodular  rheumatism.  In  the  latter 
case  we  find  changes  in  the  joints  and  symmetry  of  the  lesions.  The  same 
statement  applies  to  the  deformities  of  paralysis  agitans,  and  it  must  be 
added  that  the  two  diseases  may  coexist.  In  some  cases  gout  determines 
muscular  contractures  and  deformities  like  those  of  nodular  rheumatism, 


T^TTKUMATIf  AXD  DYSTIIOI'IIK '   1)I.<^EASK.S  1029 

but  in  jToiity  piitioiits  they  arc  acconipuiiiiMl  hv  1o|ilii,  wliirli  aro  not  prosent 
in  rlicuniMl  ic  j>iit  icnts. 

Pathological  Anatomy.— Ail  tho  constituont  purl. 4  of  tlip  jdints  are 
affectod.  The  synovial  nionibrane  is  covered  with  vej^etations  and  villi  ; 
the  cellular  tissue  which  lines  it  is  indurated  and  thickened  ;  the  synovial 
fluid  is  scanty  or  absent  (arthritis  sicca).  The  intra-articular  ligaments 
have  in  part  disappeared,  and  the  joint  cavity  is  divided  up  }ty  bands  of 
fibrous  tissue.  The  cartilages  become  eroded  and  ulcerated,  and  finally 
disappear.  The  articular  ends  of  the  ])()ne  present  at  the  centre  the  lesions 
of  rarefying  osteitis,  and  eburnation  at  the  periphery.  Bony  processes,  or 
osteophytes,  often  form  a  kind  of  crown  around  the  ends  of  the  bone.  The 
small  bones  of  the  carpus  are  sometimes  ankylosed  together.  Subluxa- 
tions and  luxations  are  frequent.  The  ligaments,  the  tendons,  and  their 
sheaths,  are  invaded  by  the  inflammatory  process,  which  has  a  sclerous 
tendency. 

From  the  histological  point  of  view  the  changes  in  the  cartilage  are 
those  which  have  been  described  under  the  name  of  villous  condition,  the 
ground  substance  being  pushed  aside,  and  reduced  to  a  shreddy  condition  by 
the  falling  out  of  the  cartilaginous  capsules.  The  eburnated  layer  at  the 
extremities  of  the  bone  is  due  to  the  conversion  of  the  deep  embryonic 
cartilage  cells  into  bone  cells.  Enchondroses  develop  by  the  same 
process. 

The  treatment  of  nodular  rheumatism  may  be  thus  summed  up  :  Inter- 
nally— preparations  of  iodine  and  arsenic  ;  externally — painting  with  tincture 
of  iodine  over  the  diseased  joints.  Hydrothermal  cures,  sulphur,  or  arsenical 
baths  may  be  prescribed. 

3.  Partial  Chronic  Rheumatism. 

This  variety  of  chronic  rheumatism,  which  produces  deformity  of  the 
bones,  is  confined  to  a  few  joints,  and  has  but  little  tendency  to  become 
general.  Partial  chronic  rheumatism  and  the  swellings  upon  the  fingers 
known  as  Heberden's  nodules  belong  to  this  variety. 

(a)  Partial  chronic  rheumatism,  or  senile  arthritis,  is  almost  special  to 
old  age.  It  affects  the  large  joints  ;  the  knee  and  the  hip  are  most  often 
affected  {morbus  coxce  senilis).  The  lesions  are  practically  the  same  as 
those  described  in  the  preceding  section.  The  disease  is  almost  always 
chronic  from  the  first,  although  it  may  follow  acute  rheumatism  (Adams)  or 
acute  arthritis. 

The  joint  affection,  which  is  often  painless  at  its  onset,  is  sometimes 
the  seat  of  acute  attacks  of  pain  ;  they  are  not  provoked  by  palpation  and 
percussion.  The  diseased  joint  is  deformed,  and  the  deformity  is  due  to 
hydarthrosis,  to  foreign  bodies,  to  bony  growths,   which  are  sometimes 


1930  TEXT-BOOK  OF  MEDICINE 

large,  and  to  swelling  of  tlie  epiphyses.  Movement  is  difficult,  and  is  often 
accompanied  by  intra- articidar  creaking.  The  lesion  may  result  in  anky- 
losis, feom  fusion  of  the  articular  surfaces,  or  by  reason  of  the  peripheral 
osteophytes. 

(6)  Another  form  of  chronic  partial  rheumatism  is  described  under  the 
name  of  chronic  rheumatism  of  the  phalanges  or  Heberden's  nodes.  This 
variety  has  no  connection  with  gout.  It  is  characterized  by  small  nodes, 
situated  at  the  joints  of  the  terminal  phalanges  ;  these  nodes  are  due  to  an 
enlargement  of  the  bony  nodules  normally  present  in  this  region.  The 
extremity  of  the  finger  is  usually  displaced  to  the  right  or  to  the  left ;  the 
joint  is  rigid,  but  does  not  creak.  The  other  joints  of  the  hand  are  generally 
but  little  afiected.  The  disease  is  more  special  to  old  age  ;  it  is  hereditary, 
and  often  coexists  with  migraine,  asthma,  or  sciatica. 

4.  Fibrous  Chronic  Rheumatism. 

The  lesions  of  the  fibrous  tissues  (tendons,  ligaments,  bands,  and 
aponeuroses),  which  have  only  a  secondary  importance  in  the  forms  above- 
described,  may  become  of  the  highest  importance  in  some  cases,  and  cause 
the  disease  to  assume  the  character  of  a  fibrous  rheumatism.  The  faulty 
positions  and  the  deformities  of  the  fingers  and  of  the  hand  are  very  marked 
— as,  for  instance,  in  a  remarkable  case  published  by  Jaccoud.  The  ends  of 
the  bones  are  displaced  and  form  prominences,  but  we  find  here  neither 
sweUing  of  the  epiphyses  nor  osteophytes,  as  in  nodular  rheumatism. 
Intra-articular  creaking  is  absent. 

The  treatment  of  chronic  rheumatism,  and  especially  of  cases  with  a 
tendency  to  deformity,  consists  in  the  application  of  superheated  air  at 
130°,  180°,  or  200°  C,  and  the  results  obtained  are  sometimes  remarkable. 
In  the  obstinate  forms  of  gonorrhoeal  talalgia  this  treatment  produces  rapid 
improvement. 

Abarticular  Rheumatism. 

If  it  be  difficult  to  define  the  limits  of  rheumatism,  even  when  the  joints 
participate  m  the  morbid  changes,  this  delimitation  is  much  more  difficult 
when  we  are  dealing  with  abarticular  rheumatism— that  is  to  say,  rheuma- 
tism which  afiects  the  organs,  the  muscles,  or  the  nerves,  and  spares  the 

joints. 

While  studying  acute  articular  rheumatism  we  have  already  reviewed 
the  visceral  manifestations  which  may  occur  during  the  rheumatic  attack, 
and  we  have  seen  that  almost  all  the  organs  and  systems  may  be  attacked 
by  acute  rheumatism,  but  we  had  there  the  troubles  in  the  joiats  as  the 
criterion  of  the  rheumatic  nature  of  these  visceral  afiections. 

On  the  other  hand,  hi  the  condition  now  under  discussion   the   joint 


rnEUMATIC  AND  PYSTROPHTC  DISEASES  IQ.-'i 

localizations  are  wanting,  and  wc  tlion  ask  ourselves  what  must  bo  iiioludod 
in  the  categor}-  of  true  rheumatic  ailoctions  and  what  must  be  excluded. 

One  individual  suffers  from  facial  neuralgia  or  from  sciatica,  and  the 
trouble  reappears  as  the  result  of  chills  or  variations  in  the  weather.  Is 
this  a  sufficient  reason  for  admitting  the  rheumatic  origin  of  the  neuralgia  ? 
Another  suffers  from  muscular  pains,  such  as  torticollis,  pleurodynia,  or 
lumbago.  Is  it  right  to  say  that  he  is  suffering  from  muscular  rheumatism  ? 
Confusion  has  arisen  in  consequence  of  an  {etiological  idea  which  has  been 
imperfectly  interpreted.  As  chill  is  one  of  the  causes  of  neuralgia,  and  also 
one  of  the  most  active  causes  of  rheumatism,  we  have  readily  fallen  into  the 
habit  of  attributing  to  rheumatism  all  troubles  arising  from  the  common 
influence  of  chill. 

Do  we  not  daily  speak  of  rheimiatic  facial  paralysis  when  rheumatism 
often  has  nothing  to  do  with  the  pathogenesis  of  this  paralysis  ?  And  the 
same  statement  applies  to  certain  f onns  of  tetany. 

"What  part  has  not  been  assigned  to  the  rheumatic  diathesis  by  including 
imder  this  denomination  a  crowd  of  morbid  conditions  and  fimctional 
troubles  of  digestive,  uterine,  nervous  origin,  etc.,  while  their  nature  and 
origin  were  by  no  means  clearly  elucidated  ! 

In  truth,  I  do  not  say  that  these  troubles  may  not  be  of  a  rheumatic 
nature,  but  we  must  be  strict  in  the  appreciation  of  setiological  ideas  before 
admitting  that  an  abarticular  morbid  change  is  essentially  rheumatic  ;  we 
must  have  good  reasons  for  doing  so,  and  inquire  into  the  heredity,  the 
previous  medical  history,  and  the  constitution  of  the  patient. 

The  previous  medical  history  furnishes  valuable  information.  If  a 
patient,  at  some  period  of  his  life,  has  suffered  from  acute  or  from  chronic 
rheumatism,  we  have  some  reason  for  considering  the  abarticular  troubles 
which  he  may  show  later  as  being  related  to  the  rheumatism.  If  a  child 
born  of  rheumatic  parents  suffers  from  eczema,  sycosis,  psoriasis,  headache 
(Bazin),  muscular  pains,  nervous  spasms  (tics),  we  may,  up  to  a  certain  point, 
put  these  troubles  down  to  rheumatic  heredity.  If  a  patient  presents 
abarticular  troubles  of  a  rheumatic  nature,  although  he  has  never  had 
articular  symptoms,  we  may  prejudge  the  rheumatic  nature  of  these 
troubles  if  the  patient,  by  reason  of  his  constitution,  form  one  of  the  great 
family  of  arthritics  (diabetes,  biliary  lithiasis,  obesity).  It  must  be  added 
that  the  possibQity  of  gouty  troubles  (gout  being  also  a  member  of  this 
morbid  family)  sometimes  complicates  the  diagnosis. 

We  find  muscular  rheumatism,  but  it  is  often  difficult  to  allow  for  this 
muscular  rheumatism,  inasmuch  as  the  muscle  is  not  the  only  tissue  at 
fault,  and  we  do  not  always  know  whether  we  are  dealing  with  myositis, 
neuritis,  or  with  neuralgia.  Thus,  in  the  affection  described  under  the  name 
of  atrophic  deltoid  rheumatism  (Duchenne),  and  characterized  by  sharp 


1932  TEXT-BOOK  OF  MEDICINE 

pains  in  the  shoulder  and  the  deltoid,  with  paresis  and  rapid  atrophy  of  the 
muscle,  we  iind  lesions  of  myositis,  neuritis,  and  periarthritis,  so  that  the 
name  atrophic  scapular  rheumatism  is  preferable  (Sabourin).  Lumbago, 
torticollis,  and  pleurodynia  are  often  rheumatic  in  nature. 

Neuralgia  is  common  in  rheumatic  patients ;  sciatica  is  the  most  recent 
form. 

I  have  already  mentioned  certain  eruptions  in  acute  rheumatism.  "  Dry 
circumscribed  eczema,  pseudo-sycosis  of  the  upper  or  of  the  lower  lip,  simple 
sycosis  of  the  upper  lip,  solitary  or  very  discrete  psoriasis,  psoriasis  with 
large  patches  afiecting  the  palm  of  the  hand  or  the  sole  of  the  foot,  and 
scarlatiniform  psoriasis,  limited  to  the  genital  organs,  acne  rosacea,  cica- 
tricial acne  pilaris,  etc.,  stand  in  the  forefront  of  the  affections  which  we  have 
recognised  most  frequently  in  rheumatic  persons,  and  present  such  definite 
characters  that  we  can  prejudge  their  rheumatic  nature  and  the  arthritic 
condition  of  the  patient  "  (E.  Besnier). 

Acute  iritis  sometimes  supervenes  between  attacks  of  acute  rheumatism ; 
chronic  irido-choroiditis  accompanies  the  chronic  disease. 

CEdema  is  one  of  the  most  interesting  of  the  abarticular  manifestations. 
We  have  already  noted  the  oedema  which  accompanies  congestion  of  the 
periarticular  tissues  during  an  attack  of  acute  or  of  subacute  rheumatism, 
and  the  more  or  less  coloured  oedema  associated  with  the  rheumatic  exan- 
themata. The  articular  manifestations  may  be  insignificant,  and  yet  the 
oedema  may  be  of  considerable  extent.  This  hypercrinia  of  the  cellular 
tissue  belongs  to  the  course  of  rheumatism.  In  other  patients,  although  the 
rheumatic  diathesis  be  never  betrayed  except  by  some  chronic  and  more  or 
less  painful  swellings  of  the  joints,  rheumatic  oedema  may,  at  a  given  mo- 
ment, invade  a  region,  a  limb,  or  the  legs,  and  remain  there  in  an  obstinate 
fashion.  This  oedema  has  nothing  in  common  with  the  oedema  of  cardiac 
lesions  or  of  nephritis  ;  it  is  the  result  neither  of  cachexia  nor  of  venous 
obliteration.  It  does  not  make  the  prognosis  grave,  and  it  represents  one 
of  the  manifestations  of  the  rheumatic  diathesis  in  the  subcutaneous  cellular 
tissue  (Potain). 

Again,  in  rheumatic  patients  we  see  a  prominence  which  fills  up  the 
supraclavicular  hollow,  where  it  stands  out  in  relief  to  the  extent  of  an 
inch  or  more.  This  swelling,  which  is  elastic,  but  not  painiul,  does  not  take 
the  imprint  of  the  finger ;  it  is  neither  reducible  nor  fluctuating ;  it  is  accom- 
panied by  no  change  in  the  colour  of  the  skin.  It  has  been  called  supra- 
clavicular pseudo-lipoma  by  VemeuU.  It  is  probably  due  to  the  accumu- 
lation of  adipose  tissue  (Verneuil),  or  to  serous  infiltration  (Potain). 


IMII'.IMATIC   AND    I  )\  STl;()l'l  I  K  '   IHSKASKS  1933 

III.— PSEUDO-EHEIJMATISM  DUE  TO  GONOKRIK.EA, 
TUBERCULOSIS,  ETC. 

Gonorrhceal  Rheumatism — This  form  occurs  during  the  course  or 
about  llie  (Icclino  of  bleiuiorrhagia.  It  assumes  various  fispects,  according 
as  its  chief  manifestations  are  articular  or  abarticular.  Those  manifestations 
of  the  gonorrhceal  infection  differ  so  notaldy  from  true  rheumatism  that 
confusion  is  not  possible.  Gonorrliceal  pseudo-rlicumatism  may  show  some 
analogy  with  genuine  articular  rheumatism.  We  may  find  with  the  joint 
pains,  visceral  manifestations,  such  as  endocarditis,  pericarditis,  pleurisy, 
or  cerebral  troubles. 

If  the  reader  will  turn  to  the  section  on  Gonorrhoea,  he  will  find  that 
these  various  visceral  manifestations  are  caused  by  the  gonococcal  infection, 
and  not  by  the  rheumatism. 

The  morbid  troubles  in  the  serous  cavities  and  in  the  joints  are  found 
in  a  modified  form  in  various  infective  conditions,  such  as  gonorrhoea, 
scarlatina,  dy.'^entery,  mumps,  etc.  From  the  point  of  view  of  their  nature 
and  their  origin,  the  forms  of  infective  pseudo-rheumatism  must  be  clearly 
distinguished  from  true  rheumatism,  which  is  also  an  infectious  disease. 

If,  however,  the  distinction  is  clearly  marked  from  the  pathogenic  point 
of  view,  it  is  not  always  so  complete  from  the  clinical  one,  and  in  some  cases, 
apart  from  the  discovery  of  gonorrhoea,  it  would  be  very  difficult  to  say 
whether  the  case  were  one  of  true  rheumatism  or  of  pseudo-rheumatism. 

Tubercular  Rheumatism. — Tubercular  rheumatism  presents  two  chief 
varieties — primary  or  secondary.  The  primary  form  "  opens  the  patho- 
logical scene,  and  is  the  first  manifestation  of  the  tubercular  infection." 
The  secondary  form  appears  in  a  patient  who  "  has  previously  been  attacked 
by  tuberculosis  or  is  actually  tubercular  "  (Poncet). 

Primary  Tubercular  Rheumatism. — The  joint  troubles  are  the  first 
indication  of  tuberculosis,  which  so  far  is  latent,  and  their  symptomatic 
value  may  be  considerable.  The  joints  are  affected  by  Koch's  bacillus  or 
by  its  toxines,  and  the  lesions  may  run  the  course  of  a  tuberculization  of 
the  joint  or  may  resolve  completely,  as  in  one  of  my  cases,  where,  remark- 
able to  relate,  in  spite  of  the  presence  of  the  bacillus  in  the  joint,  resolu- 
tion took  place  just  as  completely  as  in  the  case  of  ordinary  tubercular 
pleurisy. 

This  tubercular  rheumatism  sometimes  begins  like  acute  or  subacute 
rheumatism,  and  generally  attacks  several  joints.  It  is  not,  however, 
frank  in  character.  "  It  presents  great  fixity  in  its  localization,  disappears 
slowly,  and  very  often  leaves  traces  of  its  passage.  It  does  not  return  in 
the  joint  first  affected,  as  in  the  case  of  true  rheumatism.  It  usually  affects 
two  or  three  joints,  rarely  more,  and  is  oligo-articular  "  (Maillant).     While 


1934  TEXT-BOOK  OF  MEDICINE 

less  mobile  ttan  rlieiimatism,  it  is  also  less  transient,  and  tends  to  become 
fixed.     The  salicylate  treatment  has  no  action  upon  it. 

The  duration  is  variable.  Although  the  fever  may  be  moderate,  the 
general  condition  is  quickly  afiected,  and  the  affection  often  terminates  in 
one  of  the  following  ways  :  The  joint  troubles  disappear,  but  the  tuber- 
culosis invades  the  viscera  or  the  serous  membranes.  The  joint  becomes 
more  and  more  involved,  with  fungous  arthritis,  white  swelling,  and  possiblj)' 
with  multiple  ankyloses  (Poncet).  Sometimes  the  rheumatism  passes  into 
the  chronic  condition,  affecting  the  small  joints  of  the  hand  and  of  the  feet, 
as  in  chronic  arthritis  deformans.  Lastly,  recovery  is  possible  without 
ulterior  tuberculization,  as  in  the  case  of  my  patient  in  the  Hotel-Dieu.  It 
is  probable  that  cases  of  this  kind  are  not  very  rare,  but  they  have  so  far 
passed  unnoticed.  We  see  a  patient  suffering  from  fluid  in  the  knee-joint, 
and  we  think  of  arthritism,  "  which  has  a  broad  back,"  and  we  make  a 
diagnosis  of  rheumatic  arthritis.  Nowadays  we  are  not  content  with  such 
a  superficial  diagnosis.  We  withdraw  some  of  the  fluid  from  the  joint, 
examine  for  lymphocytosis,  and  inoculate  guinea-pigs.  In  short,  we  act  as 
in  a  case  of  pleural  effusion,  and  we  find  that  the  so-called  rheumatic  hydrar- 
throsis is  sometimes  a  tubercular  hydrarthrosis  of  a  curable  nature. 

The  diagnosis  of  primary  tubercular  pseudo-rheumatism  is  often  difficult, 
and  we  must  always  think  of  tubercular  rheumatism  when  we  cannot  deter- 
mine the  cause  of  an  infective  rheumatism.  Laboratory  researches,  ex- 
amination of  the  articular  fluid  (cyto-diagnosis),  inoculation  of  guinea-pigs, 
and  Arloing  and  Courmont's  sero-diagnosis,  are  indispensable  procedures  in 
forming  an  opinion. 

The  articular  lesions  vary  in  proportion  to  the  tuberculization  of  the 
joint.  They  may  result  in  miliary  tuberculosis  of  the  serous  membrane  or 
in  white  swelling,  or  they  may  continue  to  be  inflammatory,  and  run  the 
ordinary  course  of  rheumatism  (Poncet). 

If  the  quantity  of  fluid  in  the  joint  is  considerable,  aspiration  is  per- 
formed. In  other  cases  cryogenin,  in  dos.es  of  J  to  1  gramme  daily,  has  a 
beneficial  action  upon  the  joint  lesions,  and  also  upon  the  pain.  We  may 
at  the  same  time  employ  counter-irritation  in  all  its  forms,  and  prescribe 
general  tonics — arsenic,  lecithin,  and  glycero-phosphates.  In  chronic  cases 
the  thermal  cures  of  Salies-de-Beam,  Biarritz,  Bourbon-l'Archambault,  and 
Dax  give  good  results.  Here,  as  in  other  forms  of  pseiido-rheumatism, 
salicylate  treatment  produces  no  appreciable  effect. 

Secondary  Tubercular  Rheumatism. — In  this  case  the  joint  troubles 
occur  in  a  patient  who  is  already  suffering  from  tuberculosis  of  the  serous 
membranes  (rare  cases)  or  of  the  viscera.  We  must,  however,  be  on  our 
guard  against  "  labelling  as  tubercular  every  case  of  acute  arthritis  in 
individuals  suffering  from  a  tubercular  lesion,  and  in  particular  phthisical 


RHEUMATIC  AXP  in'STKOrTTTC  DISEASES  1935 

patients  "  (Bezan^on).     Experimontal  verification,  with  the  assistance  of  all 
the  means  at  our  disposal,  must  contribnto  largely  to  the  diagnosis. 

The  evolution  of  secondary  tubercular  rheumatism  has  nothing  to  dis- 
tinguish it  from  the  primary  form.  Simple  arthralgia,  acute,  subacute,  or 
chronic  and  deforming  joint  lesions  comprise  the  jjrincipal  varieties. 
Recovery  may  occur,  although  the  primary  focus  continues  its  course,  as 
in  the  cases  of  Bentz,  in  which  the  initial  lesions,  Pott's  disease,  and  osteitis 
of  the  tibia  remained  active,  while  the  joint  troubles  disappearod  without 
ending  in  definite  articular  tuberculosis. 

Scarlatinal  Rheumatism. — The  rheumatism  of  scarlatina  may  simulate 
true  rheumatism,  although  it  more  often  assumes  the  characters  of  infective 
pseudo-rheumatism.  It  appears,  as  a  rule,  during  the  decline  of  the  disease, 
and  its  seats  of  election  are  the  wrist  and  the  instep.  It  is  often  so  slight 
that  the  pain  is  only  revealed  by  pressure  on  the  parts.  Pyogenic  bacteria 
are  frequently  associated  with  scarlatina,  and  scarlatinal  arthritis  may 
sometimes  end  in  suppuration.  Pleurisy  and  pericarditis,  which  may 
develop  simultaneously  with  the  joint  lesions,  also  show  a  tendency  towards 
pundent  change.  For  further  details,  I  would  refer  the  reader  to  the  section 
on  Scarlatina. 

Dysentery. — Dysentery  is  sometimes  accompanied  by  arthritis.  This 
is  Stoll's  rheumatic  form.  The  joint  manifestations  supervene  at  an  ad- 
vanced period  of  the  disease,  sometimes,  indeed,  during  convalescence. 
According  to  the  particular  case,  one  or  several  joints  are  affected  simul- 
taneously or  in  succession.  The  arthritis  is  sometimes  transient ;  at  other 
times  obstinate,  as  in  gonorrhceal  arthritis. 

Mumps  are  sometimes  accompanied  by  joint  troubles,  and  even  by  endo- 
carditis, as  has  been  pointed  out  in  the  section  on  Mumps. 

Pregnancy  leads  to  such  changes  in  the  economy  that  rheumatism  may 
be  notably  modified  in  the  pregnant  woman  (Hanot).  The  puerperal  con- 
dition constitutes  a  favourable  state  for  the  development  of  secondary 
arthritis,  which  sometimes  ends  in  suppuration  and  ankylosis. 

Pneumonia  may  also  be  accompanied  by  simple  or  by  suppurative 
arthritis,  due  to  infection  by  the  pneumococcus  or  to  secondary  infections. 

Erysipelas  may  also  be  accompanied  or  followed  by  joint  troubles  of 
various  kinds,  such  as  hydrarthrosis  and  simple  or  suppurative  arthritis. 

Typhoid  fever  is  another  infectious  disease,  in  the  course  of  which  simple 
or  suppurative  arthritis  may  supervene. 

Certain  intoxications  (iodism,  plumbism,  food-poisoning)  and  auto- 
intoxications are  capable  of  giving  rise  to  rheumatic  symptoms. 

In  many  of  the  cases  of  infective  arthritis  just  reviewed  we  find  the 
pathogenic  agent  in  the  diseased  joint — gonococcus,  pneimiococcus,  Bacillus 
typhosus,  streptococcus. 


1936  TEXT-BOOK   OF  MEDICIKE 

In  other  cases  we  find  only  agents  of  secondary  infection.  Sometimes, 
indeed,  the  fluid  from  the  joint  is  sterile,  and  we  then  ask  whether  we  must 
hold  the  toxines  guilty,  or  whether  it  is  not  more  correct  to  admit  the  dis- 
appearance of  the  microbes. 

Treatment.— As  a  general  rule,  we  employ  the  drugs  used  in  true  rheu- 
matism. Gonorrhoeal  arthritis  and  puerperal  arthritis,  which  so  frequently 
assume  the  subacute  type,  must  be  treated  from  the  onset  by  energetic  local 
measures,  such  as  bleeding,  leeches,  cupping,  blisters,  and  the  cautery. 
These  cases  may  well  be  treated  by  the  measures  which  I  saw  Trousseau 
employ,  and  which  I  have  myself  used  with  success.  I  have  described  it* 
under  the  name  of  Trousseau's  Cataplasm.     Its  composition  is  as  follows  : 

Take,  according  to  the  size  of  the  diseased  joint,  3  or  4  pounds  of  bread, 
4  pounds  being  necessary  for  the  knee,  while  2  pounds  are  sufficient  for  the 
wrist.  Cut  the  bread  in  pieces,  taking  care  to  remove  all  the  crust,  and 
soak  the  pieces  in  water  for  about  five  minutes. 

When  the  bread  is  taken  out  of  the  water,  it  is  quite  soaked.  It  is  then 
placed  in  a  cloth  or  in  a  serviette,  and  a  portion  of  the  water  which  has  been 
absorbed  is  expressed  by  twisting  the  cloth.     The  bread  is  then  only  damp. 

It  is  next  placed  in  a  bain-marie,  where  it  is  allowed  to  remain  for  three 
hours.  When  it  is  taken  out  of  the  bain-marie  we  have  a  kind  of  dryish 
paste,  which  is  gradually  softened  by  the  addition  of  camphorated  alcohol. 
The  cake  is  kneaded  until  it  has  acquired  the  consistency  of  plum-pudding 
or  of  putty.  This  is  the  most  delicate  part  in  the  manufacture  of  the 
plaster,  and  this  degree  of  consistency  must  be  obtained.  If  the  cataplasm 
be  too  soft,  it  softens  down  under  the  pressure  exercised  over  the  joint, 
and  if  it  be  too  hard,  it  is  no  longer  homogeneous,  but  forms  small  lumps, 
and  the  dried  parts  may  excoriate  the  skin.  It  is,  therefore,  essential  to 
exercise  great  care  as  to  the  consistency  of  the  cataplasm.  When  we  are 
unaccustomed  to  use  it,  we  are  always  liable  to  make  it  too  soft,  either 
because  the  bread  has  not  been  sufficiently  squeezed  before  placing  it  in 
the  bain-marie,  or  because  too  large  a  quantity  of  camphorated  alcohol  has 
been  added  too  quickly. 

The  paste  prepared  in  the  above  manner  is  spread  out  on  a  linen  com- 
press in  the  form  of  an  elongated  rectangle  of  such  a  size  that  the  whole 
joint  may  be  covered.  The  cataplasm  should  be  nearly  J  iach  thick  at  its 
edges,  in  order  to  avoid  too  rapid  drying  of  the  thinner  parts.  A  solution 
of  the  following  composition  is  then  poured  over  the  surface  of  the  poultice  : 

Camphor         . .         . .  . .  . .  . .  . .     7  parts. 

Extract  of  opium     . .         . .         ..         . .         . .     5     „ 

Alcohol  . .  . .  . .  . .  . .  . .     Sufficient  to  make  it 

liquid. 

*  Dieulafoy,  Gazette  Hebdo^^  No.  48.     1879. 


iniKUMATlC  AND  J)YSTl;<  »I'II  K'   DfSK  \SI<:S  1037 

The  cataplasm  is  now  finished,  and  the  applicjaiion  is  more  simple.  It 
is  placed  directly  upon  the  diseased  joint,  and  covered  over  by  oiled  silk 
to  prevent  evaporation.  The  whole  is  fixed  firmly  by  a  flannel  bandage 
several  feet  in  length,  and  secured  with  tapes.  The  length  of  the  tapes 
varies  according  to  the  size  of  the  joint,  and  consequently  to  the  size  of  the 
poidtice. 

The  diseased  joint,  thus  enveloped,  is  kept  at  rest.  The  compression 
sliould  be  fairly  firm,  but  not  so  firm  as  to  produce  oedema  in  the  subjacent 
parts.  We  may  prevent  oedema  by  taking  care  to  surround  these  parts 
with  a  roller  bandage.  A  reverse  may  be  used  in  order  to  prevent  displace- 
ment of  the  turns. 

The  cataplasm  is  thus  applied,  and  allowed  to  remain  in  situ  for  from 
eight  to  ten  days.  It  is  removed  after  this  period,  and  it  is  surprising  to 
find  the  cataplasm  as  fresh  and  as  moist  as  if  it  had  just  been  applied.  The 
strong  smell  of  camphor  is  still  present,  and  not  a  trace  of  mustiness  is  to 
be  seen.  The  skin  which  has  remained  so  long  in  contact  with  the  cataplasm 
is  absolutely  healthy.  It  is  only  excoriated  if  the  cataplasm,  being  too  thin 
at  its  edges,  has  become  dried  or  has  been  spread  out  by  ill-applied  com- 
pression. A  second  or  a  third  application  must  be  made  if  one  does  not 
suffice. 

IV.  GOUT. 

Following  the  example  of  old  writers,  it  is  customary  to  describe  regular 
and  irregular  gout. 

Regular  Gout. 

Acute  Gout. — The  attack  of  gout  is  only  an  episode  in  the  life  of  the 
gouty,  especially  in  the  hereditary  disease,  which  is  the  most  common.  A 
patient  who  will  some  day  become  gouty  usually  experiences  from  an  early 
age  some  of  the  manifestations  which  form  part  of  the  gouty  diathesis. 

At  the  age  of  fourteen  or  fifteen  years  he  is  subject  to  migraine  or  epis- 
taxis.  Haemorrhoids  and  eczema  appear  somewhat  later,  and  then,  about 
the  age  of  twenty-five  and  for  a  series  of  years,  he  complains  of  dyspepsia, 
with  flatulence,  heaviness  in  the  stomach,  distension  of  the  abdomen,  acid 
eructations,  constipation,  pruritus  ani,  and  urine  which  contains  thick 
deposits  of  urates  or  of  uric  acid. 

Some  patients  have  attacks  of  asthma,  which  reappear  at  mgre  or  less 
lengthy  intervals ;  others  suffer  from  hepatic  colic,  renal  colic,  and  attacks 
of  boils,  or  show  early  baldness  and  a  notable  tendency  to  obesity.  The 
gouty  diathesis  may  appear  in  these  different  forms  without  ending  in 
articular  gout,  and  when  the  attack  of  gout  appears  it  does  not  do  so  before 
the  age  of  thirty  or  forty  years. 


1938  TEXT-BOOK  OF  MEDICIXE 

The  attack  of  gout  is  usually  ushered  in  by  some  premonitory  symp- 
toms. Tlie  patient  becomes  morose  and  irritable  without  reason,  his  temper 
becomes  worse,  and  he  complaios  of  inaptitude  for  work,  of  vertigo,  and  of 
dyspepsia.  The  gout  is  at  hand,  and  the  economy  is,  as  it  were,  saturated 
with  it — totum  corpus  est  "podagra  (Sydenham) — and  the  gouty  person  who 
has  had  several  previous  attacks  knows  perfectly  well  what  is  pendiug. 

The  attack  of  gout,  whether  it  has  or  has  not  been  preceded  by  pre- 
monitory troubles,  runs  the  following  course  :  The  sufferer  goes  to  bed  and 
falls  asleep,  but  between  midnight  and  three  o'clock  in  the  morning — ^for  it 
is  almost  always  in  the  middle  of  the  night  that  the  first  attacks  of  gout 
appear — he  is  awakened  by  a  sharp  pain  situated  in  the  metatarso-phalangeal 
articulation  of  the  big  toe  (podagra).  The  pain  becomes  intolerable  iu 
three  or  four  hours  ;  the  patient  is  a  prey  to  absolute  torture,  and  cannot 
bear  the  contact  of  the  clothes,  dreads  the  vibration  of  the  bed  caused  by 
persons  walking  about  the  room  or  by  carriages  passing  in  the  street.  These 
agonizing  pains  are  not  confined  to  the  joitit  invaded.  They  sometimes 
extend  to  the  foot  and  the  leg,  and  the  patient  compares  them  to  boiling  oil 
or  to  molten  lead  flowing  along  the  affected  limb.  Towards  morning — "  at 
cock-crow  "  {sub  galli  cantu),  says  Sydenham — ^the  paios  diminish,  the  chills 
which  accompany  them  disappear,  the  patient  falls  asleep,  there  is  slight 
perspiration,  and  the  day  is  less  painful ;  but  towards  evening  and  during 
the  night  the  pains  reappear  with  all  their  severity,  to  lessen  again  in  the 
morning ;  they  alternate  in  this  fashion  for  four,  five,  six,  or  eight  days. 

Let  us  now  study  the  appearance  of  the  diseased  parts.  The  veins  of 
the  invaded  and  of  the  neighbouring  regions  are  extremely  swollen ;  the 
skin  of  the  big  toe  is  bright  red,  shiny,  and  recalls  the  appearance  of  onion- 
peel  (Trousseau).  The  redness  spreads  and  fades  insensibly.  It  reaches 
its  maximum  on  the  second  day,  and  then  gives  place  to  a  violet  tint.  The 
tissues  are  swollen,  and  oedema,  lasting  some  days,  is  seen.  After  the  attack 
the  sldn  desquamates  to  a  slight  extent,  and  itching  is  felt. 

The  attack  of  gout  is  accompanied  by  general  symptoms,  known  as 
gouty  fever.  The  congestion  of  the  face  and  the  headache  of  the  onset 
yield  after  two  or  three  days.  The  skin  is  dry,  and  the  morning  sweats 
have  neither  the  abundance  nor  the  acidity  seen  in  articular  rheumatism. 
The  temperature  increases  up  to  the  fourth  or  to  the  fifth  day.  It  may 
reach  103°  E.  at  night,  and  falls  about  a  degree  in  the  morning.  The  fever 
is  accompanied  by  thirst,  anorexia,  and  constipation.  The  urine  is  red, 
loaded  with  urates  and  uric  acid,  and  sometimes  contains  albumin.  If  a 
blister  is  applied,  the  serous  fluid  usually  contains  crystals  of  uric  acid, 
though  less  in  the  neighbourhood  of  the  invaded  joints  than  at  other  points. 
The  blood,  which  during  an  attack  of  gout  contains  an  excess  of  uric  acid, 
only  contains  traces  after  the  attack. 


EHEUMATIC  AND  DYSTEOPHIC  DISEASES  1939 

After  the  attack  the  patient  has  difficulty  in  walking,  and  the  diseased 
joint  does  not  regain  its  suppleness  for  some  weeks  ;  but  the  general  h<;alth 
remains  excellent — better,  indeed,  than  before  the  attack.  It  might  be 
said  that  this  acute  episode  has  played  the  part  of  u  salutary  emunctory. 
Perhaps  it  is  true  to  say  that  the  gouty  fever  has  played  a  useful  part  in 
determining  more  intense  combustion,  and  in  eliminating  and  destroying 
the  uric  acid  (Bouchard). 

The  attack  of  gout  does  not  always  run  the  foregoing  course.  I  have  so 
far  considered  only  the  first  or  the  early  attacks,  but  in  some  patients, 
especially  in  those  who  have  had  several  previous  attacks,  the  course  of 
events  is  somewhat  different.  In  the  first  place,  the  gout  does  not  remain 
limited  to  one  toe,  but  invades  both  big  toes  in  succession,  and  then  other 
joints — foot,  knee,  hand,  elbow,  etc.  The  attacks,  instead  of  coming  on 
during  the  months  of  January  and  February,  appear  in  the  early  spring- 
time or  at  the  end  of  the  autumn.  These  attacks  appear  in  the  form  of 
successive  paroxysms — that  is  to  say,  the  patient  experiences  a  series  of 
attaclvs,  each  of  which  is  sHght,  and  separated  by  a  few  days  of  improve- 
ment. 

The  muscular  form  of  gout  has  been  carefully  described  by  Grandmaison, 
and  the  attack  may  be  isolated  or  be  concurrent  with  articular  gout.  I 
have  seen  it  limited  to  the  calf,  with  intense  congestion  and  painful  oedema, 
and  distension  of  the  venous  network. 

An  indi\adual  may  have  only  one  attack  of  gout  in  his  life,  but  this  is 
rare,  and  the  subsequent  attacks  are  sometimes  separated,  especially  the 
first  ones,  by  an  interval  of  several  years. 

Chronic  Gout. — Chronic  gout,  as  a  rule,  attacks  old  people.  It  is  rarely 
chronic  from  the  first,  and  is  preceded  by  more  or  less  frequent  attacks  of 
acute  gout.  Chronic  gout  resembles  the  acute  disease,  with  successive 
paroxysms,  "  with  this  capital  difference — that  its  attacks  are  longer,  and 
that  in  the  intervals  the  patient  is  never  completely  free  "  (Trousseau). 
Further,  the  disease  attacks  several  joints  at  once,  and  the  joint  swellings 
persist  indefinitely.  Thus,  while  the  patient  suffering  from  acute  gout 
regains  after  the  attack  complete  freedom  of  movement,  the  sufferer  from 
chronic  gout  becomes  helpless — his  feet,  knees,  and  hands  are  deformed ; 
walking  is  difficult  or  impossible.  Acute  attacks  may  supervene  in  chronic 
gout. 

The  history  of  the  tophus  belongs  to  chronic  gout.  The  tophus  is  a 
concretion  formed  of  urate  of  soda,  of  urate  and  of  phosphate  of  lime. 
These  concretions  develop  in  the  subcutaneous  cellular  tissue  and  in  the 
thickness  of  the  sldn.  They  form  small  nodular  tumours,  which  are 
sessile  or  pedunculated,  and  which  vary  in  size  from  a  small  pea  to  a  pigeon's 
egg.     They  usually  develop  in  the  hands,  in  the  neighbourhood  of  the  joints 


1940  TEXT-BOOK  OF  MEDICINE 

of  the  fingers,  wMcli  they  help  to  deform.  They  are  not  symmetrical.  The 
tophi  appear  after  the  attack,  during  the  remission  stage.  They  are  at 
first  composed  of  a  semifluid  mass,  which  raises  the  skin,  without  causing 
changes  in  it.  In  a  short  time  the  mass  becomes  solid  and  hard,  and  ia- 
creases  in  size  with  each  fresh  attack  of  gout.  In  some  cases  the  tophus 
is  reabsorbed ;  the  skin  sometimes  ulcerates,  and  the  contents  of  the  tophus 
are  discharged  externally.  Some  gouty  patients  sufier  for  a  long  time  from 
chalky  fistulse,  which  may  become  inflamed. 

The  tophi  develop  in  points  other  than  in  the  neighbourhood  of  joints. 
They  are  frequent  in  the  external  ear,  at  the  edge  of  the  helix,  and  on  the 
inner  surface  of  the  pinna.  They  have  also  been  seen  on  the  eyelids  and 
on  the  alse  nasi.  Although  tophi  develop,  as  a  rule,  after  attacks  of  articular 
gout,  it  must  be  added  that  they  may  appear  in  persons  who,  though  of 
the  gouty  diathesis,  have  not  shown  articular  troubles.  This  gravel  of  the 
skin,  as  Trousseau  calls  it,  is  a  certain  sign  of  the  gouty  diathesis. 

I  had  under  my  care  ia  the  Avenue  Gabriel  a  lady  of  gouty  stock,  who 
had  never  had  an  attack  of  gout.  She  was  subject  to  renal  colic,  and  had 
a  large  tophus  in  the  forearm. 

Chronic  gout  is  very  serious,  because  it  tends  to  weaken  the  organism  to 
such  an  extent  that  it  has  received  the  names  of  atonic  and  asthenic  gout. 
This  cachectic  condition,  which  comes  on  more  or  less  early,  according  to 
the  patient,  is  hastened  by  multiple  complications,  such  as  diabetes,  dys- 
pepsia, and  changes  in  the  kidneys,  heart,  and  great  vessels. 


Irregular  or  Visceral  Gout. 

Larval  gout,  retrocedent  gout,  and  organic  changes  of  gouty  origin  are 
included  under  this  heading. 

Larval  Gout. — The  articular  changes  which  constitute  the  attack  of 
acute  or  of  chronic  gout  are  the  most  genuine  and  evident  expression  of  the 
gouty  diathesis,  but  this  diathesis  also  reveals  itself  by  other  manifesta- 
tions, such  as  migraine,  asthma,  gravel,  haemorrhoids,  diabetes,  and  ecze- 
matous  eruptions. 

These  various  forms  may  appear  in  an  individual  who  has  not  sufiered 
from  an  attack  of  articular  gout,  and  they  may,  indeed,  remain  in  the 
condition  of  larval  gout,  without  ending  in  the  more  genuine  manifestations 
of  the  articular  disease.  As  a  rule,  articular  gout  is  preceded  many  years 
previously  by  some  of  the  manifestations  of  larval  gout.  In  adolescence 
we  find  migraine  and  haemorrhoids  ;  in  adult  age  asthma,  dyspepsia,  gravel, 
and  eczema ;  later,  the  articular  disease  appears.  In  some  cases  articular 
gout  alternates  with  attacks  of  asthma  or  of  renal  colic.  These  different 
varieties  form  so  clear  a  part  of  the  same  diathesis  that  the  parent  with 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  1041 

articular  gout  begets  children  who  will  present  the  manifestations  of  larval 
gout,  and,  vice  versa,  parents  suffering  from  larval  gout  beget  children  who 
inherit  the  articular  disease. 

Retrocedent  Gout. — The  name  of  retrocedent  or  metastatic  gout  has 
been  given  to  troubles  which  are  more  or  less  sudden,  and  which  supervene 
in  the  course  of  an  attack  of  articular  gout. 

A  patient  is  attacked  by  gout,  and,  as  a  result  of  untimely  treatment, 
or  of  some  disturbing  cause,  or  even  without  any  appreciable  reason,  the 
articular  congestion  is  aborted  at  its  onset,  and  the  gout,  seizing  on  some 
organ,  causes  certain  complications. 

In  the  digestive  system  we  may  find  cesophagisra,  dysphagia,  attacks  of 
cardialgia,  characterized  by  terrible  cramps  of  the  stomach,  and  by  uncon- 
trollable vomiting,  with  cold  sweats,  algidity,  and  a  tendency  to  syncope. 
Sometimes  the  gastric  manifestations  assume  the  inflammatory  form,  fever 
appears,  and  hsemorrhagic  or  phlegmonous  gastritis  supervenes.  Let  us 
note  also  intestinal  colic,  with  or  without  enteritis. 

In  the  nervous  centres  we  find  troubles  similar  to  those  of  cerebral 
rheumatism — violent  headache,  delirium,  epileptiform  convulsions,  stupor, 
apoplectiform  conditions,  and  coma. 

Aphasia  forms  part  of  these  cerebral  troubles.  In  some  cases  it  might 
be  said  that  gout  strikes  the  mesencephalon  or  the  bulb.  The  patient 
suddenly  experiences  palpitation,  laryngeal  spasms,  respiratory  distress, 
lipothymia,  and  may  die  suddenly  in  syncope. 

The  Visceral  Lesions  of  Gout. — Permanent  lesions  occur  in  certain 
organs  as  a  result  of  the  gouty  diathesis.  We  may  not«  segmentary  myo- 
carditis (Renaut  and  Landouzy) ;  fatty  degeneration  of  the  heart,  favouring 
fatal  syncope  ;  aortitis  and  atheroma  of  the  aorta,  which  is  associated  with 
angina  pectoris  ;  arterio-sclerosis  and  atheroma  of  the  arteries,  which  pave 
the  way  for  cerebral  symptoms  and  gangrene  of  the  limbs  ;  phlebitis  and 
emboli,  chronic  congestion  of  the  liver,  and  the  manifestations  of  gout  in 
the  kidney,  which,  on  account  of  their  importance,  I  discuss  in  detail. 

Gout  and  the  Kidney. — In  the  gouty  person  the  kidney  is  the  organ 
most  often  attacked.  In  the  gouty,  or  in  the  individual  bom  of  gouty 
stock,  whether  he  may  or  may  not  have  had  an  attack  of  articular  gout, 
the  disease  may  show  itself  in  the  kidney  under  various  forms,  of  which 
gravel,  renal  colic,  nephritis,  albuminuria,  and  haematuria  are  the  principal 
ones. 

Gravel. — As  a  matter  of  fact,  gouty  persons  suffer  from  gravel  to  a 
more  or  less  marked  degree  and  for  a  more  or  less  lengthy  period.  Every 
individual  who  is  tainted  with  the  gouty  diathesis  passes  uric  acid  in  excess, 
either  in  the  shape  of  sand  or  of  gravel.  It  is,  indeed,  because  he  passes 
this  excess  of  uric  acid  that  he  is  to  a  certain  degree  free  from  articular  gout. 
^  123 


1942  TEXT-BOOK  OF  MEDICINE 

If  the  gouty  person  were  able  to  pass  this  excess  of  uric  acid  in  the  form 
of  sand  all  would  be  weU,  for  the  uric  sand  does  not  cause  renal  colic  ;  but, 
in  addition  to  sand,  the  patient  passes  gravel,  as  a  rule,  at  the  expense  of 
renal  colic. 

It  is  certain  that  three-quarters  of  the  persons  who  suffer  from  renal 
colic  are  of  the  gouty  diathesis,  and  it  may  be  said  of  renal  colic  that  it  is 
an  attack  of  renal  gout.  Out  of  150  gouty  persons,  48  had  suffered  from 
renal  colic  (Lecorche). 

In  most  cases  the  trouble  commences  with  renal  colic,  and  the  articular 
disease  appears  later.  It  may  come  on  ten,  twenty,  or  thirty  years  after 
the  first  attack  of  colic.  Lecorche  quotes  the  case  of  a  patient  who  had 
his  first  attack  of  gout  thirty-four  years  after  his  first  attack  of  colic.  During 
this  long  space  of  time  he  had  had  twenty-five  or  thirty  attacks  of  colic. 
It  might  be  said  that  the  expulsion  of  sand  or  of  gravel,  with  or  without 
colic,  removes  the  risk  of  articular  gout  up  to  a  certain  point,  and  the  more 
the  patient  suffers  from  gravel,  the  less  has  he  to  fear  an  attack  of  gout ; 
but  if  the  passage  of  sand  or  gravel  cease,  the  gout  may  become  articular. 
"  It  is  precisely  because  the  uric  acid  no  longer  takes  the  renal  channel  for 
its  elimbiation  that  the  joints  become  affected.  As  long  as  the  excess  is 
eliminated  by  the  kidneys,  the  joints  are  free  from  an  attack  "  (Lecorche). 
This  assertion,  without  being  absolute,  contains  a  large  degree  of  truth. 

In  other  cases,  which,  it  is  true,  are  more  rare,  the  attacks  of  articular 
gout  are  the  first  to  occur,  and  the  colic  appears  later.  It  may  be  remarked 
that  in  certain  gouty  patients  the  attacks  of  articular  gout  cease  or  diminish 
in  severity  when  renal  colic  appears.  One  of  Lecorche's  patients,  who 
had  had  attacks  of  articular  gout  for  thirteen  years,  did  not  suffer  from  a 
single  one  after  the  appearance  of  the  renal  colic.  Lastly,  we  find  oases  in 
which  the  articular  attacks  alternate  with  the  renal  attacks. 

In  spite  of  the  close  relations  between  articular  gout  and  renal  calculus, 
a  patient  born  of  gouty  stock  may  only  have  lithiasis  and  renal  colic,  and 
may  recover  without  suffering  from  articular  gout. 

Gouty  Kidney — Nephritis. — The  morbid  series  often  commences  with 
gravel,  and  goes  on  to  nephritis.  Renal  lithiasis  and  colic  occur  at  first, 
and  the  lesions  of  nephritis,  which  chiefly  affect  the  interstitial  tissue, 
supervene  later.  In  other  cases,  on  the  contrary,  gouty  nephritis  arises 
insidiously,  without  having  been  preceded  by  the  severe  s3anptoms  of  renal 
colic.  The  formation  and  the  elimination  of  the  uric  acid  occur  in  sUence, 
but  they  pave  the  way,  nevertheless,  for  fibrous  lesions  in  the  kidney.  The 
gouty  person,  therefore,  has  his  kidneys  somewhat  exposed,  and  if  attacks 
of  renal  colic,  thanks  to  the  prolonged  expulsion  of  the  uric  acid  in  the 
urine,  may,  up  to  a  certain  point,  relieve  the  patient  from  the  risk  of  an 
attack  of  articular  gout,  the  reverse  side  of  the  question  shows  the  possible 


RHEUMATIC  .\ND  DYSTUOnilC  DISEASES  VJ-Vi 

prospect  of  uuphritis,  with  all  its  consociuences.  Nephritis  is  the  more  to 
be  (Irt'iult'd,  as  the  arterioles  of  the  kidney  are  the  more  rapidly  damaged, 
arterio-sclerosis  being  the  appanage  of  the  gouty. 

Two  chief  causes  dominate  the  evolution  of  gouty  nephritis  :  On  the  one 
hand,  the  presence  and  the  elimination  of  irritating  substances,  such  as  uric 
sand  and  gravel ;  on  the  other  hand,  the  arterio-sclerotic  degeneration  of  the 
renal  vessels. 

The  lesions  of  the  gouty  kidney  are  well  known  (Garrod,  Charcot, 
Comil).  Their  evolution  is  very  slow.  At  the  end  of  the  process  the  gouty 
kidney  is  a  type  of  the  contracted  kidney.  The  capsule  is  thickened  and 
adherent.  Cysts  are  frequent.  We  find  on  section  that  the  cortical  sub- 
stance is  almost  completely  atrophied.  The  histological  examination  reveals 
interstitial  nephritis.  Fibrous  tissue  predominates  everywhere.  At  various 
spots,  but  especially  in  the  glomeruli,  arterio-sclerosis  is  very  marked. 

The  characteristic  of  the  gouty  kidney,  however,  is  the  presence  of 
crystals  of  uric  acid  and  deposits  of  urate  of  soda.  Uric  acid,  in  the  form 
of  sand  or  of  yellowish  or  brownish  concretions,  is  deposited  in  the  excretory 
apparatus  of  the  kidney — that  is  to  say,  in  the  straight  tubules,  papillae, 
calyces,'and  peh^s — and  also,  though  more  rarely,  in  the  secretory  apparatus 
of  the  kidney — that  is,  in  the  convoluted  tubules  and  in  the  periphery  of 
the  lab}Tinth.  The  urate  of  soda  is  deposited  chiefly  in  the  region  of  the 
pyramids,  either  in  the  interior  of  the  uriniferous  tubules  or  externally  in 
the  connective  tissue. 

The  symptoms  of  gouty  nephritis  are  similar  to  those  of  chronic  inter- 
stitial nephritis,  with  the  predominance  of  arterio-sclerosis.  The  major 
complications  of  Bright's  disease  are  slow  in  showing  themselves,  and  are 
usually  preceded  by  the  minor  symptoms  of  Brightism,  with  or  without 
albuminuria.  We  see  gouty  persons  who  have  not  albuminuria,  and  in 
whom  the  renal  lesion  reveals  itseK  by  the  minor  complications  of  Brightism, 
or  by  some  severe  sjmptoms  of  Bright's  disease. 

Some  of  these  patients  consult  us  for  dyspepsia,  with  or  without  vomit- 
ing ;  for  headache,  which  they  term  migraine ;  for  continuous  or  for 
paroxysmal  dyspepsia,  which  they  look  upon  as  asthma.  And,  as  gouty 
persons  often  suffer  from  dyspepsia,  migraine,  and  asthma,  we  are  liable 
to  agree  too  readily  with  their  diagnosis,  and  we  sometimes  wrongly  attribute 
their  troubles  to  the  gouty  diathesis.  On  closer  inspection,  however,  we 
see  that  these  troubles  are  neither  asthma  nor  migraine  ;  they  are  symptoms 
of  Bright's  disease.  The  urine  may  for  the  moment  be  free  from  albumin, 
but  it  matters  little  :  the  gouty  person  in  question  is  none  the  less  a  case 
of  Bright's  disease.  When  we  make  a  careful  inquiry,  we  find  the  minor 
complications  of  Brightism — poUakiuria,  crysesthesia,  dead  fingers,  cramps 
in  the  calves,  and  electrical  shocks.     We  find  an  increase  of  the  arterial 

123—2 


1944  TEXT-BOOK  OF  MEDICINE 

tension,  or  a  hruit  de  galop.  If  we  investigate  tke  toxicity  of  the  urine,  we 
find  it  diminislied. 

Lastly,  the  symptoms  of  Bright' s  disease  dominate  the  situation  in  some 
gouty  persons.  The  other  manifestations  of  gout  appear  to  be  extinguished, 
and  these  patients  succumb  to  renal  disease  and  ureemia. 

Gouty  Albuminuria. — I  have  said  that  in  a  gouty  person  albuminuria 
may  be  present  as  a  transitory  or  as  a  permanent  condition,  without  being 
absolutely  associated  with  the  progressive  renal  lesions  of  Bright's  disease. 
It  is,  therefore,  essential  to  state  exactly  the  prognostic  value  of  gouty 
albuminuria.  A  person  who  suffers  from  articular  gout  may  pass  albumin 
for  years  without  showing  symptoms  of  Bright's  disease.  I  know  gouty 
persons  who  have  passed  large  quantities  of  albumin  for  three,  five,  and 
ten  years,  and  yet  they  have  never  shown  the  minor  troubles  of  Brightism. 

At  the  Necker  Hospital  I  have  often  talked  with  a  physician  who 
was  gouty,  and  who  had  for  several  years  passed  large  quantities  of  albumin 
in  the  urine,  without  having  ever  experienced  any  symptom  of  Bright's 
disease.  I  have  seen  a  young  man  who  is  subject  to  attacks  of  articular 
gout,  and  who  has  passed  albumin  for  three  years,  the  urine  containing, 
when  I  examined  it,  more  than  2  grammes  of  albumin  per  litre,  but  its 
toxicity  was  absolutely  normal.  This  patient  has  not  the  least  sign  of 
Brightism.  There  is,  therefore,  a  gouty  albuminuria,  which  may  last  for 
years,  without  resulting  in  Bright's  disease.  From  the  point  of  view  of 
the  prognosis,  these  facts  are  of  great  importance. 

This  analysis  of  cases  proves  that  in  the  gouty  diathesis,  as  in  the  in- 
fectious diseases,  the  morbid  acts  of  the  kidney  may  be  dissociated,  as 
I  have  tried  to  prove  in  my  communication  to  the  Academic  de  Medecine.* 
On  the  one  hand,  albuminuria  may  be  absent — at  least,  for  a  time — in  gouty 
nephritis,  and,  on  the  other  hand,  albuminuria,  as  we  shaU  see  later,  may 
exist  alone,  to  the  exclusion  of  any  symptom  of  Bright's  disease,  and  it 
may  acquire  importance  as  regards  prognosis  only  by  its  conjunction  with 
signs  of  urinary  iasufficiency. 

Haematuria. — Heematuria  in  the  gouty  is  associated  with  gravel  and 
with  renal  calculi.  If  the  reader  will  turn  to  the  section  on  Renal  Calculus, 
he  will  find  a  description  of  this  hasmaturia.  Gouty  persons  may  sufier 
from  hsematuria  which  has  nothing  to  do  with  a  calcidus,  and  the  haema- 
turia appears  in  their  case  just  as  epistaxis  or  haemorrhoids  do  in  other 
persons,  because  the  congestion  affects  the  kidneys  instead  of  affecting  the 
hsemorrhoidal  vessels.  Lecorche  has  reported  five  cases  of  this  gouty 
haematuria,  and  I  have  seen  one  case  at  Troyes  in  a  patient  who  feared 
renal  cancer.  Gouty  haematuria  is  preceded  or  accompanied  by  pain  in  one 
or  in  both  kidneys.  The  pain  is  due  to  the  congestion  of  the  organ  or  to 
*  Seance  des  6  et  20  Juin.  1893. 


RHEUMATIC  AND  DYSTROPIITr!  DISEASES  1945 

tho  passage  of  clots  through  thn  urotor,  and  perhaps  also  to  the  momentary 
ohstrurtiim  of  the  ureter.  The  urine  is  hrovviiish,  reddish,  or  Ijloody, 
according  to  the  quantity  of  blood  passed.  TIk;  hicmorrhage  may  bo 
repeated  several  times  daily  for  several  days  or  weeks. 

Gouty  Congestion  of  the  Kidney. — As  I  have  said  above,  gouty  con- 
gestion of  the  kidney  exists.  In  some  cases  the  congestion  coincides  with 
renal  colic  ;  in  other  cases  it  is  independent.  It  must  be  said,  however, 
that  it  chiefly  affects  kidneys  already  damaged  by  lithiasis.  The  course  of 
events  is  as  follows  :  The  patient  has  a  feeling  of  swelling  and  of  heaviness 
in  one  of  the  kidneys.  This  feeling  spreads  to  the  ureter  and  to  the  testicle. 
The  testicle  becomes  tender,  congested,  and  swollen.  The  onset  of  renal 
colic  is  then  feared,  but  the  symptoms  do  not  increase  in  severity.  The 
urine  takes  on  a  yellow  colour,  and  a  deposit  of  uric  acid  is  found.  The 
look  of  the  water  subsequently  passed  is  cloudy,  as  though  a  few  drops  of 
ink  had  been  added.  The  brownish  urine  in  the  specimen-glass  has  a 
cloudy  look,  and  a  dark  deposit  of  uric  acid  and  blood  forms  at  the  bottom 
of  the  glass.  The  renal  congestion  may  be  accompanied  by  painful  swelling 
of  certain  joints — in  the  knee,  in  the  foot,  and  especially  in  the  big  toe. 
The  symptoms  then  cease  in  an  abortive  maimer. 

etiology — Pathogenesis. — Gout — or,  rather,  the  gouty  diathesis — may 
be  acquired,  but  it  is  hereditary  in  two-thirds  of  the  cases. 

Gouty  heredity  means  the  heredity  of  the  diathesis  as  a  whole.  Thus, 
gouty  parents  beget  children  who  may  have  all  the  other  manifestations  of 
the  diathesis  except  gout.  They  may  be  asthmatical  or  may  suffer  from 
urinary  and  biliary  lithiasis,  to  which  I  have  added  sabulous  typhlo-colitis 
and  appendicular  lithiasis,  but  yet  they  escape  articular  gout.  On  the 
other  hand,  parents  who  suffer  from  asthma,  gravel,  or  renal  troubles,  but 
who  have  never  suffered  from  the  articular  manifestations  of  gout,  beget 
children  who  are  affected  by  true  articular  gout.  These  facts  have  been 
clearly  stated  by  Trousseau. 

Gout  is  more  frequent  in  men  than  in  women.  It  is  the  appanage  of  the 
wealthy  classes,  and  it  is  probable  that  good  living,  excessive  use  of  wine, 
and  want  of  exercise  favour  its  development.  Gout  may  appear  from  an 
early  age,  but  this  is  exceptional.  The  first  attack  of  gout  occurs  earlier  when 
the  disease  is  hereditary  than  when  it  is  acquired,  and  usually  shows  itself 
between  the  ages  of  thirty  and  forty  years.  In  gouty  persons  an  injury, 
a  shock,  a  strain,  a  long  walk,  or  tight  boots  suffice  to  bring  on  an  attack. 

It  has  been  said  that  gout  is  due  to  an  excess  of  uric  acid  in  the  blood, 
but  this  uric  dyscrasia  alone  is  not  sufficient  to  explain  gout,  for  in  many 
cases  the  dyscrasia  appears  in  an  acute  state  (acute  diseases)  or  as  a  chronic 
condition  (cirrhosis,  leucocythsemia),  without  the  slightest  manifestation  of 
gout  supervening. 


1946  TEXT-BOOK  OF  MEDICINE 

According  to  Bouchard,  the  causes  of  the  exaggerated  formation  of  uric 
acid  are  of  less  importance  than  the  causes  of  its  retention  in  the  blood. 
The  latter  are  diminution  of  the  alkalinity  of  the  blood,  and  the  predomi- 
nance of  oxalic  and  lactic  acids.  The  predominance  of  acids  is  a  condition 
favouring  the  precipitation  of  the  uric  acid,  whether  in  the  free  state  or  in 
the  form  of  urates.  This  dyscrasic  condition,  with  the  predominance  of 
acid,  is  said  to  result  from  the  fact  that  in  gout  an  exaggerated  formation, 
or  too  slow  a  destruction  of  the  organic  acids,  takes  place.  It  is,  therefore, 
a  manifestation  of  delayed  nutrition. 

Diagnosis — Prognosis. — The  diagnosis  between  acute  gout  and  acute 
rheumatism  presents  no  difficulty,  but  we  cannot  say  the  same  with  regard 
to  the  chronic  forms  of  these  two  diseases.  I  have  discussed  the  explana- 
tion under  Nodular  Rheumatism.  I  must  say  that,  in  addition  to  the 
common  cases,  in  which  each  of  these  diseases  shows  its  normal  character, 
we  find  mixed  or  intermediate  cases,  in  which  gout  and  rheumatism  appear 
to  occur  together. 

The  diagnosis  of  irregular  gout  is  often  difficult.  The  patient's  ante- 
cedents must  be  inquired  into,  and  the  question  of  heredity  must  be 
examined. 

The  gravity  of  gout  depends  upon  the  possibility  of  the  complications 
of  retrocedent  gout  and  metastatic  troubles,  and  upon  the  development  of 
visceral  changes  (gouty  nephritis,  arterio-sclerosis,  fatty  degeneration,  and 
rupture  of  the  heart). 

Pathological  Anatomy. — It  may  be  said  that  the  gouty  person  is  im- 
pregnated with  uric  acid  and  urates.  The  uric  acid  is  in  excess  in  the 
blood.  It  increases  at  the  approach  of  the  attack,  and  diminishes  or  dis- 
appears for  a  time  after  it.  This  uricsemia,  however,  is  met  with  in  other 
conditions  (lead-poisoning,  albuminuria),  and  is  not  special  to  gout. 

Urate  of  soda  is  found  in  the  form  of  crystals  in  the  cartilages  of  the 
diseased  joints,  in  the  ligaments,  tendons,  and  bursse,  under  the  periosteum, 
and,  lastly,  in  the  cellular  tissue  and  in  the  skin,  where  the  accumulations 
of  urate  of  soda  receive  the  name  of  tophi. 

The  excess  of  uric  acid  in  the  blood  is  easily  demonstrated  in  the  semm 
taken  from  a  blister  or  from  dry-cupping.  In  each  case  a  few  drops  of  acetic 
acid  are  added  to  the  serum  on  a  watch-glass ;  some  threads  of  cotton  are 
placed  in  the  fluid.  After  twenty-four  hours  the  threads  are  covered  with 
crystals  of  uric  acid.  It  must  be  stated  that  during  an  attack  of  gout  the 
serous  fluid  in  a  blister  from  the  region  of  the  congested  joint  does  not  contain 
uric  acid,  while  the  serum  from  a  blister  at  any  other  point  shows  the  opposite 
condition.  We  find  urate  of  soda  in  the  secretions  of  the  gouty  person,  m 
the  serum  of  the  pleura,  or  of  the  pericardium. 

When  the  joint  lesion  is  studied  from  the  histological  point  of  view,  we 


RHEUMATIC  AND  DYSTROPHTC  DISEASES  1947 

find  that  tlio  deposits  of  urate  of  soda  which  impregnate  the  cartilages  are 
first  laid  down  around  the  cartilage  cells,  without  changing  the  structure  of 
the  cartilage.  Later,  in  chronic  gout  the  cartilages  change,  and  we  some- 
times find  the  lesions  of  arthritis  sicca,  but  the  articular  and  periarticular 
incrustations  of  urate  of  soda  predominate. 

The  incrustation  of  the  cartilages  begins  during  the  first  attack  of  gout, 
and  persists  in  the  intervals  between  the  attacks.  This  change  is  special 
to  gout,  and  is  not  found  in  any  variety  of  rheumatism.  Whether  the 
deposits  of  urates  which  occur  during  an  attack  of  gout  come  from  the 
blood  or  are  formed  in  the  tissues  of  the  joint  is  a  question  which  has  not 
been  cleared  up. 

Treatment. — The  first  care  of  the  physician  in  the  case  of  a  person  who 
is  born  of  gouty  stock,  or  who  has  presented  some  of  the  symptoms  of  the 
diathesis,  is  to  delay  or  to  prevent  the  outburst  of  the  gouty  attack.  This 
prophylactic  treatment  should,  if  possible,  commence  in  infancy,  and 
measures  to  increase  nutrition,  such  as  exercise  in  the  open  air,  cold  baths, 
rubbing,  and  massage,  should  be  ordered.  The  patient  must  be  forbidden 
to  take  large  meals,  to  eat  fatty  substances,  to  drink  fermented  liquors,  or 
to  indulge  in  excess  of  any  kind.  Alkaline  preparations  for  dyspepsia  and 
Vichy  water  should  be  taken  in  moderation. 

What  treatment,  however,  should  be  employed  in  the  attack  of  gout  ? 
Must  we  treat  the  attack,  or  must  we  leave  it  to  nature  ?  We  have  all  the 
desired  measures  at  hand  to  lessen  the  attack  or  even  to  abort  it.  The 
preparations  of  colchicum  are  wonderful  agents  in  this  respect.  Tincture 
of  colchicum  seeds,  given  in  doses  of  from  8  to  10  drops,  repeated  two  or 
three  times  a  day,  extract  of  colchicum  seeds,  and  colchicum  wine  will 
relieve  the  acute  pains  of  gout,  and  shorten  the  duration  of  the  attack. 

Similar  results  may  be  arrived  at  with  all  the  more  or  less  famous  pre- 
parations, such  as  Lartigue's  pills  and  Laville's  solution,  in  which  veratrine 
and  colchicum  are  the  chief  ingredients.  Salicylate  of  soda  in  large  doses, 
antipyrin,  alone  or  with  salicylate,  and  aspirin  may  be  efficacious. 

Such,  then,  are  the  drugs  which  may  be  employed  for  the  attack  of  gout, 
but  it  is  necessary  to  know  precisely  how  far  intervention  must  be  carried. 
Sydenham  was  careful  not  to  intervene  during  the  attacks  of  gout  to  which 
he  was  subject,  and  Trousseau  and  many  others  iiave  followed  the  advice 
of  Sydenham.  The  attack  must  be  considered  as  a  kind  of  emunctory 
which  must  be  respected,  especially  in  elderly  persons.  If  we  cut  short 
the  attack  of  gout,  we  may  expose  the  patient  to  the  terrible  complica- 
tions of  retrocedent  gout.  The  gouty  person  who  moderates  the  severity 
and  cuts  short  the  duration  of  his  attack  of  gout  does  not,  as  a  rule,  experi- 
ence the  same  after-feeling  of  health  as  does  the  gouty  patient  m  whom 
the  attack  has  run  its  ordinary  course.     He  is  more  subject  to  early  recur- 


1948  TEXT-BOOK  OF  MEDICINE 

rence,  is  more  troubled  by  other  manifestations  of  the  diathesis,  and  is  more 
exposed  to  the  conversion  of  his  disease  into  chronic  or  into  atonic 
gout. 

It  is,  therefore,  necessary  to  respect  attacks  of  acute  gout,  to  avoid  local 
measures  (leeches,  injections  of  morphia,  blisters)  which  may  suppress  the 
articular  congestion,  to  withhold  violent  purgatives  at  the  onset  of  the 
attack,  and  to  be  content  with,  mild  anodyne  treatment. 

For  the  latter  purpose,  I  employ  antipjrrin  in  doses  of  from  30  to  45 
grains  daily,  given  in  cachets,  alternated  with  cachets  of  salicylate  of  soda 
in  a  daily  dose  of  from  30  to  60  grains. 

There  are,  however,  cases  in  which  it  is  necessary  to  intervene  more 
energetically,  as  when  the  gout  tends  to  show  a  chain  of  paroxysms, 
which,  by  its  duration,  weakens  the  patient.  We  must  also  employ  ener- 
getic treatment  when  the  disease  afiects  the  organs,  "  since  nothing  worse 
than  this  can  happen,"  and  this  is  the  time  to  have  recourse  to  anti- 
gouty  medicines.  The  principles  formulated  as  to  the  danger  of  energetic 
treatment  in  an  attack  of  acute  gout  are  not  accepted  to-day  by  all  observers. 
See,  from  his  experience,  is  of  opinion  that  the  attack  of  gout  may  be  treated 
vigorously,  and  he  found  that  salicylic  preparations  gave  excellent  results, 
provided,  of  course,  that  the  condition  of  the  heart  and  kidneys  is  watched, 
and  that  we  do  not  expose  the  patient  to  incomplete  elimination  and 
accumulation  of  the  drug. 

The  hygiene  of  gouty  persons  is  similar  in  every  way  to  the  prophy- 
lactic measures  above  indicated.  To  avoid  excesses  of  every  land,  to  take 
moderate  exercise,  to  use  cutaneous  stimulants,  such  as  baths,  lotions,  or 
massage,  to  avoid  heavy  meals,  "  high  "  foods,  game,  truffles,  acid  foods 
and  drinks,  sorrel,  tomatoes,  vinegar,  and  fatty  foods,  which,  combined  with 
proteid  matter,  may  become  a  powerful  excitant  of  uricsemia.  Generous 
wines  and  alcoholic  drinks  should  be  forbidden,  and  pure  water,  with  the 
addition  of  white  wine,  or  with  cider,  must  be  the  usual  drink.  Beer  is  not 
allowed.  Alkaline  waters,  taken  after  meals  or  in  the  morning  on  an  empty 
stomach,  are  of  undoubted  value.  In  short,  the  gouty  person  must  be 
careful  during  his  whole  life.  The  cures  of  Vichy,  Carlsbad,  ContrexeviUe, 
and  Vittel  give  excellent  results. 


V.  DIABETES  MELLITUSj 

Pathogenesis. — Sugar  is  indispensable  to  life.  It  is  fixed  in  the  ana- 
tomical elements  of  the  body,  and  undergoes  changes  therein.  It  serves 
for  the  repair  of  the  tissues  ;  it  is  utilized  for  combustion,  and  is  a  source  of 
heat  and  energy. 

The  blood  normally  contains  sugar  in  proportion  of  about  1  per  1,000. 


RTIEUMATIC  AND  DYSTROPHIC  DISEASES  1949 

This  physiolof:rical  condition  is  culled  glycaemia.  (riycsornia  results  from 
the  e(|uilibriuin  which  exists  in  the  economy  between  the  supply  and 
demand  for  sugar.  By  reason  of  this  equilibrium  the  quantity  of  sugar 
remains  practically  the  same,  althouf^h  the  quantity  of  sugar  taken  with  tlie 
food  may  be  variable,  and  although  there  be  no  emunctory  for  the  excretion 
of  the  saccharine  principles. 

In  the  pathological  state,  however,  the  equilibrium  between  the  supply 
and  the  demand  for  sugar  is  disturbed  :  glycaemia  gives  place  to  hyper- 
glycsemia,  and  the  sugar  in  the  blood  amounts  to  3,  4,  or  5  parts  per  1,000  ; 
indeed,  5'3  parts  per  1,000  (Pavy^)  have  been  found — and  symptoms  of 
diabetes  appear  with  tliis  hyperglycacmia. 

The  following  problem  requires  solution  from  the  point  of  view  of  the 
pathogenesis  of  diabetes  :  By  what  means  does  normal  glycajmia  give  place 
to  pathological  hyperglycsemia  ?  In  attempting  to  answer  this  question, 
let  us  study  the  chemistry  of  the  sugar  in  the  organism — a  study  which  had 
been  absolutely  ignored  before  the  great  discoveries  of  the  illustrious 
physiologist,  Bernard. 

The  sugar  in  the  economy  and  that  in  the  blood  have  different  origins. 
In  the  first  place,  they  come  from  the  starchy  and  saccharin  material  of 
the  food — starch,  dextrin,  cane-sugar,  and  the  sugars  from  milk  and  fruits. 
These  materials,  converted  into  glucose  by  the  saliva  and  by  the  pancreatic 
and  intestinal  juices,  are  carried  by  the  portal  vein  to  the  liver.  But  they 
may  neither  remain  in  the  liver  nor  pass  through  it  in  the  condition  of 
sugar.  They  are  converted  and  fixed  there  (Pavy)  in  the  form  of  animal 
starch  or  glycogen,  which  is  converted  into  glucose,  and  is  carried  away 
in  the  hepatic  veins  (Bernard). 

Starchy  foods,  however,  are  only  one  of  the  sources  of  glycogen.  The 
albuminoid  foods  are  also  utilized  by  the  liver.  Thus,  in  animals  fed  ex- 
clusively on  meat  for  several  months  the  liver  cell  continues  to  form  glycogen 
(Bernard). 

Fats,  glycerin,  and  gelatin  also  serve  for  the  production  of  glycogen. 

Furthermore,  it  is  not  solely  from  the  recently  ingested  food  that  the 
liver  obtains  the  elements  of  glycogen,  for,  in  addition  to  the  direct  nutri- 
tion, which  is  renewed  daily  with  the  food,  we  find  an  indirect  nutrition, 
which  takes  place  at  the  expense  of  reserve  foodstuffs  previously  stored  up 
m  the  tissues  and  organs.  The  anatomical  elements  are  the  seat  of  incessant 
changes.  The  waste  of  living  cells  is  not  aU  destined  to  be  excreted  by  the 
emunctories.  The  larger  portion  of  this  waste  is  taken  up  by  the  circulation, 
and  the  liver  contains  a  part  of  the  elements  necessary  for  the  elaboration 
of  the  saccharin  principles  of  the  economy.  Glycogen  "  is  thus  an  inter- 
mediary stage  by  which  certain  substances  of  disassimilation  may  again 
oecome  assimilable  "  (Bouchard). 


1950  TEXT-BOOK  OF  MEDICINE 

Such,  then,  is  the  origin  of  glycogen  suggested  by  Bernard,  and  studied 
by  Pavy  and  Rouget  under  the  name  of  liver-starch  and  zoamilin. 

The  glycogenic  function  of  the  liver  is  comparable  to  the  fimction  of 
vegetables.  They  both  form  saccharin  material,  and  the  form(\tion  of 
starch  is  effected  in  the  whole  animal  series  by  a  mechanism  analogous  to 
that  -which  is  seen  in  the  vegetable  kingdom  (Bernard).. 

There  are  two  distinct  phenomena  in  the  formation  and  in  the  evolution 
of  the  immediate  saccharin  principle  :  (1)  The  creation  of  amylaceous 
matter  in  the  hepatic  cell — ^that  is  to  say,  secretion  of  glycogen ;  (2)  the 
chemical  phenomenon  which  produces  successive  transformations  in  this 
immediate  principle.  Glycogen  is  an  assimilation  product  of  the  hepatic 
cell.  It  is  fixed  and  stored  in  the  liver  as  a  reserve  element  of  the  economy. 
It  probably  undergoes  there  the  action  of  a  ferment  produced  in  the  liver  ; 
by  the  action  of  this  ferment  the  glycogen,  which  is  converted  into  glucose, 
passes  into  the  veins  and  into  the  whole  economy.  During  life  these  two 
orders  of  phenomena — the  formation  of  glycogen  and  its  conversion  by  the 
ferment — take  place  at  the  same  time ;  but  after  death  the  formation  of 
glycogen,  which  is  the  vital  act,  is  arrested,  while  its  decomposition  into 
secondary  products,  which  is  the  chemical  act,  continues.  And  therefore 
we  may  wash  the  liver  of  an  animal  repeatedly,  and  find  that  it  stiU 
contains  traces  of  glucose  after  successive  washings  (Bernard). 

An  attempt  has  been  made  to  generalize  the  glycogenic  function.  Rouget, 
having  found  glycogen  in  other  tissues — the  muscles,  for  example,  although 
in  small  proportions — thought  that  glycogenia  was  a  general  nutritive 
act,  and  not  a  special  function  of  the  Hver.  The  presence  of  glycogen  in 
a  large  number  of  tissues  has  not,  however,  the  importance  which  some 
would  assign  to  it.  "  These  are  phenomena  subjected  to  aU  the  eventualities 
of  alimentation,  and  to  aU  the  varieties  seen  in  the  accidental  phenomena 
of  the  economy,  which  must  be  distinguished  from  the  constant  functions  " 
(Bernard).  "  Without  doubt,  sugar  as  well  as  glycogen  exists  in  the 
muscle,  but  in  the  muscle,  left  to  itself,  the  glycogen  disappears  without 
the  sugar  increasing.  In  the  muscle,  which  contracts,  the  glycogen  dis- 
appears, and  lactic  acid  forms,  but  not  sugar.  Further,  by  contraction 
the  sugar  disappears  at  the  same  time  as  the  glycogen "  (Bouchard). 
Normal  glycogenia,  therefore,  which  is  the  constant,  invariable,  and  necessary 
function,  is  imposed  upon  the  liver,  which,  by  its  glycogenic  function, 
regulates  the  glycsemia. 

The  liver-sugar,  which  is  continually  poured  into  the  blood,  is  used 
in  various  ways.  One  part  becomes  fixed  in  the  tissues,  there  to  undergo 
fresh  changes  and  to  serve  for  their  repair.  It  is  not  exactly  known  in  what 
form  the  glucose  of  the  blood  is  fixed  in  the  tissues.  In  some  cases — as  in  the 
muscles,  for  example — it  is  probable  that  it  passes  back  again  into  glycogen. 


RHEUM ATTC  AND  DYSTROPHIC  DISEASES  lOni 

Another  part  of  tlio  sugar  servos  for  roinbustion,  for  the  functional  activity 
of  the  organs,  for  niuscuhxr  contraction,  and  becomes  an  ag(mt  of  energy 
and  heat.  Sugar  is  a  plastic  and  respiratory  food,  and  just  as  glycogen  is 
converted  into  sugar,  so  sugar  may  pass  back  into  glycogen.  The  question 
is  one  of  hydration  and  dehydration. 

Normal  glycooraia  results  from  the  equilibrium  which  occurs  in  the 
economy  between  the  supply  and  demand  for  saccharin  principles.  When 
this  equilibrium  is  upset,  and  too  much  sugar  is  produced  or  too  little  sugar 
is  used  up,  an  accumulation  in  the  blood  results.  We  have  hyperglycsemia, 
with  all  its  consequences.  An  excess  of  sugar  is  produced  if  the  liver,  by 
reason  of  functional  hyperactivity,  elaborates  too  large  a  quantity  of  glycogen, 
or  if  the  tissues  of  the  economy,  by  reason  of  an  exaggerated  disassimilation, 
furnish  an  excess  of  materials  for  glycogen.  Too  little  sugar  is  used  up 
if  the  assimilation  of  the  saccharin  principles  is  turned  aside  from  its  true 
end,  or  if  the  consumption  becomes  insufficient.  At  this  point  the  theories 
of  diabetes  commence. 

These  theories  are  very  numerous,  and  no  one  is  applicable  to  every 
case. 

According  to  Bernard,  the  question  is  one  of  degree,  between  tran- 
sient glycosuria  and  diabetes.  This  is  the  idea  which  Jaccoud  has  always 
expressed,  when  he  says  any  case  of  glycosuria  may  end  in  diabetes. 
Bernard  thinks  that  diabetes  is  due  to  an  exaggerated  production  of 
glycogen,  without,  however,  reducing  the  diabetes  to  a  simple  hyperactivity 
of  the  liver,  as  writers  have  been  too  prone  to  repeat  by  wrongly  stating 
his  theory  under  the  name  of  the  hepatic  theory.  Bernard  looked  at  the 
question  from  a  more  extensive  point  of  view,  and  admitted  the  general 
trouble  in  nutrition,  with  special  reaction  on  the  liver.  "  If,  by  a  process 
of  excessive  disassimilation,  the  organ  wastes  the  reserve  depot,  of  which 
the  liver  is  the  seat,  the  sugar  is  poured  into  the  blood  in  abnormal  quantity, 
and  hence  hyperglycaemia  and  glycosuria  appear.  The  hepatic  source, 
however,  is  not  exhausted.  It  continues  to  assimilate  the  materials  requisite 
for  the  formation  of  glycogen,  and  consequently  of  sugar.  It  redoubles 
its  activity  in  order  to  replace  the  sugar  eliminated,  and  exhausts  the 
organism  in  order  to  provide  for  this  exaggerated  demand  for  saccharin 
material." 

The  present  tendency  is  to  attribute  diabetes  to  a  general  perversion 
of  the  nutritive  processes,  without  giving  the  liver  the  importance  which 
was  assigned  to  it  by  Bernard.     Are  we  on  the  right  track  ?  • 

This  perversion  of  the  nutritive  processes  has  been  variously  inter- 
preted. According  to  some  authorities,  there  is  an  abnormal  decomposition 
of  tissue,  by  which  an  excess  of  glycogen  is  set  free.  According  to  other 
authorities,  it  is  the  normal  glycogen  which  is  not  sufficiently  used  up  by 


1952  TEXT-BOOK  OF  MEDICINE 

tie  economy,  because  of  the  diminution  in  tlie  glycolytic  ferment  (Lepine) ; 
thence  arises  the  residue  and  excess  of  glycogen. 

The  former  theory  admits  the  decomposition  of  the  proteid  substances  into 
glycogen  and  urea  (Jaccoud).  According  to  the  other  theory,  the  sugar  is  not 
properly  burnt  up  (Mialhe)  in  the  tissues,  or  the  ferment  which  effects  the 
decomposition  of  sugar  is  wanting.  According  to  Bouchard,  the  nutritive 
trouble  which  leads  to  diabetes  is  characterized  "  primarily  and  essentially 
by  a  lack  or  insufl&ciency  of  assimilation,  and  in  particular  by  an  absence  of 
the  consumption  of  the  sugar  in  the  anatomical  elements."  The  excess  of 
sugar  which  is  not  utilized  accumulates  in  the  blood,  and  hyperglycsemia 
results.  Diabetes  would  therefore  enter  into  the  class  of  morbid  conditions, 
due  to  a  "  slackening  in  the  nutrition."  This  slackening  of  the  nutritive 
processes  affects  the  elaboration  of  sugar  and  constitutes  diabetes,  just  as 
it  favours  biliary  or  renal  lithiasis  and  obesity,  when  it  depends  on  the 
defective  elaboration  of  cholesterin  or  nitrogenous  matter  and  of  fat. 

At  the  present  time  the  hepatic  theory  of  diabetes  has  somewhat  returned 
to  favour  (Glenard,  Triboulet).  Hyperhepatia  appears  to  account  for 
diabetes  in  undeniable  cases  where  the  liver,  whether  hypertrophied  or  not, 
not  does  present  any  lesions  (Gilbert  and  P.  LerebouUet). 

In  Germany  a  renal  theory  of  diabetes  exists  (Klemperer).  The  discovery 
of  phloridzin-glycosuria  has  appeared  to  give  it  a  certain  basis,  but  we  must 
await  fresh  researches. 

.etiology. — Diabetes  may  be  divided  into  essential  and  symptomatic 
(Lecorche).     The  so-called  symptomatic  diabetes  is  rarely  a  true  diabetes. 

Symptomatic  diabetes  of  nervous  origin  is  sometimes  caused  by  lesions 
of  the  bulb  and  of  the  brain,  such  as  tumours  of  the  fourth  ventricle, 
traumatism  of  the  occipital  region,  general  concussion  from  carriage  or 
railway  accidents.  These  lesions  produce  glycosuria  more  often  than 
diabetes.  In  other  cases  diabetes  is  associated,  not  so  much  with  a  lesion 
of  the  nervous  centres,  as  with  a  neujosis  (epilepsy,  paralysis  agitans). 

One  form  of  symptomatic  diabetes  is  partly  associated  with  lesions 
of  the  liver  or  of  the  pancreas.  We  shall  see  later  what  opinion  should  be 
held  of  bronzed  diabetes,  associated  with  a  certain  form  of  hepatic  cirrhosis. 

Changes  in  the  pancreas  are,  according  to  Lancereaux,  the  origin  of  a 
wasting  diabetes.  This  pancreatic  diabetes,  resulting  from  functional 
inactivity  of  the  pancreas,  has  as  its  special  characters  early  appearance 
of  intestinal  troubles,  frequent  fatty  stools,  and  rapid  wasting.  I  shall  refer 
to  it  under  the  Symptoms  of  Diabetes. 

•Malarial  fever  appears  to  play  some  part  in  the  development  of  glycosuria 
and  of  diabetes  (Burdel,  Vemeuil). 

Essential  or  true  diabetes  is  hereditary  or  acquired.  Heredity  is 
manifested  when  the  diabetes  appears  in  children  born  of  diabetic  parents. 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  1053 

between  the  ages  of  six  months  and  one  to  two  years.  In  the  great  majority 
of  cases  diabetes  is  associated  with  the  gouty  diathesis,  or  with  a  nervous 
heredity. 

To  the  arthritic  source  belong  the  various  manifestations  which  Bazin 
has  collected  under  the  name  of  arthritism,  and  which  Bouchard  has 
described  under  the  name  of  disease  caused  by  slackening  of  nutrition. 
In  this  group  we  find  gout,  asthma,  rheumatism,  gravel,  gall-stones,  obesity, 
and  diabetes.  Manifestations  of  this  morbid  group  are  frequently  met  with 
in  the  same  individual  or  in  the  same  family.  They  are  transmissible  by 
heredity,  and  may  undergo  changes  in  their  transmission.  Thus  a  gouty 
individual  who  has  or  has  not  had  diabetes  himself  begets  children  who 
suffer,  on  the  one  hand,  from  diabetes,  and,  on  the  other  hand,  from  asthma, 
gout,  or  calculi.     These  cases  are  extremely  frequent. 

To  the  nervous  source  belongs  the  diabetes  which,  in  the  same  family, 
is  associated  with  dementia,  epilepsy,  hysteria,  tabes,  general  paralysis, 
or  exophthalmic  goitre.  I  have  often  found  this  nervous  heredity,  with  its 
mutations.  It  is  sufficient  to  glance  at  the  table  of  statistics  published  on 
this  subject  to  see  the  frequency  of  this  nervous  association,  with  its  heredi- 
tary mutations.  To  quote  examples  :  An  epileptic  father  had  five  children, 
of  whom  four  were  epileptics  and  one  diabetic.  A  diabetic  father, 
who  died  from  diabetic  coma,  had  three  children :  the  first  diabetic, 
the  second  tabetic,  and  the  third,  for  the  time  being,  free.  A  grand- 
mother of  unsound  mind  had  a  nervous  daughter,  who  begot  an  epileptic 
son  and  a  diabetic  daughter.  I  may  repeat  that  the  most  usual  origins  of 
hereditary  diabetes  are  the  arthritic  and  the  nervous  sources,  which  are 
sometimes  united.  In  other  cases  diabetes  is  acquired,  although  it  may  be 
difficult  to  establish  the  pathogenesis. 

The  social  position  has  a  great  influence  upon  the  development  of 
diabetes.  Worms  has  published  interesting  statistics  on  this  subject. 
He  found  that  the  urine  in  607  persons  doing  heavy  manual  work,  which, 
as  a  rule,  demands  great  muscular  and  respiratory  activity,  did  not  contain 
sugar  in  appreciable  doses.  Of  those  given  to  more  or  less  severe  intellectual 
labour — such  as  scientists,  physicians,  artists,  and  statesmen — he  found 
glycosuria  in  10  per  cent.  In  these  persons  repeated  analyses  have  proved 
that  the  condition  is  not  one  of  simple  alimentary  or  transitory  glycosura, 
but  rather  a  true  diabetes. 

A  conjugal  form  of  diabetes  has  been  described,  the  husband  and  the 
wife  both  sufiering  from  the  disease.  Lecorche  has  seen  conjugal  diabetes 
six  times  in  114  cases.  Debove  has  seen  it  five  times  in  fiity-nine  cases. 
Marie  has  published  a  very  interesting  case.  Several  theories  have  been 
proposed  to  explain  conjugal  diabetes.  Teissier  is  inclined  to  believe  in 
contagion,  but  other  authors  invoke  the  similarity  of  the  mode  of  life  in 


1954  TEXT-BOOK  OF  MEDICINE 

Kusband  and  wife,  wlio  are  nourished  in  the  same  manner,  participate  in 
the  same  occupations,  in  the  same  mode  of  existence,  and  in  the  same 
vicissitudes. 

The  onset  is  usuaUj  insidious,  and  many  persons  pass  an  ounce  of  sugar 
daily  without  knowing  it — that  is  to  say,  they  are  diabetic  for  months  or 
for  years  before  the  warning  symptom  appears.  Sometimes  this  symptom 
is  striking  :  the  thirst  is  acute  and  the  urine  is  abundant,  or  perhaps  a  car- 
buncle appears,  and  the  patient  is  himself  put  on  the  track  of  the  diagnosis 
by  this  warning  symptom  (Jaccoud),  The  warning  symptom  in  diabetes, 
however,  is  often  quite  different.  The  patient  complains  of  obstinate 
balanitis,  of  sexual  incapacity,  of  visual  troubles  (amblyopia),  of  gingivitis, 
or  of  falling  out  of  the  teeth,  of  itching,  of  neuralgia,  or  of  muscular  pains. 
One  patient  wastes,  another  loses  strength  without  apparent  cause.  Women 
frequently  suffer  from  pruritus  vulvae,  with  or  without  eczema.  In  the 
presence  of  these  various  symptoms,  although  the  thirst  is  not  exaggerated, 
the  urine  should  always  be  analyzed,  and  diabetes,  the  hidden  cause  of  these 
troubles,  is  often  discovered,  to  the  great  astonishment  of  the  patient. 

In  order  to  draw  attention  to  these  symptoms,  I  have  grouped  them  under 
the  name  of  the  minor  symptoms  of  diabetes.  They  are  comparable  to 
the  minor  symptoms  of  Brightism,  and,  like  them,  they  are  apparently 
of  small  importance.  So,  too,  they  pass  unnoticed  in  those  who  do  not 
know  of  them,  and  yet  in  both  cases,  if  they  are  well  known,  they  give  an 
immediate  clue  to  the  diagnosis. 

Salivary  Symptoms. — In  the  diabetic  patient  the  saliva  is  acid,  because 
of  the  presence  of  lactic  acid,  produced  by  the  fermentation  of  the  sugar. 
The  Leptothrix  huccdis  finds  an  excellent  culture  medium  therein.  As  the 
result  of  these  new  conditions,  the  mouth  becomes  dry  (it  is  noticed  when 
speaking),  the  tongue  becomes  pasty  and  studded  with  papillse,  the  gums 
soften  and  bleed  easily  (noticed  on  cleaning  the  teeth).  In  some  cases 
alveolo-dental  periostitis  appears  (expulsive  gingivitis),  and  causes  displace- 
ment, loosening,  and  falling  out  of  the  teeth.  These  various  symptoms, 
which  may  be  isolated  or  associated,  and  which  are  sometimes  incomplete, 
often  permit  the  discovery  of  diabetes  in  persons  who  have  neither  polyuria 
nor  polydipsia,  and  who  have  no  idea  of  theic  condition. 

Ocular  Symptoms. — I  do  not  allude  here  to  diabetic  cataract,  which 
is  a  symptom  of  the  highest  importance,  and  cannot  escape  notice ;  nor 
do  I  aUude  to  ocular  paralysis,  or  to  lesions  of  the  fundus  oculi.  We  shall 
have  to  consider  them  later  among  the  complications.  I  aEude  to  those 
apparently  insignificant  troubles,  which  consist  in  weakness  of  the  sight, 
following  diminution  in  the  power  of  accommodation  (premature  presbytia). 
"  A  healthy  man  teUs  you  that  his  sight,  previously  good,  has  become 
markedly  weak ;  that  for  some  time  he  has  been  obliged,  when  reading, 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  1955 

to  hold  the  book  at  a  diatauce,  and,  later,  to  employ  HpectaclcH  ;  tliat 
he  has  been  forced  to  change  his  glasses  every  month  for  stronger  ones. 
This  fact  alone  will  give  us  cause  to  ask  whether  the  patient  has  albuminuria 
or  diabetes.  In  default  of  other  symptoms  which  may  not  exist,  this  one 
will  show  you  the  way,  and  the  examination  of  the  urine  will  clear  up  the 
diagnosis  "  (Trousseau). 

Cutaneous  Symptoms. — Here,  again,  I  do  not  allude,  of  course,  to  the 
most  marked  symptoms,  such  as  carbuncles  or  eruption  of  boils,  which  at 
once  point  to  diabetes ;  I  speak  of  more  trifling  symptoms,  which,  for  tliis 
reason,  deserve  to  take  a  place  among  the  minor  troubles  of  diabetes.  We 
find,  on  the  one  hand,  severe  general  pruritus,  in  which  no  cutaneous 
eruption  is  present,  but  which  is  so  obstinate  as  to  dishearten  the  patient. 
On  the  other  hand,  we  find  eczema,  which  may  be  limited  to  the  genitalia, 
and  which  produces  most  severe  itching.  An  attentive  observer  has,  from 
these  symptoms,  recognized  diabetes  in  persons  who  had  neither  polyuria 
nor  excessive  thirst. 

Nervous  Symptoms. — Nervous  symptoms  are  met  with  at  every  turn 
in  the  history  of  diabetes.  I  shall  here  content  myself  with  reviewing  the 
milder  symptoms,  which  are  of  an  indefinite  character.  Many  persons,  in 
the  absence  of  a  thorough  examination,  are  said  to  be  sufiering  from  melan- 
cholia, neurasthenia,  or  other  neurosis,  when  they  are  really  sufiering  from 
diabetes.  One  patient  complains  of  lassitude,  for  which  he  can  give  no 
reason.     He  becomes  lazy,  and  everything  tires  him. 

Another  patient  complains  of  muscular  pains,  lumbago,  pleurodynia, 
sciatica,  and  hyperaesthesia  ;  and  the  condition  is  put  down  to  rheumatism 
instead  of  diabetes. 

A  third  patient  has  sensory  troubles  in  the  lower  limbs,  and  a  syringo- 
myelic dissociation  of  sensibility,  which  at  first  gives  the  idea  of  some 
disease  of  the  spinal  cord  (Vergely). 

A  fourth  patient  sufiers  from  psychical  symptoms,  loss  of  memory, 
tendency  to  sleep,  inaptitude  for  work — symptoms  put  down  to  the  onset 
of  a  cerebral  lesion,  when  they  are  really  due  to  diabetes. 

Genital  Symptoms. — Age  or  excesses  are  too  often  held  to  account 
for  sexual  weakness  which  is  due  to  diabetes. 

Urethritis,  balanitis,  and  phimosis  belong  to  the  diabetic  manifestations 
which  are  especially  obvious.  The  prolonged  contact  of  a  few  drops  of  altered 
urine  and  the  acetic,  alcoholic,  lactic,  and  butyric  fermentation  in  the 
saccharin  urine,  and  the  possible  appearance  of  smaU  fungi,  analogous  to 
the  aspergillus  (Friedrich),  explain  these  genital  diabetides.  The  urethritis, 
localized  to  the  anterior  part  of  the  urethra,  causes  a  whitish  or  colourless 
discharge,  accompanied  by  acute  pruritus,  and  too  often  mistaken  for 
gonorrhoea.     Sometimes  the  glans  is  red  and  swollen,  and  we  find  balanitis, 


1956  TEXT-BOOK  OF  MEDICINE 

which  may  last  for  months  without  the  patient  suspecting  the  cause.  The 
prepuce  is  often  red,  inflamed,  and  covered  with  ulcerated  vesicles,  which 
resemble  those  of  herpes,  and  are  painful  on  contact  with  the  urine.  A 
degree  farther  and  phimosis  appears.  Many  patients  who  have  diabetes, 
urethritis,  and  balanitis  do  not  speak  of  it,  because  they  think  that  they  are 
suffering  from  sjrphilis,  and  the  condition  goes  on  to  phimosis.  If  they 
consult  an  inexperienced  physician,  the  nature  of  the  phimosis  is  misunder- 
stood, and  an  operation  is  advised,  which  may  lead  to  grave  results  (because 
the  patient  has  diabetes),  when  medical  treatment  would  have  relieved 
the  condition,  even  though  it  is  of  long-standing.  With  Terrier  I  saw  a 
diabetic  patient  in  whom  phimosis  of  two  months'  duration  was  cured  by 
diet  and  medical  treatment. 

Such  are  the  minor  troubles  of  diabetes,  which,  either  grouped  or 
isolated,  may  give  the  diagnosis  in  the  absence  of  the  more  important  re- 
vealing signs. 

The  initial  period  of  diabetes,  which  is  more  or  less  latent,  lasts  as  long 
as  the  diabetes  is  moderate.  If  the  sugar  increase,  the  disease  shows 
itself  by  symptoms  which  may  be  more  or  less  marked,  but  which  are  rarely 
wanting.  These  symptoms  include  unusual  dryness  of  the  mouth  and 
throat,  unquenchable  thirst,  and  abundant  urine,  which  presents  special 
characters.     These  symptoms  will  now  be  described  in  detail. 

{a)  Glycosuria,  or  the  presence  of  sugar  in  the  urine,  depends  upon  hyper- 
glycsemia.  In  the  normal  condition  the  sugar  in  the  blood  (1  per  1,000) 
has  no  tendency  to  pass  into  the  urine,  but  as  soon  as  the  hyperglycsemia 
reaches  2 '50  per  1,000  glycosuria  appears.  The  passage  of  sugar  in  the 
uriue  is  favoured  by  the  quantity  of  water  which  the  sugar  takes  up  from 
the  blood,  each  gramme  of  sugar  fixing  7  grammes  of  water.  In 
extreme  cases  the  quantity  of  water  taken  up  into  the  blood  may  reach 
400  grammes. 

At  the  onset  of  the  disease  the  glycosuria  is  transient  and  intermittent. 
In  ordinary  cases  the  quantity  of  sugar  passed  in  the  twenty-four  hours 
is  from  25  to  60  grammes.  It  may  exceed  1,000  grammes  in  very  severe 
forms  of  diabetes.  "  If  there  is  hypergenesis,  the  quantity  of  sugar  lost 
within  twenty-four  hours  is  truly  without  limit,  and  it  has  no  other  boundaries 
than  those  of  the  abnormal  formation,  which  may  be  double,  treble,  or 
quadruple  the  physiological  formation.  This  quantity  may  be  fixed  approxi- 
mately at  200  grammes  a  day  (Jaccoud).  The  glycosuria  is  increased  by 
taking  saccharin  and  farinaceous  foods.  When  we  suppress  these  foods,  the 
glycosuria  improves  or  disappears  if  the  diabetes  is  slight ;  in  grave  cases 
the  glycosuria  persists.  This  caused  Jaccoud  to  say  that  in  the  first  stage 
the  diabetic  makes  sugar  from  starchy  food.  At  a  more  advanced  period 
he  elaborates  sugar  from  his  own  tissues  (autophagia).     Sugar  may  dis- 


RHEUMATIC  AND  DYSTROPHIC  DISIOASES  1057 

appear  inomeritiirily  from  the  urinn  as  a  result  of  an  inflammation  or  of  a 
febrile  disease.     It  diminishes  markedly  in  the  consumptive  stage. 

In  diabetes  the  quantity  of  sugar  passed  from  day  to  day  is  extremely 
variable,  apart  from  variations  in  diet  and  hygiene.  Worms  has  clearly 
shown  this  variability  in  the  quantity  of  sugar  passed.  As  a  matter  of  fact, 
no  fixed  relation  exists  between  these  quantities. 

A  diabotic  patient  goes  to  his  doctor  and  says  "  I  pass  52  grammes  of  sugar  "  aa 
unconcornodly  as  ho  would  say  I  am  fifty-two  years  old,  and  ho  shows  an  analysis 
giving  this  amount.  The  urine  is  examined,  and  is  found  to  contain  10  or  80  grammes 
of  sugar.  On  the  evening  before  we  might  have  found  20  or  10  grammes,  and  on  the 
no.xt  day  we  might  find  perhaps  2  or  75  grammes  (Worms).  I  have  often  seen  diabetic 
patients  who  thought  themselves  ill  because  they  had  had  their  urine  analyzed  two 
or  three  days  apart  in  different  laboratories.  They  had  come  to  their  physician  and 
told  him,  with  some  emphasis  :  "  I  have  had  my  water  examined  by  two  analysts — 
one  found  IS  grammes  and  the  other  45.  One  of  the  two  is  quite  in  the  wrong."  It  is 
not  the  analyst  who  has  made  a  mistake,  but  the  patient,  who  wrongly  interprets  the 
facts.  The  glycosuria  may  be  absolutely  different  on  different  days.  The  urine  passed 
after  meals  contains  the  largest  quantity  of  sugar. 

The  urine  is  colourless,  acid,  and  of  a  specific  gravity  which  increases 
from  1018,  the  normal  amount,  to  10.32  or  1060,  because  of  the  dissolved 
sugar.  We  often  find  marked  increase  of  the  urea  (60  grammes  instead  of 
25  grammes),  of  the  chlorides  (36  grammes  instead  of  10  grammes),  and  of 
the  phosphoric  acid  (10  grammes  instead  of  2  grammes). 

Diabetic  sugar  is  practically  analogous  to  vegetable  glucose.  It  turns 
polarized  light  to  the  right,  but  it  disappears  more  quickly  than  vegetable 
glucose  when  it  is  injected  into  the  blood.  It  is  easy  to  discover  the  sugar 
in  the  urine.  The  reagent  most  used  is  Fehling's  solution,  which  yields 
a  red  or  orange-yellow  precipitate  on  boiling.  Quantitative  analysis  is 
made  by  means  of  the  saccharometer. 

Diabetic  urine,  in  contact  with  linen  or  with  clothes,  often  leaves  dusty 
spots  when  it  dries. 

(6)  Polyuria  (abundance  of  urine)  accompanies  glycosuria,  but  does  not 
exactly  follow  the  variations  of  the  latter.  It  is  probably  due  to  an  excess 
of  intravascular  tension  caused  by  the  water  in  the  blood.  The  diabetic 
who  passes  50  grammes  of  sugar  in  the  twenty-four  hours  may  not  pass 
more  than  2  litres  of  urine.  The  polyuria  rarely  reaches  10  to  12  litres, 
and  is  less  than  in  diabetes  insipidus. 

(c)  Polydipsia  (increase  of  thirst)  is  associated  with  the  preceding  symp- 
toms. Hyperglycsemia,  by  modifying  the  normal  conditions  of  osmosis, 
attracts  water  from  the  tissues  to  the  blood.  This  dehydration  produces 
thirst,  dryness  of  the  mouth  and  throat,  and  diminution  of  the  pulmonary 
and  cutaneous  excretions.  It  probably  enters  largely  into  the  production 
of  the  cutaneous,  muscular,  and  nervous  troubles.  Certain  diabetics 
n.  124 


1958  TEXT-BOOK  OF  MEDICINE 

who  sufier  from  incessant  thirst,  drink  20  to  30  pints  of  fluid,  in  the  twenty- 
four  hours.  The  polydipsia  is,  however,  less  in  diabetes  meUitus  than  in 
diabetes  insipidus. 

Some  patients  pass  large  quantities  of  sugar  in  the  urine,  and  yet  their 
thirst  is  practically  normal. 

{d)  Polyphagia  (increased  appetite),  which  is  less  constant  than  poly- 
dipsia, depends  upon  the  marked  loss  of  sugar,  salts,  and  urea  by  the 
organism.  This  exaggeration  of  the  appetite  compensates  for  a  time  the 
losses  sustained  by  the  diabetic,  and  some  persons  remain  well  nourished. 
After  a  time,  however,  dyspeptic  troubles  supervene,  the  enormous  quantity 
of  food  taken  is  not  digested,  the  wasting  progresses,  and  the  period  of 
cachexia  commences. 

Pancreatic  diabetes,  which  is  one  of  the  forms  of  wasting  diabetes, 
appears  suddenly,  without  prodromata.  The  patient  can  state  the  month, 
and  even  the  day,  on  which  the  first  symptoms  appeared  (Lapierre). 
This  sudden  onset  is  marked  by  gastro -intestinal  troubles  (vomiting  and 
abundant  diarrhoea),  by  jaundice,  or,  lastly,  by  lumbar  and  epigastric  pains. 
The  usual  and  cardinal  signs  of  diabetes  appear  rapidly,  and  the  disease  is 
severe  from  the  first  (Lancereaux). 

The  polyphagia,  and  especially  the  polydipsia,  are  marked.  The  thirst 
is  unquenchable,  and  the  hunger  is  generally  very  great.  Polyuria  is 
excessive,  and  patients  pass  5,  10,  or  15  litres  of  clear  urine  in  the  twenty- 
four  hours.  The  specific  gravity  is  almost  always  over  1030.  The  glycos- 
uria may  exceed  1,000  grammes  a  day,  and  the  enormous  quantity  of 
1,800  grammes  of  sugar  has  been  noted.  It  is  diminished  neither  by  diet 
nor  by  treatment.  This  glycosuria  is,  in  exceptional  cases,  accompanied 
by  lipuria  (Thirolat),  rarely  by  albuminuria,  but  constantly  by  azoturia 
(Lancereaux),  independent  of  nourishment  and  general  treatment. 

The  general  condition  is  rapidly  and  profoundly  afiected.  The  wasting, 
which  always  appears  early,  results  in  extreme  emaciation ;  the  incessant 
loss  of  sugar  and  of  urea  produce  a  true  autophagism.  The  skin  becomes  dry, 
wrinkled,  and  scaly,  while  the  hair  and  the  nails  usually  fall  out.  The 
strength  diminishes  from  day  to  day.  Fatigue  renders  walking  at  first 
distressing,  and  later  impossible.  The  exhausted  patient  often  suffers  from 
profuse  diarrhcea,  which  is  horribly  foetid  and  sometimes  fatty.  A  profound 
state  of  cacheida,  with  some  pyrexia,  soon  follows,  and  in  the  immense 
majority  of  cases  death  is  caused  by  pulmonary  tuberculosis,  the  natural 
end  of  this  form  of  diabetes.     Coma  is  rare. 

The  course  of  pancreatic  diabetes  differs  from  that  of  constitutional 
diabetes.  The  disease  does  not  last  for  ten,  twenty,  or  thirty  years,  but 
runs  its  course,  on  an  average,  in  two  years,  though  death  may  supervene 
in  a  few  months.     The  gravity  of  the  prognosis  is  therefore  self-evident. 


RHEUMATIC  AND  DYSTROPJIIG  DISEASES  I'.ir.O 

Complications. 

The  secondary  or  inconstant  symptoms  and  tbc  complications  which 
may  supervene  iin  the  course  of  diabetes  are  so  numerous  and  varied  that  it 
is  necessary  to  divide  them  into  groups. 

Cutaneous  Symptoms. — Retraction  of  the  palmar  fascia  is  often 
seen.  The  skin  is  rough  and  dry ;  eczema,  simple  or  gangrenous  ecthyma 
(Hardy) ;  erythema  of  the  vulva  and  of  the  groin  ;  intertrigo  of  the  labial 
commissure  (Hardy) ;  friability  of  the  nails ;  and  preputial,  vulvar,  or 
cutaneous  pruritus  are  frequently  seen.     Zona  has  been  noted  by  Vergely. 

Carbuncle,  Cellulitis,  Gangrene.— Boils,  carbuncles,  cellulitis,  and 
diabetic  gangrene  may  appear  as  early  or  late  complications.  They  may  be 
seen  in  patients  who  do  not  pass  more  than  30  to  60  grammes  of  sugar  daily. 

Moreover,  diabetes  induces  a  liability  to  parasitism.  The  lung  of  a 
diabetic  patient  is  a  favourable  medium  for  the  tubercle  bacillus.  The  skin 
and  cellular  tissue  are  readily  invaded  by  the  microbes  of  suppuration. 
The  multiplication  of  these  microbes,  which  have  most  often  entered  through 
a  graze  or  through  a  scratch  in  the  skin,  is  singularly  favoured  by  the  presence 
of  sugar  in  the  tissues  (Bujvid).  Necrosis  and  gangrene  result  from  circu- 
latory troubles,  but  the  saprogenic  microbes  frequently  assist  in  the  develop- 
ment of  inflammatory  moist  gangrene. 

Boils  and  carbuncles  are  very  frequent  in  diabetes. 

The  carbuncle  is  almost  always  single,  and  is  situated  on  the  nape  of 
the  neck,  on  the  back,  or  on  the  buttock.  Its  onset  is  insidious,  without 
sharp  reaction  or  acute  pain.  It  may  be  complicated  by  gangrene  and 
cellulitis,  but  yet  it  recovers  fairly  often  after  elimination  of  the  sloughs. 
In  123  cases  of  diabetes  Marchal  saw  carbuncles  on  seventeen  occasions. 
Cellulitis,  which  is  quite  as  frequent  as  carbuncle,  is  rarely  primary ;  but  a 
simple  scratch,  a  prick  (Verneml),  erysipelas,  or  some  wound,  may  in  a 
diabetic  become  the  starting-point  of  the  cellulitis. 

Diabetic  cellulitis  does  not  present  the  acute  reaction  of  a  true  inflam- 
mation. It  is  often  diffuse,  and  may  end  in  gangrene  of  the  cellular  tissue 
or  in  phagedsena,  with  fatal  infection  and  adynamia.  The  cellulitis  may 
appear  at  any  period  of  the  disease,  although  it  usually  occurs  at  a  late 
stage.  It  develops  with  such  rapidity  that  it  demands  the  greatest  atten- 
tion on  the  part  of  the  surgeon  who  is  performing  an  operation  on  a  diabetic 
patient.     Intervention  is,  however,  necessary. 

Inflammations  in  diabetic  patients  show  a  notable  tendency  to  end  in 
gangrene,  both  in  cases  of  visceral  and  cutaneous  lesions  (lung,  tonsils, 
genital  organs).  Sometimes,  indeed,  the  initial  inflammatory  stage  presents 
such  a  shght  reaction  that  only  gangrene  appears  to  be  present ;  but,  in 
addition  to  these  gangrenous  troubles,  which  appear  to  be  secondary,  and 

124—2 


1960  TEXT-BOOK  OF  MEDICINE 

which  foUow  pneumonia,  carbuncle,  erysipelas,  or  other  causes,  we  find  in 
the  diabetic  a  primary  gangrene  which  is  somewhat  similar  to  the  so-caUed 
senile  gangrene. 

Diabetic  gangrene  chiefly  afiects  the  lower  limbs,  and  may  assume 
various  forms.  In  some  cases  it  is  dry  and  superficial.  It  chiefly  invades 
the  toes  in  the  form  of  painful  erythematous  patches,  which  are  sometimes 
symmetrical.  The  patches  end  in  dark  eschars,  which  may  heal  or  may 
extend,  causing  mummification  of  large  areas  of  skin.  Gangrenous  patches 
may  also  appear  on  other  parts  of  the  body. 

In  some  cases  the  gangrene  invades  aU  the  tissues  of  the  limb.  The 
toes  are  painful,  the  skin  becomes  bluish  and  cold,  oedematous  swelling 
appears,  blebs  form,  sanious  fluid  flows  away,  and  the  eschar  invades  the 
deep  parts,  laying  bare  the  muscles  and  the  tendons. 

The  pathogenesis  of  this  gangrene  is  multiple.  We  may  incriminate 
arteritis  obliterans,  blood  conditions,  the  lower  resistance  of  the  diabetic 
tissues,  and  the  presence  of  saprogenic  and  pyogenic  microbes.* 

Gangrene  of  the  penis  is  a  more  rare  complication.  It  sometimes  runs 
a  fulminant  course. 

(Edema  in  the  course  of  diabetes  has  various  origins.  It  may  result 
from  concomitant  albuminuria,  from  venous  thrombosis,  or  from  cachexia. 
In  other  cases  it  runs  a  rapid  course,  and  is  probably  of  neurovascular 
origin  (See). 

Perforating  Ulcer. — Among  the  trophic  troubles  of  diabetes  I  may 
specially  mention  perforating  ulcer  of  the  foot.  As  we  shall  see  later,  the 
disease  may  limit  its  action  to  the  soft  parts,  but  in  other  cases  it  attacks  the 
bones  and  joints.     A  benign  and  a  grave  form  may,  therefore,  be  described. 

In  a  diabetic  patient  perforating  ulcer  of  the  foot  may  appear  under- 
neath the  little  toe  and  at  the  heel,  but  its  seat  of  election .  is  beneath  the 
big  toe.  The  onset  is  usually  painless,  and  the  condition  resembles  a  corn. 
This  corn  exfoliates,  a  pustule  forms,  and  is  gradually  followed  by  an  ulcer. 
The  ulcerated  parts  are  painless,  and  a  zone  of  anaesthesia  is  sometimes 
found.  The  patient  takes  some  precautions,  but  continues  to  walk  about, 
and  the  perforating  ulcer  thus  lasts  for  months  and  years.  The  ulceration 
recovers  under  influence  of  rest  and  of  treatment,  but  is  subject  to  recur- 
rences. The  above  is  the  benign  form  of  perforating  diabetic  ulcer.  The 
soft  parts  alone  are  afiected.  The  skeleton  is  intact,  and  we  find  neither 
gangrene  nor  secondary  infection. 

The  disease,  however,  does  not  always  run  this  course.     In  some  cases 

perforating  ulcer  spreads  deeply,  afiecting  the  bones  and  joints.     It  gives 

rise  to  necrosis,  and  results  in  sequestra — fistulee,  ankylosis,  and  deformity 

of  the  afiected  parts.     In  other  cases  perforating  ulcer  is  associated  wiih 

*  Vide  Appendix,  "  Treatment  of  Gangrene  with.  Superheated  Air." 


rJIEUMATIC  AXI)  DYSTItorirrC  DISEASES  19G1 

socondary  iiifocLious — suppuniLiou,  gangrene,  ct'llulilis,  and  erysipelas. 
This  fact  proves  that  the  prognosis  of  perforating  nicer  in  diabetes  must 
be  given  with  reserve. 

The  perforating  ulcer  in  diabetes  must  not  be  confounded  with  that 
seen  in  tabes.  In  the  former  case  it  accompanies  symptoms  of  diabetes  ; 
in  the  latter,  those  of  tabes. 

Digestive  Troubles. — In  the  diabetic  the  mouth  is  dry,  the  salivary 
secretion  is  diminished,  the  tongue  is  thickened,  red,  sometimes  pilous  or 
cracked.  The  pilous  appearance  is  due  to  an  exaggerated  proliferation  of 
the  epithelium  which  surrounds  the  papillaj.  Dental  caries  is  frequent, 
and  is  the  result  of  alveolo-dental  periostitis.  The  teeth,  although  healthy, 
are  pushed  out  from  the  alveoli  (Magitot).  These  phenomena  are  due  to 
changes  in  the  saliva,  and  probably  to  the  presence  of  an  acid  derived  from 
the  fermentation  of  the  sugar. 

Dyspepsia  is  rare — or,  at  least,  slow  to  appear — in  spite  of  the  quantity 
of  fluid  taken  by  the  patient.  The  liver  is  fairly  often  hypertrophied,  and  in 
some  cases  shows  the  lesions  of  pigmentary  cirrhosis  described  elsewhere. 

Ocular  Troubles. — We  have  already  noted  the  diminution  in  the  power 
of  accommodation.  Let  us  also  note  paresis  of  the  sphincter  (mydriasis). 
The  cornea  is  sometimes  affected  (neuroparalytic  keratitis,  ulcerations  of 
the  cornea).  The  iris  is  often  attacked  (iritis — sometimes  plastic,  sometimes 
with  hypopyon). 

Cataract  is  one  of  the  more  frequent  and  more  important  complications 
of  diabetes.  It  is  usually  double.  While  it  is  soft  in  young  patients,  it 
does  not  differ  in  the  elderly  from  the  ordinary  senile  cataract.  Its  course 
varies  in  rapidity  according  to  the  severity  of  the  diabetes. 

The  fundus  oculi  may  also  be  affected.  Diabetic  retinitis  is  charac- 
terized by  more  or  less  extensive  haemorrhages,  and  by  exudation  in  the 
form  of  white  rounded  spots  scattered  over  the  retina.  Contrary  to 
retinitis  in  Bright's  disease,  the  spots  are  not  formed  of  large  patches,  and 
do  not  assume  a  star  shape  around  the  macula.  The  affection  is  sometimes 
complicated  by  white  atrophy  of  the  optic  nerve ;  this  atrophy  marches 
progressively,  and  is  not  preceded  by  oedema  of  the  papillse.  The  atrophy 
may  exist  alone,  independent  of  glycosuric  retinitis  (Lecorche).  Lastly, 
we  sometimes  see  transient  amblyopia,  which  is  not  accompanied  by  ophthal- 
moscopic lesions.  It  is  transient,  and  appears  to  be  due  to  troubles  of 
innervation. 

Paralysis  of  the  Motor  Muscles  of  the  Eye.— I  have  devoted  to  these 
paralyses  a  clinical  lecture,  of  which  the  following  is  the  summary  :  I  have 
been  able  to  coUect  74  cases  of  paralysis  of  the  oculo-motor  nerves  in 
diabetics — to  wit,  45  cases  of  the  sixth  pair,  17  of  the  third  pair,  6  of  the 
fourth  pair,  and  6  of  external  ophthalmoplegia.     In  all  the  cases  which  I 


1962  TEXT-BOOK  OP  MEDICINE 

have  just  quoted  diabetes  alone  was  the  cause.  No  other  setiological  factors 
were  present,  and  the  patients  were  free  from  syphilis,  tabes,  and  hysteria, 
as  well  as  from  general  paralysis  and  cerebral  tumour — in  fact,  they  were 
affected  only  by  diabetes. 

The  first  point  to  note  is  that  in  diabetics  paralysis  of  the  sixth  pair  of 
nerves  is  three  times  as  frequent  as  paralysis  of  the  third  pair.  In  syphilis 
and  in  tabes  partial  or  total  paralysis  of  the  third  pair  is  most  frequently 
seen  ;  hence  the  precept  that  in  paralysis  of  the  sixth  pair  of  nerves  diabetes 
must  first  be  thought  of.  Paralyses  of  the  oculo-motor  nerves  in  diabetes 
are  most  often  transitory.  They  supervene  suddenly,  and  then  improve  and 
disappear.  Their  mean  duration  is  about  three  months.  In  the  three 
cases  which  I  have  seen  they  lasted  two  and  a  half  months  and  three  months 
respectively.  They  may  recover,  however,  more  quickly ;  but,  on  the  other 
hand,  they  may  persist  longer.  Recurrences  are  not  rare.  The  diabetic 
person,  who  some  months  or  some  years  previously  has  had  paralysis  of 
the  sixth  pair,  but  who  has  completely  recovered,  may  suffer  later  from 
paralysis  of  the  sixth,  of  the  third,  or  of  the  fourth  nerve,  either  in  one  or 
both  eyes. 

In  five  cases  the  paralysis  extended  progressively  to  all  the  motor 
muscles  in  the  form  of  unilateral  or  bilateral  external  ophthalmoplegia. 
In  Blanc's  case,  quoted  by  Sauvineau,  ophthalmoplegia  affected  both  eyes, 
and  was  followed  by  paresis  of  both  hypoglossal  and  inferior  facial  nerves. 
In  one  of  Sauvineau' s  cases  the  ophthalmoplegia  was  progressive  and  uni- 
lateral ;  in  another  case  the  patient  had  paralysis  of  the  left  third  nerve, 
and  eighteen  months  later  right  progressive  ophthalmoplegia  which  lasted 
for  eight  months. 

There  are  cases  in  which  the  ocular  palsies  of  diabetes  may  be  the 
prelude  of  severe  complications  and  of  fatal  polioencephalitis  (Koenig). 

Such,  then,  from  the  point  of  view  of  their  evolution,  are  the  various 
appearances  which  the  ocular  paralyses  of  diabetes  may  assume.  The 
appearance  of  paralysis  of  an  oculo-motor  nerve  in  diabetics  is  not  neces- 
sarily related  to  the  severity  of  the  glycosuria.  In  seventy-four  cases  which 
I  have  collected  I  find  patients  who  have  been  affected  by  paralysis  while 
they  passed  200,  100,  50,  20,  12,  and  3  grammes  of  sugar  a  day.  Sometimes, 
indeed,  the  glycosuria  disappeared  when  the  paralysis  supervened.  There 
is  no  direct  relation  between  the  abundance  of  the  glycosuria  and  the 
appearance  of  the  paralysis. 

I  must  next  describe  some  special  symptoms  which  I  have  seen  in  certain 
cases.  Thus,  one  of  my  patients  at  the  Hotel-Dieu  (550  grammes  of  sugar 
in  twenty-four  hours)  was  affected  for  a  week  previous  to  the  development 
of  sixth-nerve  paralysis  with  severe  and  contiauous  temporo-orbital  neuralgia. 
The  pains  were  clearly  localized  to  the  temporal  and  periorbital    region, 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  19G3 

and  (lid  not  encroach  upon  the  rest  of  tlio  face.  They  increased  on  prcsRure, 
lasted  day  and  night  without  respite,  and  ceased  only  when  the  paralysis 
declared  itself.  There  was  no  question  of  ordinary  headache  in  this  case, 
but  of  a  clearly  localized  neuralgia,  which  seemed  to  depend  upon  the  same 
provoldng  cause  as  the  paralysis.  In  short,  it  was  my  opinion  that  the 
patient  was  suffering  from  painful  paralysis  of  the  sixth  nerve.  I  know 
that  this  coupling  is  scarcely  classical,  but  my  case  is  not  isolated.  Although 
pain  accompanying  paralysis  of  the  oculo-motor  nerves  has  not,  as  far  as 
I  know,  attracted  special  attention,  I  find  this  symptom  noted  in  several 
cases  which  have  very  kindly  been  placed  at  my  disposal.  ' 

Thus,  in  ono  of  Lapersonne's  patients  paralysis  of  the  sixth  pair  was  accompanied 
by  neuralgia.  In  one  of  Galezowski's  patients  jiaralysis  of  the  third  pair  of  nerves  was 
accompanied  by  such  acute  pain  that  ophtlialmic  zona  was  at  first  thought  of.  In  one 
of  Koenig's  patients  paralj^sis  of  the  sixth  pair  was  preceded  and  accompanied  by  a 
constricting  pain  aroimd  the  right  eye.  In  Nattan-Larrier's  case  the  paralysis  of  the 
sixth  pair  was  preceded  by  severe  temporo-orbital  neuralgia,  which  lasted  during  the 
whole  period  of  the  paralysis,  and  did  not  disappear  until  the  paralysis  was  cured. 
In  a  diabetic  patient  of  Buge  paralysis  of  the  fourth  pair  was  accompanied  by  pain  in 
both  temples.  In  a  diabetic  patient  of  Charcot  paralysis  of  the  third  pair  was  accom- 
panied by  facial  neuralgia.  In  one  of  Sauvineau's  diabetic  patients  paralysis  of  the  left 
third  nerve  was  accompanied  by  slight  pains  in  the  left  side  of  the  head. 

We  have,  then,  several  diabetic  patients  in  whom  paralysis  of  an  oculo- 
motor nerve  has  been  preceded,  accompanied  or  followed  by  neuralgic 
pains  in  the  temporal  region,  with  or  without  periorbital  radiation  on  the 
side  of  the  paralysis.  This  is  not  a  simple  coincidence,  and  the  two  symp- 
toms (pain  and  paralysis)  are  associated  here,  as  in  painful  paralysis  of  the 
seventh  pair  (faoial  nerve). 

Pulmonary  Complications. — The  respiratory  function  is  especially  dis- 
turbed in  some  diabetics.  Their  breathing  resembles  that  of  the  tree-frog. 
They  absorb  less  oxygen,  give  off  less  carbonic  acid  and  less  water- vapour, 
and  their  lungs  are  in  a  state  of  receptivity  favourable  to  the  agents  of 
suppuration,  gangrene,  tuberculosis,  and  pneumonia. 

The  larynx  may  be  affected  in  the  diabetic.  The  laryngitis  declares 
itself  by  dryness  in  the  throat  (Leichtenstern),  and  loss  of  voice  if  con- 
versation is  prolonged.  On  laryngoscopic  examination,  the  larynx  and  the 
vocal  cords  have  a  dry  look. 

Diabetics  are  exposed  to  congestion  of  the  lungs,  to  broncho-pneumonia, 
which  is  sometimes  so  severe  that  the  patient  may  succumb  in  one  or  two 
days  (Bouchardat's  fulminant  pneumonia).  As  a  rule,  pneumonia  in 
diabetics  does  not  run  a  frank  course  or  cause  a  high  temperature.  It  may 
readily  give  rise  to  suppuration  and  gangrene,  because  the  pathogenic 
agents  of  these  complications  have,  as  we  have  said,  a  marked  predilection 
for  the  lung. 


1964  TEXT-BOOK  OF  MEDICINE 

Nevertheless,  true  pneumonia  may  occur  in  diabetics,  the  sugar  dis- 
appearing from  tlie  urine  during  the  pneumonia,  defervescence  taking  place 
classically  on  the  ninth  day,  and  the  sugar  reappearing  immediately  after 
recovery. 

Diabetes  Mellitus  and  Pulmonary  Tuberculosis. — I  believe  pulmonary 
tuberculosis  to  be  one  of  the  most  frequent  and  severe  complications  of 
diabetes  meUitus.  Every  individual,  whether  young  or  old,  who  sufiers 
from  diabetes  is  liable  to  pulmonary  tuberculosis. 

According  to  Bradsley,  nearly  all  diabetic  patients  die  of  phthisis. 
Bouchardat  says  that  he  found  tuberculosis  nineteen  times  in  nineteen 
autopsies  upon  diabetic  patients.  Contour,  in  his  thesis  in  1844,  considers 
tuberculosis  as  the  inevitable  consequence  of  diabetes.  According  to 
Lecorche,  tuberculosis  is  the  most  frequent  complication  of  diabetes,  and 
Griensinger  has  said  that  out  of  100  diabetics  43  die  of  phthisis. 

Tuberculosis  does  not  affect  only  the  wasted  and  cachectic  diabetics, 
whose  daily  loss  of  sugar  amounts  to  some  hundred  grammes,  but  it  also 
strikes  down  those  whose  health  is  apparently  excellent,  and  whose  daily 
loss  of  sugar  may  not  exceed  30  to  40  grammes. 

In  one  of  Hanot's  cases,  relating  to  a  diabetic  with  a  large  liver  who  became  tuber- 
cular, the  quantity  of  sugar  was  only  about  15  grammes.  In  one  of  Tapret's  cases  a 
strong  man,  suffering  from  gout  and  such  trifling  diabetes  that  the  glycosuria  only 
amounted  to  a  few  grammes,  nevertheless  became  tubercular. 

In  my  lecture  devoted  to  tuberculosis  in  diabetics*  I  have  quoted 
examples  of  a  similar  nature. 

Sometimes,  indeed,  the  diabetes  is  so  slight  that  the  patient  who  comes 
to  consult  us  for  tuberculosis  (or  for  so-caUed  bronchitis)  is  ignorant  of  the 
fact  that  he  is  a  diabetic.  His  thirst  is  in  no  way  increased,  and  the  quantity 
of  urine  passed  does  not  exceed  the  normal.  Indeed,  we  only  discover  the 
revealing  signs  of  diabetes,  such  as  genital  eczema,  gingivitis,  and  boils,  by 
careful  examination.  An  analysis  of  the  urine  then  reveals  a  daily  quantity 
of  from  20  to  25  grammes  of  sugar.  The  patient  has  had  diabetes  without 
his  knowledge,  and  tuberculosis  has  been  grafted  upon  the  diabetes. 

The  examples  of  this  kind  concern  the  most  common  form  of  pulmonary 
tuberculosis  in  diabetes — namely,  the  insidious  apyretic  form,  which  simu- 
lates ordinary  bronchitis.  The  patient,  who  thinks  that  he  is  sufieriag 
from  a  cold,  commences  to  cough  and  to  spit,  and  feels  so  little  anxiety 
that  he  does  not  seek  advice.  The  cold,  however,  is  obstinate,  the  sputum 
is  thick  and  sometimes  streaked  with  blood,  the  appetite  faUs,  strength 
declines,  and  the  patient  then  decides  to  seek  advice.  Before  any  examina- 
tion the  patient,  who  has  been  coughing  for  some  weeks,  already  awakens 
our  suspicions,  and  we  find  jerky  expiration,  with  some  moist  and  crackling 
*  Dieulafoy,  Clinique  Medicale  de  VEotd-Dieu,  1905,  13™*  legon. 


RHKUMATIC  AND  DYSTROPHIC  DISEASES  19C5 

sounds  at  one  of  the  apices.  Exainiriation  of  the  sj)utura  reveals  barilli. 
The  patient  has  become  tubercuhxr. 

The  tubercuh)ais  has  scarcely  become  installer!  when  the  scene  changes. 
A  diabetic  who,  without  losing  his  strength  and  without  wasting,  has  borne 
severe  diabetes  of  some  duratitm  grows  weak  and  wastes  after  the  appear- 
ance of  tuberculosis.  As  a  rule,  he  does  not  know  that  he  has  become 
tu])ercular,  and  believes  that  he  is  suffering  from  an  ordinary  bronchitis, 
and  yet  he  is  astonished  at  the  change  in  himself.  He  feels  anxious,  blames 
the  diet  and  the  treatment  prescribed,  when  the  condition  is  really  due  to 
tuberculosis. 

We  must,  therefore,  be  on  guard  if  a  diabetic  patient  develops  a  cough. 
As  far  as  I  am  personally  concerned,  I  do  not  like  the  onset  of  coryza  in 
diabetes,  for  I  always  dread  the  hatching  of  diabetic  tuberculosis,  which  is 
far  more  severe  than  the  ordinary  form.  I  do  not  say  that  diabetic  tuber- 
culosis is  absolutely  incurable,  since  some  cases  respond  to  treatment,  and 
may  even  recover,  but  they  are  the  exception.  Diabetic  tuberculosis  is 
difficult  to  dislodge,  and  the  association  of  tuberculosis  in  diabetes  creates 
a  very  threatening  situation. 

Let  us  next  consider  acute  miliary  tuberculosis,  which  may  be  grafted 
upon  diabetes,  as  the  following  examples  show  : 

One  of  Tapret's  patients,  with  200  grammes  of  sugar,  was  stricken  down  with  acute 
febrile  tuberculosis,  which  in  three  weeks  caused  cavernous  lesions,  and  death  in  three 
months.  A  patient  of  Hutinel,  with  100  to  120  grammes  of  sugar,  was  taken  ill  with 
tubercular  broncho-pneumonia  of  both  lungs,  which  proved  fatal  in  a  few  weeks. 
Letulle's  patient,  with  about  400  grammes  of  sugar,  was  stricken  down  with  miliary 
tuberculosis,  and  died  in  eight  days.  The  autopsy  revealed  tubercular  nodules  in  most 
of  the  organs,  but  especially  in  the  lungs,  Hver,  and  kidneys.  Further,  the  apex  of  the 
right  lung  and  one  of  the  glands  at  the  hilum  of  the  limg  showed  older  tubercular 
lesions. 

Some  authors  have  thought  that  tuberculosis  in  diabetes  predisposes  less 
to  haemoptysis  than  ordinary  tuberculosis.  This  idea  is  wrong.  Schmidt 
found  hsemoptysis  in  twenty-six  cases  of  diabetic  tuberculosis.  Lecorche 
has  seen  hsemoptysis  sometimes  at  the  onset,  sometimes  at  an  advanced 
period  of  diabetic  tuberculosis,  and  in  four  cases  the  amount  of  haemorrhage 
was  considerable.  For  my  part,  I  have  fairly  often  seen  abundant  and 
repeated  hsemoptysis  in  diabetic  patients  with  tuberculosis.  In  my  clinical 
lecture  I  have  reported  a  case  which,  for  want  of  room,  I  cannot  reproduce 
here  in  detail. 

A  man,  fifty-five  years  of  age,  had  suffered  from  diabetes  for  several  years.  He  had 
only  passed  from  25  to  30  grammes  of  sugar  and  a  small  quantity  of  albumin.  One 
day  he  was  seized  with  profuse  haemoptysis,  as  the  revealing  sign  of  tuberculosis  in 
the  apex  of  the  right  lung.  The  sputum,  though  scanty,  contained  bacilli.  From  this 
time  on  the  haemoptysis  reappeared  fairly  frequently,  and  two  years  later  he  succumbed 
during  an  attack  of  haemoptysis. 


1966  TEXT-BOOK  OF  MEDICINE 

Diabetes  of  traumatic  origin  may  favour  an  outburst  of  tuberculosis. 
Hutinel  has  communicated  the  following  case  to  me  : 

A  youth,  bom  of  healthy  parents,  had  enjoyed  excellent  health,  until  one  day,  in 
a  railway  collision,  he  received  a  violent  shock.  Shortly  after  the  accident  he  was  taken 
iU  with  polyuria  and  polydipsia.  The  urine  was  examined,  and  showed  the  presence 
of  150  grammes  of  sugar.  Rapid  wasting  supervened,  and  signs  of  pulmonary  tuber- 
culosis appeared.  The  phthisis,  which  defied  aU  treatment,  ran  a  rapid  course,  and 
the  yoimg  man  died  in  eight  months  from  pulmonary  tuberculosis  grafted  upon  trau- 
matic diabetes. 

Such,  then,  are  the  various  forms  that  pulmonary  tuberculosis  may 
assume  in  diabetes.  The  fact  which  surprises  me  is  that  the  diabetic  patient 
is  so  rarely  attacked  by  tubercular  pleurisy,  whereas  he  is  so  often  affected 
by  pulmonary  tuberculosis ;  and  the  contrast  is  the  more  astonishing  as 
pleurisy  is  one  of  the  commonest  manifestations  of  tubercular  infection. 
It  is  difficult  to  explain  why  the  pleura  in  the  diabetic  is  spared  to  such  an 
extent  when  his  lung  is  spared  so  little.  We  meet  with  any  number  of  cases 
of  diabetic  phthisis,  whereas  cases  of  tubercular  pleurisy  in  diabetes  are 
comparatively  rare.     To  quote  cases  : 

A  man  came  into  the  Bichat  Hospital  for  severe  diabetes.  The  glycosuria  mounted 
to  800  grammes  daily.  The  disease  was  of  four  months'  duration.  At  this  time  the 
man  was  suffering  from  polydipsia,  polyuria,  polyphagia,  and  rapid  wasting.  The 
diabetes  improved  to  a  marked  extent  as  the  result  of  diet  and  of  antipyrin.  Pain 
appeared,  however,  on  the  right  side  of  the  chest,  the  cough  was  frequent,  the  ex- 
pectoration was  abundant,  and  signs  of  phthisis  were  evident  at  the  right  apex.  Some 
days  later  an  effusion  appeared,  in  the  right  pleura.  The  patient  became  cachectic 
and  died.  The  autopsy  revealed  a  cavity  in  the  lung.  The  pleura  contained  3  litres 
of  serous  fluid. 

With  Ramon,  I  saw  a  lady  suffering  from  diabetes  and  pleurisy,  and  at  the  Hotel- 
Dieu  I  have  had  a  diabetic  who  was  taken  iU  with  right  hsemorrhagic  pleurisy  of  a 
tubercular  character,  from  which  he  recovered. 

It  follows,  therefore,  that  pulmonary  tuberculosis  in  all  its  forms  may 
complicate  diabetes  meUitus,  and  we  may  see  slow,  rapid,  miliary,  or  haemop- 
toic  tuberculosis.  This  terrible  complication  is  seen  in  diabetics  of  all 
ages — children,  adults,  and  elderly  people.  The  most  common  form  is 
ordinary  tuberculosis,  which  at  first  simulates  bronchitis,  or  a  cold  "  which 
has  no  end." 

The  pathogenesis  of  the  tuberculosis  is  difficult  to  explain.  Writers 
were  formerly  iaclined  to  consider  phthisis  in  diabetics  as  the  final  expres- 
sion of  severe  and  cachectic  diabetes.  We  know  that  it  is  often  quite 
otherwise,  because  tuberculosis  is  grafted  upon  slight  diabetes  and  also  upon 
diabetes  of  traumatic  origin.  All  this  proves  that  the  saccharin  medium 
constitutes  in  the  diabetic  a  soU  extremely  favourable  to  the  fixation  and 
growth  of  Koch's  bacillus.     I  am  content  to  note  the  fact  without  pro- 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  19C7 

pounding  theories.  A  healthy  individual  becomes  diabetic.  He  is  then 
more  likely  than  another  to  become  tubercular,  no  matter  what  is  the  cause 
and  origin  of  the  diabetes. 

According  to  Bouchard,  "  diabetic  phthisis  exists  almost  exclusively  in 
patients  who  also  suffer  from  albuminuria.  I  have  seen,  says  he,  albu- 
minuria absent  only  once  in  diabetic  phthisis,  and  I  have  seen  phthisis 
supervene  in  18  per  cent,  of  diabetic  patients  with  albuminuria,  while,  in 
the  total  number  of  cases  of  diabetes  phthisis  only  supervened  in  8  per 
cent."  My  opinion  differs  from  that  of  Bouchard,  and  I  do  not 
attach  the  same  prognostic  value  to  albuminuria.  It  is,  of  course,  better 
if  a  diabetic  has  not  albuminuria,  but  in  many  cases  albuminuria  is  an 
epiphenomenon  without  grave  results,  and,  in  my  opinion,  without  direct 
association  with  tuberculosis.  Thus,  out  of  twelve  diabetics  with  tuber- 
culosis mentioned  in  my  clinical  lecture,  eight  did  not  suffer  from  albu- 
minuria. We  must  also  take  into  account  the  frequent  cases  in  which  the 
diabetic  patient  already  had  tuberculosis  when  the  albuminuria  appeared. 

As  regards  treatment,  prophylaxis  should  occupy  a  very  large  place, 
Diabetes  produces  a  soil  favourable  to  the  fixation  and  growth  of  Koch's 
bacillus,  and  the  diabetic  ought,  therefore,  as  far  as  possible,  to  avoid  all 
causes  of  contamination.  A  diabetic  patient  placed  in  a  hospital  ward  with 
tubercular  patients  is  more  liable  than  others  to  take  the  infection.  A 
diabetic  who  has  a  tubercular  wife  or  child  in  his  family  should  carry  out 
strict  hygiene  in  order  to  avoid  contagion.  Diabetics  born  of  tubercular 
stock  ofier  a  soil  doubly  favourable  to  the  hatching  of  tuberculosis,  and 
should  take  precautions  in  consequence. 

Nervous  Complications. — The  sensory  or  motor  troubles  of  peripheral 
origin  may  be  set  down  to  neuritis.  As  regards  the  sensory  troubles, 
anaesthesia  and  hypergesthesia  have  both  been  seen.  Neuralgia  may  affect 
the  intercostal,  sciatic,  trigeminal,  and  vagus  nerves  (Peter).  It  is  some- 
times symmetrical  (Worms).  In  a  series  of  learned  monographs,  Vergely 
has  called  attention  to  attacks  of  angina  pectoris  associated  with  diabetes, 
to  diabetic  zona,  and  to  the  syringomyelic  dissociation  of  sensibility  in 
diabetics. 

The  motor  troubles  are  very  varied.  Some  diabetics  experience  painful 
lassitude  and  excessive  muscular  fatigue,  principally  in  the  muscles  of  the 
legs  and  of  the  loins.  This  muscular  atony  is  explained  by  the  dehydration 
of  the  muscles  and  by  the  insufficiency  of  oxygen  destined  for  muscular 
respiration  (See).  It  is  probable  that  a  diminution  in  nerve  power  is  also 
associated  with  it.  We  find  paralyses  which  are  sometimes  partial  and 
limited  to  one  arm  or  to  a  group  of  muscles,  such  as  the  muscles  of  the  face, 
of  the  tongue,  or  of  the  larynx,  or  which  are  at  other  times  general,  and 
take  the  form  of  hemiplegia  or  of  paraplegia.     These  paralyses  may  super- 


1968  TEXT-BOOK  OF  IVIEDICINE 

vene  at  all  periods  of  th.e  disease.  They  Kave  tKe  ciiaracteristie  of  being 
incomplete  and  transitory. 

In  certain  cases  the  paralyses  depend  upon  cerebral  arteritis  obliterans, 
atheroma,  softening,  and  cerebral  or  meningeal  haemorrhage.  These  various 
lesions,  according  to  the  case,  provoke  apoplexy,  hemiplegia,  or  aphasia. 

The  cerebral  troubles  occupy  an  important  place  in  the  history  of 
diabetes.  The  patient  becomes  apathetic,  lazy,  and  has  attacks  of  somno- 
lence, lacking  "  the  appetite  for  thought "  (Lasegue).  The  symptom- 
complex  of  the  cerebral  troubles  includes  restlessness,  delirium,  aphasia, 
which  is  generally  transitory,  and  coma.  Coma  is  one  of  the  most  dread 
complications  of  diabetes  (Kussmaul).  In  Frerichs'  statistics,  of  250  deaths 
caused  by  the  complications  of  diabetes  coma  figures  153  times. 

Diabetic  coma  is  usually  ushered  in  by  vomiting,  diarrhoea,  abdominal 
pains  which  simulate  peritonitis  (Jaccoud),  or  by  dyspnoea,  and  this  fact 
gives  it  the  greatest  analogy  with  ursemia,  from  which  it  difiers,  however, 
in  the  absence  of  convulsions  and  of  contractions,  and  in  the  condition  of 
the  respiration,  which  does  not  assume  the  Cheyne-Stokes  type.  The 
dyspnoeic  phase  is  usually  preceded  or  accompanied  by  restlessness,  which 
gives  place  to  progressive  depression.  The  temperature  drops,  the  patient 
faUs  into  collapse,  and  death  occurs  in  a  few  days. 

In  a  second  variety  (vertiginous  form)  headache  and  vertigo  are  the 
chief  symptoms.  In  the  third  variety  the  symptoms  comprise  a  smaU  and 
irregular  pulse,  cyanosis,  and  coldness  of  the  body,  so  that  Jaccoud  has 
called  it  the  cardiac  form.  These  two  last  varieties  also  end  in  coma,  and 
carry  ofi  the  patient  in  a  few  days  or  in  a  few  hours.  Coma  appears  at  all 
periods  of  diabetes,  but  is  more  frequent  in  young  patients,  and  especially 
as  the  result  of  traveUing,  fatigue,  violent  exercise,  or  overwork,  whence 
the  precept  that  the  diabetic  patient  should  abstain  from  every  cause  of 
fatigue.  The  pathogenesis  of  these  cerebral  troubles  has  been  variously 
interpreted.  Among  the  theories,  of  which  no  one  is  absolutely  satisfactory, 
dehydration  of  the  nerve  centres  and  acetonemia  have  been  invoked. 

Acetonaemia  is  said  to  result  from  the  absorption  of  acetone  formed  at 
the  expense  of  the  glucose.  The  partisans  of  this  theory  depend  upon  the 
fact  that  acetone  has  been  found  in  the  breath  (odour  of  chloroform),  in 
the  urine,  and  ia  the  vomit  of  patients  with  diabetic  coma.  The  theories 
which  attribute  the  intoxication  to  acetone  or  to  acetic  acid  are,  however, 
insufficient. 

In  some  cases  sudden  death  occurs.  It  is  probably  due  to  cardiac 
syncope  (cardiac  form  of  coma). 

Course — Termination. — Diabetes  is  generally  insidious  in  its  onset. 
There  is,  however,  an  acute  form,  which  is  sudden  in  its  onset,  and  which 
runs  a  rapid  course.     In  the  slow  and  chronic  form  of  diabetes  the  first 


RHb:UMATIC  AND  DYSTROPHIC;  DISEASES  19G9 

period  is  of  indefinite  duration.  I  say  indefinite,  because  for  several  years 
we  may  find  10,  20,  and  30  graniiiics  of  sugar  in  the  urine,  although  the 
severe  symptoms  of  diabetes,  such  as  polydipsia  and  polyuria,  are  not  suHi- 
ciently  marked  to  sound  the  alarm.  Often,  too,  the  appetite  is  increased, 
the  patient  grows  stouter,  and  we  hear  these  diabetics  congratulating  them- 
selves  on  their  excellent  health.  In  spite  of  this  apparent  health,  and  in 
ignorance  of  their  malady,  they  are  exposed  to  many  complication.s — 
balanitis,  phimosis,  sexual  weakness,  expulsive  gingivitis,  attacks  of  boils, 
carbuncles,  muscular  fatigue,  cataract,  erythema  of  the  vulva  and  of  the 
groin,  pruritus  vulvse,  and  intertrigo  of  the  labial  commissures  (Hardy). 
If  they  escape  pulmonary  tuberculosis,  they  are  none  the  less  liable  to 
gangrene,  abscesses,  cerebral  troubles,  and  coma.  At  this  period  appro- 
priate treatment  and  suitable  hygiene  may  keep  them  in  a  state  of  adequate 
equilibrium.  It  is  often  suflficient  to  regulate  the  diet  in  order  to  lessen  the 
glycosuria. 

As  the  disease  progresses  the  symptoms  become  marked ;  the  polydipsia 
and  the  glycosuria  increase ;  treatment  has  less  effect ;  the  quantity  of  sugar 
in  the  urine  sometimes  remains  high,  in  spite  of  the  suppression  of  saccharin 
and  starchy  food,  the  sugar  forming  at  the  expense  of  the  proteids  (Jaccoud). 
Examination  of  the  urine  often  reveals  albumin,  and  phosphates  and  sul- 
phates in  excess,  pointing  to  a  more  general  perversion  of  the  metabolism. 
The  proteid  matter  amounts  to  as  much  as  50  and  60  grammes  daily. 
Azoturia  is,  therefore,  present.  In  spite  of  these  losses  in  sugar,  mineral 
salts,  and  urea,  the  patient  practically  maintains  his  equilibrium  if  the 
digestive  functions  allow  him  to  compensate  for  the  loss  by  taking  abundant 
nourishment. 

We  must  now  turn  our  attention  to  azoturia  and  albuminuria,  which 
have  been  variously  interpreted  from  the  point  of  view  of  pathogenesis  and 
of  prognosis. 

Albuminuria  appears  at  a  given  moment  in  two-thirds  of  patients  with 
diabetes.  We  may  see  it  just  as  much  in  the  slight  as  in  the  severe  cases. 
It  is  e^^dently  a  somewhat  dangerous  complication,  but  it  has  not  quite 
the  gravity  attributed  by  Rayer  and  others,  who  thought  that  it  indicated 
Bright's  disease,  Bright's  disease  may  certainly  complicate  diabetes,  and 
render  the  prognosis  gloomy  in  arthritics  with  diabetes.  We  find  post 
mortem  the  lesions  of  the  small  gouty  kidney,  but  this  is  an  exception. 
Albuminuria  in  diabetics  has  another  origin,  and  it  is  probable  that  it  arises 
"  in  a  more  profound  change  of  nutrition,  the  anatomical  elements  allowing 
the  expulsion  of  the  albuminoid  material  without  having  caused  it  to 
undergo  the  chenadcal  changes  which  should  reduce  it  to  the  condition  of 
crystalloid  matter "  (Bouchard).  Albuminuria  has  no  direct  relation 
with   azoturia.     I    have   often  seen   albuminuria   supervene   in    diabetics 


1970  TEXT-BOOK  OF  MEDICINE 

wlio  were  on  too  rigorous  a  diet.     I  shall  return  to  this  question  under 
Treatment. 

Azoturia,  or  excess  of  urea  in  the  urine,  is  usually  regarded  as  a  con- 
stant and  serious  fact.  Bouchard  is  not  of  the  same  opinion.  In  100 
diabetics,  he  found  the  urea  normal  in  40,  lowered  in  20,  and  increased  in  40. 
Azoturia  is  present  in  slight  as  weU  as  in  severe  diabetes.  It  must  be 
remembered  that  marked  azoturia  (80  to  100  grammes  daily)  makes  the 
prognosis  very  grave,  unless  these  losses  are  compensated  by  rich  and  abun- 
dant nourishment.  According  to  certain  authors  (Jaccoud),  glycosuria  and 
azoturia  are  two  phenomena  which  have  a  common  origin.  Bouchard,  on 
the  other  hand,  considers  them  as  independent,  and  having  no  relation 
"  either  in  the  series  of  cases  or  in  the  successive  phases  of  a  single  case." 

Azoturia  intervenes  on  its  own  account  gradually  or  suddenly,  with 
marked  oscillations.  It  represents,  like  diabetic  albuminuria,  a  superadded 
trouble  of  nutrition. 

Eecovery  from  diabetes  is  fairly  frequent  in  adults.  On  the  other  hand, 
we  see  cases  of  diabetes  which  treatment  holds  in  check  for  several  years, 
though  finally  they  end  fatally.  When  a  diabetic  patient  wastes,  when 
digestive  troubles  appear,  and  glycosuria  persists  in  spite  of  aU  treatment, 
the  prognosis  becomes  very  grave.  In  some  cases  the  patient  succumbs 
from  cachexia.  The  wasting  becomes  extreme,  the  temperature  is  sub- 
normal, the  albuminuria  increases,  and  the  sugar  often  diminishes  or  dis- 
appears. The  patient,  as  a  rule,  succumbs  before  this  period  of  cachexia. 
Cellulitis,  carbuncles,  gangrene,  pneumonia,  phthisis,  and  diabetic  coma  are 
among  the  many  causes  of  death. 

Pancreatic  diabetes,  as  we  have  seen,  runs  an  extremely  rapid  course. 

Defaced  Diabetes. — Under  this  term,  Achard  and  Weil  have  described 
a  constitutional  diabetes  without  glycosuria  analogous  to  Bright's  disease 
without  albuminuria.  This  diabetes  is  revealed  by  glycosuria  consecutive 
to  the  subcutaneous  injection  of  glucose.  If  a  small  quantity  of  glucose 
was  already  present  in  the  urine,  the  glycosuria  shows  a  very  marked 
increase  ;  if  glucose  was  not  present  in  the  urine,  the  appearance  of  glycosuria- 
denotes  defaced  diabetes. 

Diabetes  in  Children. — Diabetes,  though  rare  in  children,  is  extremely 
grave,  because  it  assumes  from  the  first  the  wasting  form,  with  rapid  course, 
and  because  it  frequently  terminates  in  tuberculosis  or  in  coma.  It  is  in 
children  especially  that  we  may  recognize  the  importance  of  heredity  in 
the  setiology  of  diabetes. 

Diabetes  and  the  Puerperal  State. — Simple  glycosuria  is  here  an  inci- 
dent without  special  consequences.  While  it  is  rare  during  pregnancy,  it  is 
more  frequent  at  the  commencement  of  the  nursing  period,  and  shows  itself 
by  a  loss  of  sugar  which  varies  from  50  centigrammes  to  3  grammes. 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  1071 

When  a  diabetic  woman  becomes  pregnant,  what  liuppeus  to  her  and 
hiT  child  ?  Diabetes  caust-s  premature  bii-ths  in  cJO  per  cent,  of  cases. 
Labour  usually  conies  on  at  the  seventh  month.  Reciprocally,  pregnancy 
makes  the  diabetes  active,  and  the  quantity  of  sugar  may  be  doubled  about 
the  sixth  month  of  pregnancy. 

Maternal  diabetes  is  most  serious,  both  to  the  premature  and  to  the  full- 
term  child.  In  the  latter  case  the  child  dies  in  the  proportion  of  50  per 
cent.,  either  during  labour  or  shortly  after  birth.  Labour  in  diabetic  women 
is  so  serious  that  from  30  to  40  per  cent,  die,  either  from  coma  or  from  ulterior 
complications.  In  the  face  of  such  results,  a  diabetic  woman  should  be 
advised  not  to  marry — or,  at  least,  she  should  be  warned  of  the  serious 
dangers  of  pregnancy. 

Traumatic  diabetes  will  be  discussed  in  Section  VII.  Bronzed  diabetes 
has  been  discussed  under  Pigmentary  Hypertrophic  Cirrhosis. 

The  Liver  in  Diabetes. — The  liver  is  normal  in  a  large  number  of  cases. 
It  is  neither  hypertrophied  nor  cirrhosed.  This  integrity  of  the  liver  is 
found  both  in  mild  and  in  severe  diabetes.  I  had  the  following  case  under 
my  care  : 

A  man  was  suffering  from  very  severe  diabetes  mellitus.  The  urine  had  a  specific 
gravity  of  1039.  It  contained  no  albumin.  The  amoimt  of  urea  was  62  grammes. 
The  glycosuria  was  considerable,  and  in  one  analysis  120-50  grammes  per  litre  were 
found — that  is  to  say,  1,084-50  grammes  in  9  litres,  or  more  than  a  kilogramme  in  the 
twenty-four  hovurs.  I  was  anxious  to  know  how  much  alcohol  this  sugar  represented, 
and  I  asked  Corlay  to  undertake  the  necessary  examination.  A  test  was  made  one 
day  when  the  patient  had  passed  9  htres  of  urine  containing  800  grammes  of  sugar. 
The  result  was  350  grammes  of  alcohol. 

In  spite  of  the  enormous  quantity  of  food  and  drink  taken  for  several  months,  the 
stomach  was  not  dilated,  and  the  digestive  functions  did  their  work  perfectly.  The 
liver  was  normal,  measuring  barely  11  centimetres  in  its  vertical  diameter,  and  showed 
no  hypertrophy.  He  had  not  escaped  one  of  the  most  grave  compUcations — namely, 
tuberculosis.  I  could  not  define  the  exact  onset  of  the  lung  trouble,  because  it  took 
the  insidious  form  of  a  simple  bronchitis.  For  a  year  he  had  been  subject  to  "  bron- 
chitis," and  had  several  times  been  compelled  to  Ue  up.  The  cough  was  followed  by 
thick  and  abundant  expectoration,  the  strength  was  faihng,  and  the  wasting  was 
marked,  although  the  polyphagia  had  in  no  way  diminished.  The  patient  had  no  fever, 
and  did  not  sufl'er  from  night-sweats.  Auscultation  revealed  at  the  apex  of  the  right 
lung,  both  in  front  and  behind,  signs  of  softening  ;  large  rales,  dry  and  moist  crackfing 
sounds.  The  region  was  dull  on  percussion,  and  the  vibrations  were  increased.  The 
sputum  was  muco -purulent,  and  baciUi  were  present  in  large  numbers. 

For  seven  months  the  patient  continued  to  pass  600  to  700  grammes  of  sugar  daily, 
and  the  Uver  remained  normal.  Finally  he  died,  and  the  results  of  the  autopsy  were 
as  follows  :  The  liver  was  absolutely  normal ;  it  weighed  1,450  grammes,  and  presented 
no  trace  of  cirrhosis.  The  bile -ducts  were  healthy.  The  pancreas  was  absolutely  normal, 
and  Wirsung's  duct  was  patent  from  its  origin  to  its  opening  in  the  duodenum. 

In  some  cases  of  diabetes  the  liver  is  hypertrophied  or  cirrhotic.  I  am 
not  speaking,  of  course,  of  complex  cases,  in  which  the  patient  is  both 
diabetic  and  alcoholic,  tubercular,  malarial,  or  syphilitic.     In  such  cases 


1972  TEXT-BOOK  OE  MEDICINE 

we  are  frequently  in  doubt  as  to  whether  the  hypertrophy  and  the  cirrhosis 
are  due  to  diabetes  alone,  or  to  other  previous  or  concomitant  diseases.  I 
am  not  speaking  here  of  bronzed  diabetes,  described  in  detail  under  Pig- 
mentary Cirrhosis,  but  I  allude  to  the  hepatic  complications  of  diabetes 
meUitus  alone.  Bernard,  extending  his  discovery  of  hepatic  glycogenesis  to 
the  pathogenesis  of  diabetes,  declared  that  diabetes  mellitus  must  be 
"  localized  in  the  liver,"  and  yet  treatises  on  diabetes  have  for  the  past 
fifteen  or  twenty  years  made  only  passing  mention  of  the  condition  of  the 
liver  {Frerichs,  Durand-Fardel,  Griesinger). 

Lecorche  was  the  first  to  caU  attention  to  the  frequency  of  hepatome- 
galia  in  diabetes.  We  might  almost,  says  he,  consider  hypertrophy  of  the 
liver  as  one  of  the  constant  symptoms  of  diabetes  mellitus.  This  hypertrophy 
usually  affects  the  whole  liver.     It  is  rarely  partial. 

The  researches  of  the  physicians  at  Vichy,  who  have  seen  a  very  large 
number  of  diabetics,  have  helped  to  clear  up  the  question.  Glenard  and 
Fremont  have  often  found  this  hypertrophy  of  the  Uver  (60  per  cent. ;  and 
4A  in  105).  The  researches  of  Glenard  comprise  the  examination  of  324 
cases.  He  found  that  hepatomegalia  is  the  most  frequent  of  the  organic 
changes  in  diabetes,  and  thinks  that  it  is  most  often  partial.  In  68  per  cent, 
of  the  cases  observed  by  Glenard  one  lobe,  usually  the  right,  was  hyper- 
trophied.  The  liver  was  indurated  in  the  proportion  of  38  in  200,  and  sensi- 
tive to  pressure  in  the  proportion  of  23  in  100. 

Chauffard  says  that  we  may  find  changes  in  the  liver  of  diabetics  vary- 
ing from  congestive  lesions  similar  to  those  of  the  cardiac  liver  to  typical 
cases  of  porto-bihary  and  bivenous  cirrhosis,  and  this  idea  agrees  well  with 
that  of  hepatic  phlebitis  in  diabetic  cirrhosis. 

In  my  chnical  lecture  on  the  liver  in  diabetics*  I  have  had  occasion  to 
quote  facts  concerning  hypertrophy  and  cirrhosis  of  the  liver.  To  quote 
an  example  of  hypertrophy  : 

One  of  my  patients  at  the  H6tel-Dieu  was  suffering  from  severe  diabetes.  He  drank 
from  8  to  9  litres  of  fluid,  and  passed  about  the  same  quantity  of  urine,  wliich  showed 
a  specific  gravity  of  1032.  It  contained  neither  albumin  nor  indican.  The  analysis 
showed  85-50  grammes  of  sugar  per  Utre,  or  675  grammes  daily.  The  quantity  of  urea 
was  shghtly  increased.  The  appetite  was  in  proportion  to  the  thirst.  In  spite  of  the 
enormous  quantity  of  food  and  drink  ingested,  the  digestive  functions  were  perfect, 
the  tongue  had  quite  a  rosy  colour,  the  teeth  were  not  exposed,  the  stomach  was  not 
dilated,  and  there  was  neither  constipation  nor  diarrhoea.  The  liver  in  this  patient 
was  very  large,  reaching  three  fingers'  breadth  below  the  false  ribs ;  but  it  was  not 
painful,  indurated,  or  deformed.  As  we  found  no  other  cause  to  explain  the  hyper- 
trophy of  the  hver — for  the  patient  was  neither  alcohohc  nor  suffering  from  malarial 
fever  nor  cardiac  disease  —  we  thought  of  pure  diabetic  hypertrophy.  This  hyper- 
trophy was  not  comphcated  by  cirrhosis,  for  not  a  sign  of  cirrhosis  or  of  precirrhosis 

*  Dieulafoy,  "  Le  Pole  des  Diabetiques "  {Clinique  Medicale  de  VHotd  -  Dieu, 
1903,  13"^^  lejon). 


RHEUMA'IKJ  AND  DYSTROPHIC  DISEASES  1973 

was  prcsont.  Collatoral  Lirculatioti  unci  usoitcs  wore  uljsont.  In  a  fow  woeka  tho 
situation  beuauio  worso,  and  tho  quantity  of  HUgar,  wliioh  was  always  very  largo,  varied 
from  650  to  750  granimos  daily.  Diabetic;  coma  then  appeared,  and  tho  man  died  after 
sovon  montlia'  illness. 

Tho  autopsy  furni.sluid  tho  following  results  :  Tho  pancreas  was  absolutely  normal, 
no  gravel  in  tho  pancroatie  ducts,  thus  proving  that  diabotos  may  bo  rapid  and  most 
severe,  althouuh  the  pancreas  is  healthy.  The  liver,  on  the  other  hand,  was  very  much 
enlarged,  and  weighed  2,300  grammes.  Apart  from  this  general  hypertrophy,  we 
found  no  other  lesion  in  tho  organ.  Its  consistency  and  its  colour  were  normal.  In- 
duration, fatty  changes,  cirrhosis,  and  pigmentation  were  absent.  The  hypertrophy 
was  therefore  simple,  and  tho  case  was  one  of  enlarged  diabetic  liver  without  cirrhosis. 

Gilbert  speaks  of  a  diabetic  patient  suffering  from  simple  hypertrophy  of  tho  liver. 
At  the  autopsy  the  enlarged  liver  weighed  2,510  grammes.  Fatty  degeneration  and 
appreciable  cellular  lesions  were  absent.  Tho  pancreas  was  normal.  This  case  is 
absolutely  comparable  to  that  of  my  patient,  who  also  had  severe  diabetes  and  a  very 
large  liver,  without  degeneration  and  without  cirrhotic  lesions. 

In  a  diabetic  patient  of  Tapret  the  autopsy  revealed  a  large  liver  of  2,210  grammes. 
The  organ  was  not  hard  on  section,  which  appears  to  indicate  simple  hypertrophy 
without  cirrhoses. 

Some  diabetics  may,  therefore,  have  a  very  large  liver  without  cirrhosis, 
while  others  show  hypertrophy  with  cirrhosis.  If  the  patient  is  an  alcoholic, 
as  in  Gilbert's  two  cases,  hypertrophic  cirrhosis  cannot  be  attributed  ex- 
clusively to  diabetes,  but  there  are  undoubted  cases  of  enlarged  cirrhotic 
livers  in  diabetics  without  alcoholism,  as  the  following  examples  prove  : 

Hanot,  in  a  critical  review  on  cirrhosis  of  the  hver,  reports  the  case  of  a  patient 
admitted  for  diabetes.  The  urine  contained  12  grammes  of  sugar  per  litre,  and  the 
patient  also  showed  signs  of  hepatic  cirrhosis.  She  died  of  coma,  and  the  autopsy 
gave  the  following  results  :  The  liver,  which  was  larger  than  normal,  weighed  1,900 
grammes.  Its  surface  was  nodular,  but  less  so  than  in  atrophic  cirrhosis.  On  section 
the  tissue  was  resistant,  of  a  chamois-leather  colour,  and  shghtly  granular.  Micro- 
scopical examination  showed  that  the  intralobular  vein  was  much  dilated,  being  three 
times  its  normal  diameter,  and  embedded  in  a  fibrous  coat,  surroiinded  by  a  zone  of 
embryonic  cells.  Hanot,  in  seeking  to  explain  the  pathogenesis  of  the  cirrhosis,  asks 
whether  diabetes  was  not  the  cause.  "  In  diabetes,"  says  he,  "  the  blood  of  the  intra- 
lobular vein  contains  a  much  larger  quantity  of  hepatic  sugar  than  in  the  normal 
condition.  It  would  not  be  impossible  that  this  sugar  in  excess  might,  as  regards  the 
cells  of  the  intralobular  vein,  play  the  same  part  as  that  played  by  alcohol  or  by  blood- 
pigment  with  regard  to  the  radicals  of  the  portal  vein  in  perilobular  venous  cirrhosis." 
Accordingly,  as  Triboulet  remarks,  this  intarpretation  is  probable,  and  the  action  of 
the  diabetic  poisoning  on  the  internal  coat  of  the  vessels  has  been  confirmed  byLecorche 
and  Ferraro. 

Some  years  ago,  at  the  Hotel-Dieu,  I  saw  hypertrophic  cirrhosis  with  ascites  in  a 
diabetic  patient.  The  diabetes  appeared  to  me  to  be  the  sole  cause  of  this  cirrhosis. 
A  man,  fifty-two  years  of  age,  came  under  my  care  with  his  belly  distended  by  a  peri- 
toneal effusion,  estimated  at  several  litres.  The  collateral  circiilation  was  well  marked, 
but  jaundice  was  absent.  The  ascites  was  thi-ee  months  old.  It  had  developed  slowly, 
without  pain,  and  without  any  of  the  digestive  troubles  which  almost  always  mark  the 
course  of  Laennec's  cirrhosis.  Moreover,  the  patient  had  not  the  appearance  seen  in 
cirrhosis :  he  had  preserved  his  stoutness,  his  face  was  neither  earthy  nor  bronzed, 
the  conjunctivje  were  scarcely  tinged,  and  the  urine  was  normal  in  quantity,  and 
contained  only   a   httle   urobilin,  without   any  red-brown  pigment.      The  hver,   as 

n.  125 


1974  TEXT-BOOK  OF  MEDICINE 

could  be  felt  by  dipping,  was  hypertropbied,  and  reached  an  inch  below  the  costal 
margin.  The  spleen  was  sUghtly  enlarged.  The  case  was  therefore  one  of  cirrhosis 
with  an  enlarged  hver.  The  patient  was  not  an  alcohohc,  and  had  not  suffered  from 
syphihs,  malarial  fever,  or  cardiac  disease.  There  was  nothing  ia  his  past  history  to 
explain  this  cirrhosis,  except  the  diabetes  meUitus,  from  which  he  had  suffered  for  about 
three  years,  and  which  he  had  discovered  himself.  As  be  had  great  thirst  and  one 
day  foimd  that  some  drops  of  urine  left  a  whitish  deposit,  he  conceived  the  idea  of 
having  it  examined :  140  grammes  of  sugar  were  passed  in  twenty-fom:  hours.  For 
three  years  the  glycosuria  underwent  various  changes,  according  to  the  diet  which  was 
taken. 

When  he  came  under  my  care  he  was  passing  only  12  grammes  of  sugar  daily  i 
polydipsia,  polyphagia,  and  polyuria  were  absent.  The  absence  of  any  other  eetiological 
factor  led  me  to  conclude  that  it  was  a  case  of  hypertrophic  cirrhosis  due  to  diabetes, 
but  without  any  relation  to  the  pigmentary  cirrhosis  of  bronzed  diabetes,  in  which 
the  symptoms  are  very  difierent.  I  considered  this  diabetic  hepatomegaha  as  related 
to  the  cases  of  which  I  spoke  above.  The  patient  was  put  on  the  diet  which  I  usually 
order  for  diabetics.  He  was  punctured  twice,  and  left  my  ward  four  months  later, 
showing  notable  improvement. 

I  had  under  my  care  a  patient  of  whom  I  sbaU  have  to  speak  presently  in  con- 
nection with  saccharine  ascites  in  diabetes.  This  patient,  who  was  not  alcohohc, 
had  diabetes  and  a  very  large  hver,  with  cirrhosis.  Finally  he  died,  and  the  histological 
examination  made  by  Jolly  gave  the  following  results :  The  surface  of  the  hver  was 
granular,  Ghsson's  capsule  was  somewhat  thickened,  and  the  consistency  of  the  organ 
was  notably  increased.  In  sections  of  the  hver  we  saw  with  the  naked  eye  yellowish 
points  of  the  size  of  a  hepatic  lobule,  separated  by  parts  of  a  clear  grey  colour.  A 
fragment  of  hver  was  divided  into  smaU  pieces,  which  were  fixed  by  alcohol,  Miiller's 
fluid,  and  osmic  acid.  Under  the  microscope  the  normal  topography  of  the  hver  was 
no  longer  recognizable.  The  hepatic  tissue  was  made  up  of  a  certain  number  of  islets, 
of  variable  sizes,  and  more  or  less  rounded.  These  islets  did  not  correspond  to  the 
hepatic  lobules ;  they  were  formed  of  hepatic  ceUs  in  which  the  bands  no  longer  had 
their  usual  radial  disposition.  In  the  connective  tissue,  between  the  islets,  we  found 
portal  veins,  bUe-ducts,  and  also  hepatic  veins.  In  the  centre  of  some  islets,  we  found 
the  cut  section  of  a  hepatic  vein,  surrounded  by  a  zone  of  connective  tissue.  We  also 
found  in  the  connective  bands  masses  of  lymphoid  cells  and  isolated  groups  of  hepatic 
cells.  A  few  cells  were  undergoing  granulo-fatty  degeneration.  In  short,  the  cirrhosis 
was  hypertrophic  in  character,  with  small  granules,  which  chiefly  afiected  the  portal 
system,  thus  closely  resembhng  alcohohc  cirrhosis,  although  the  patient  had  not  been 
a  heavy  drinker^ 

It  is  difficult  to  explain  tlie  difierent  pathological  varieties  of  tke  diabetic 
liver.  The  difficulty  is  quite  as  great  when  we  try  to  estimate  the  respective 
share  of  the  diabetes  and  of  the  hepatic  hypertrophy.  In  a  patient  sufiering 
from  diabetes  and  a  very  large  liver  we  cannot  always  decide  whether  the 
diabetes  has  produced  the  enlarged  liver  or  whether  the  enlarged  liver  has 
produced  the  diabetes.  Gilbert  and  LerebouUet,  in  two  cases,  admit  that 
the  enlarged  hver,  diseased  through  alcohohsm,  produced  diabetes.  On  the 
other  hand,  Hanot  admits  that  in  his  patient  it  was  the  diabetes  which 
produced  the  enlarged  hver. 

In  finding  an  explanation  for  these  apparently  contradictory  facts,  can 
we  employ  the  recent  researches  undertaken  by  several  authorities  ?  Ac- 
cording to  Gilbert  and  his  collaborators,  Weil,  Carnot,  and  LerebouUet, 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  J 075 

there  are  two  varieties  of  diabetes  which  di![)end  ujxm  a  functional  dis- 
turbance of  the  liver.  The  former  is  the  result  of  chronic  insufficiency  of 
the  liver,  and  is  called  diabetes  by  anhepatia.  The  latter  is  the  result  of 
functional  hyperactivity  of  the  liver,  and  is  known  as  diabetes  by  hyper- 
hepatia. 

Diabetes  by  anhepatia  results  from  the  fact  that  the  liver  is  chronically 
incapable  of  retaining  the  sugar  ingested  with  the  food  or  formed  in  the 
alimentary  canal.  In  such  a  case  the  glycosuria  does  not  come  from  the 
sugar  manufactured  by  the  liver,  but  from  the  sugar  in  the  foodstuffs  which 
the  liver  has  let  by.  Thus,  we  find  sugar  in  the  urine  after  meals,  while  it 
disappears  during  periods  of  fasting.  The  glycosuria  is  never  high,  and 
rarely  reaches  more  than  40  to  50  grammes.  The  quantity  of  urine  passed 
does  not  exceed  1*5  to  2  litres.  The  amount  of  urea  is  somewhat  low,  and 
varies  from  15  to  20  grammes.  Indicanuria  and  urobilinuria  are  frequent. 
This  slight  diabetes  does  not  induce  severe  symptoms — polydipsia,  polyuria, 
polyphagia,  and  autophagia — but  it  may  provoke  numerous  complications 
— boils,  carbimcles,  cataract,  genital  diabetides,  and  expulsive  gingivitis — 
proving  "  that  the  condition  is  true  diabetes,  and  not  alimentary  glycosuria." 
This  anhepatic  diabetes  is  curable.  The  prognosis  is  not  grave,  and  it  does 
not  end  in  gangrene  or  coma.  Nevertheless,  it  opens  the  door  to  tuber- 
culosis. With  regard  to  its  size,  the  liver  is  normal.  It  may,  however,  be 
enlarged. 

According  to  the  same  authorities,  diabetes  by  hyperhepatia  is  different. 
The  functional  activity  of  the  liver  is  increased,  and  the  sugar  passed  in  the 
urine  may  reach  several  hundred  grammes.  Instead  of  finding  signs  of 
hepatic  insufficiency,  with  indicanuria  and  urobilinuria,  we  see  a  notable 
degree  of  azoturia.  The  urea  is  in  excess.  The  liver  is  enlarged,  with  or 
without  cirrhotic  lesions.  This  hyperhepatic  diabetes  induces  aU  the  com- 
plications of  the  constitutional  disease — namely,  tuberculosis,  coma,  and 
cachexia.  Opotherapy — that  is  to  say,  treatment  by  liver  extract — is 
harmful  in  this  condition,  because  it  increases  the  hepatic  function.  It  is 
indicated  in  anhepatic  diabetes,  in  which  the  functions  of  the  liver  are 
insufficient.  The  diabetes  called  hyperhepatic  may,  according  to  Gilbert 
and  LerebouUet,  be  connected  with  pigmentary  hypertrophic  cirrhosis,  with 
certain  forms  of  hypertrophic  alcoholic  cirrhosis,  with  some  kinds  of  biliary 
cirrhosis,  and  with  certain  cases  of  traumatic  and  of  pancreatic  diabetes,  in 
which  the  lesions  of  the  pancreas  provoke  less  activity  in  that  organ,  and, 
consequently,  more  activity  in  the  liver.  The  latter  fact  is  proved  by 
opotherapy.  Pancreatic  extract  given  to  a  patient  suffering  from  diabetes 
with  hyperhepatia  diminishes  the  production  of  sugar,  whilst  extract  of 
pancreas  given  to  a  patient  suffering  from  diabetes  with  anhepatia  increases 
the  production  of  sugar.     "  Pancreatic  extract  is  indicated  in  cases  of 

125—2 


1976  TEXT-BOOK  OF  MEDICINE 

diabetes  from  hyperhepatia.  It  should  not  be  administered  in  diabetes 
from  anbepatia,  which  is,  on  the  other  hand,  benefited  by  hepatic  extract " 
(Gilbert). 

These  considerations  are  interesting,  and  the  distinction  between  anhe- 
patic  and  hyperhepatic  diabetes  is  ingenious,  but  the  liver  may  be  enlarged 
in  both  eases.  Further,  many  cases  of  diabetes  cannot  be  placed  in  this 
classification,  and  here,  as  often  happens  in  clinical  medicine,  the  inter- 
mediary types  somewhat  absorb  the  extreme  ones. 

Besides,  hyperhepatia  or  functional  hyperactivity  of  the  liver  is  not 
sufficient  to  explain  the  hypertrophy  of  the  organ.  I  had  under  my  care 
two  patients  who  were  not  alcoholic.  One  of  them  passed  an  average  of 
700  grammes  of  sugar  in  the  twenty-four  hours,  and  died  with  an  enlarged 
liver  weighing  2,300  grammes.  The  other  patient  for  a  long  time  passed 
about  800  grammes  of  sugar,  and  his  liver  was  absolutely  normal,  as  the 
autopsy  proved.     How  can  we  reconcile  such  divergences  ? 

If  we  admit  that  the  hypertrophy  in  the  first  patient  was  due  to  func- 
tional hyperactivity  of  the  organ,  it  is  difficult  to  explain  why  the  liver  in 
the  second  patient  preserved  its  normal  size.  I  know  that  some  may 
answer  that  functional  hyperactivity  may  exist,  whether  the  organ  is  or 'is 
not  hypertrophied.  Furthermore,  the  same  objection  is  applicable  to  the 
theory  which  considers  hypertrophy  of  the  liver  as  the  result  of  diabetes. 
If  diabetes  in  which  700  grammes  of  sugar  are  passed  (as  in  my  first  patient) 
is  capable  of  causing  an  enlarged  liver,  it  is  difficult  to  explain  why  diabetes 
with  800  grammes  (as  in  the  second  patient)  should  leave  the  liver  normal. 
And,  however  little  we  may  wish  to  reconcile  the  two  theories  of  diabetes 
capable  of  causing  an  enlarged  liver,  and  of  an  enlarged  liver  capable  of 
causing  diabetes,  we  are  engaged  in  a  vicious  circle  which  is  not  at  all 
banal,  and  the  large  liver  in  diabetes  may  be  at  the  same  time  the  thing 
created  and  the  creator.  This  fact  proves,  in  short,  that  the  pathogenesis 
of  diabetes  and  of  the  enlarged  liver  in  diabetes  is  still  shrouded  in 
obscurity. 

Saccharin  Ascites. — Sugar  may  be  found  in  ascites  of  various  origins. 
Thus,  the  fluid  of  chylous  ascites  sometimes  contains  sugar.  Bahrgebuhr, 
in  his  work  on  chylous  and  chyliform  ascites,  states  that  sugar  was  present 
seven  times  in  fifty-two  cases,  and  as  much  as  8  grammes  of  sugar  per  litre 
has  been  found  in  the  ascitic  fluid.  Guttmann,  Strauss,  and  Ballmann 
think  that  the  absence  of  sugar  is  a  proof  that  the  case  is  not  one  of  true 
chylous  ascites.  Senator,  however,  observes  that  the  absence  of  sugar 
does  not  allow  us  to  deny  the  presence  of  chyle  in  the  ascitic  fluid,  for  the 
composition  of  the  chyle  may  be  modified  by  its  admixture  with  other 
exudates. 

The  variety  of  saccharin  ascites  now  under  discussion  is  quite  different. 


RFIEUMATIC  AND  DVSTROl'lIK!  DISIOASES  1977 

It  is  consecutive  to  diabetes.     Let  ine  ({note  liere  a  case  from  my  clinical 
lecture  on  this  subject : 

A  man,  Hfty-throo  yoars  of  ago,  caiuo  undor  my  caro  \\-i(  li  (odoma  of  tho  logs  and 
ascites,  which  had  lastoil  two  months.  Tlio  ascites  was  reiatod  to  hypertrophic  cirrhosis 
of  the  Uvor,  and  tlio  cirrhosis  was  itself  associated  with  diabetes,  from  which  the  man 
was  sutforing.  Tho  diabetes,  however,  was  hotter  at  the  time.  The  quantity  of  sugar, 
wliicli  had  boon  loO  grammes  two  yoars  ago,  was  only  4-50  grammes  when  tho  patient 
came  into  hospital.  Tho  abdomen  was  tapped,  and  15  litres  of  fluid  were  drawn  off. 
Tho  fluid  reformed  so  quickly  that  in  tho  two  months  preceding  death  eight  tappings 
wore  performed,  and  gave  a  total  of  122  litres  of  fluid.  It  is  remarkable  to  note  that 
tho  a^^l•itic  fluid  contained  sugar,  and  there  was  a  fairly  direct  relationship  Ijot ween  the 
quantity  of  sugar  passed  in  tho  ui'ino  and  the  quantity  of  sugar  in  the  pcuitonoal  fluid. 
When  tho  patient  had  only  a  few  grammes  of  sugar  in  the  urine,  ho  had  practically  none 
in  the  ascitic  fluid.  When  the  sugar  in  tho  urino  increased,  the  sugar  in  the  ascitic 
fluid  was  proportionately  augmented.  Here  are  the  comparative  results  furnished  by 
several  abdominal  tappings  : 

November  14  :  16  htres  of  fluid  dra-wn  off.  Sugar  in  the  urine,  47  grammes  ;  sugar 
in  the  ascitic  fluid,  45  grammes. 

November  24 :  14  litres  of  fluid  drawn  off.  Sugar  in  the  urino,  50  grammes  ;  sugar 
in  the  ascitic  fluid,  56  grammes. 

December  4 :  16  htres  of  fluid  drawn  off.  Sugar  in  tho  urino,  52  grammes  ; 
sugar  in  the  ascitic  fluid,  56  grammes. 

December  12  :  14  litres  of  fluid  di-awn  off.  Sugar  in  the  urine,  45  grammes  ;  sugar 
in  the  ascitic  fluid,  29  grammes. 

December  21 :  15  htres  of  fluid  drawn  off.  Sugar  in  the  urine,  50  grammes  ;  sugar 
in  tho  ascitic  fluid,  50  grammes. 

December  29 :  16  litres  of  fluid  drawn  off.  Sugar  in  the  urine,  160  grammes  ; 
sugar  in  the  ascitic  fluid,  80  grammes. 

January  11 :  16  litres  of  fluid  di'awn  off.  Sugar  in  the  urine,  140  grammes ; 
sugar  in  the  ascitic  fluid,  70  grammes. 

I  would  remind  tlie  reader  that  the  patient  had  an  enlarged  cirrhotic 
liver.  The  histological  examination  has  been  described  on  p.  1918.  It  is 
clear  that  in  this  case  the  sugar  contained  in  the  blood  (hyperglycsemia) 
passed  through  the  kidneys  and  peritoneum,  and  thus  gave  rise  to  sugar 
in  the  urine  and  sugar  in  the  ascites.  Its  passage  into  the  peritoneum  was 
facilitated  by  the  slowing  of  the  circulation  in  the  portal  veins,  and  by  the 
elevation  of  blood-pressure  in  these  vessels.  The  cirrhosis  of  the  liver 
consequently  favoured  the  transudation  of  the  ascitic  fluid  and  the  passage 
of  the  sugar.  The  ascitic  fluid  with  its  sugar  passed  through  the  endo- 
thelium. 

I  am  of  opinion  that  th.e  variety  of  cirrhosis  is  of  little  import  in  the 
production  of  saccharin  ascites  in  diabetics.  The  important  fact  is  the 
presence  of  cirrhosis,  which  facilitates  ascites,  and  sugar  is  found  in  the 
ascitic  fluid  if  the  patient  sufiers  from  severe  diabetes. 

In  short,  this  case  proves  that  we  may  find  ascitic  fluid  containing  40, 
60,  and  80  grammes  of  sugar  in  diabetics  with  a  large  cirrhotic  liver.  The 
quantity  of  sugar  in  the  ascitic  fluid  varies  with  the  quantity  of  sugar  in 


1978  TEXT-BOOK  OF  MEDICINE 

the  urine.  It  increases  or  diminislies  in  direct  proportion.  The  sugar 
appears  to  me  to  favour  the  rapid  and  abundant  reproduction  of  the  ascites, 
just  as  it  favours  polyuria.  Indeed,  we  may  say  that  the  sugar  affects  the 
ascites,  just  as  it  affects  the  urine.  Saccharin  ascites  appears  to  me  to  be 
reproduced  more  quickly  and  more  severely  than  in  the  non-saccharin 
forms,  and  saccharin  ascites  in.  a  diabetic  certainly  makes  the  prognosis 
worse. 

Saccharin  ascites  in  diabetics  has  not  been,  as  far  as  I  am  aware,  the 
subject  of  any  complete  work,  but  yet  it  has  been  noted  by  certain  authors. 
Lepine,  who  has  made  most  important  researches  on  diabetes,  has  given 
me  the  results  of  his  great  experience  regarding  saccharin  ascites  in  diabetics. 
He  has  not  had  the  opportunity  of  studying  in  a  conclusive  manner  the 
quantity  of  sugar  contained  in  the  ascites  of  diabetics,  but  he  has  found  in 
some  cases  high  percentages  which  almost  express  the  quantity  of  urinary 
sugar  at  the  same  time.  He  saw  a  diabetic  woman  who  passed  70  grammes 
of  sugar  in  the  urine,  and  who  had  ascites.  She  became  phthisical,  and  the 
sugar  disappeared  from  the  urine.  The  ascites  was  tapped,  and  sugar  was 
not  found.  According  to  Lepine,  sugar  is  frequent  at  some  period  in  the 
ascites  of  diabetics,  and  it  disappears  when  it  is  absent  from  the  urine. 

When  pleurisy  occurs  in  a  diabetic  patient  it  may  be  saccharin.  I  have 
seen  two  remarkable  examples  of  this.  The  first  case  was  that  of  a  lady 
whom  I  saw  in  consultation  with  Ramon.  The  second  case  was  that  of  a 
diabetic  woman  I  had  in  the  Hotel- Dieu.  She  recovered  from  the  pleurisy, 
which  was  at  the  same  time  tubercular,  hsemorrhagic,  and  saccharic. 

Diagnosis. — I  have  dwelt  on  the  usually  insidious  onset  of  diabetes,  so 
that  we  may  be  on  our  guard  against  an  error  in  diagnosis.  If  glucose  is 
found  in  the  urine,  we  must  ascertain  whether  the  patient  is  suffering  from 
simple  glycosuria  or  from  diabetes.  This  delimitation  of  the  symptom  and 
of  the  disease  is  not  always  possible.  The  question  is  often  only  one  of 
degree,  and  what  is  thought  to  be  a  simple  glycosuria  is  the  forerunner  of 
diabetes. 

We  must  avoid  confusion  between  tabes  and  diabetes.  The  abolition 
of  the  patellar  reflexes,  the  pains  in  the  limbs,  the  expulsive  gingivitis,  the 
amblyopia,  and  the  partial  paralysis  of  the  muscles  of  the  eye,  are  aU  symp- 
toms common  to  diabetes  and  to  tabes.  In  diabetics  they  may  give  rise 
to  a  pseudo-tabes.  In  other  cases  diabetes  and  tabes  run  a  parallel  course. 
Not  that  they  depend  upon  one  another,  but  they  both  belong  to  the  same 
nervous  source,  of  which  I  spoke  under  the  etiology  of  Diabetes. 

Prognosis. — The  prognosis  in  diabetes  should  not  be  considered  as 
absolutely  bad.  The  disease  is  very  serious  in  children,  and  it  is  also  very 
formidable  when  it  runs  a  rapid  course  and  induces  cachexia  (pancreatic 
diabetes  of  some  authors).     Certain  complications  may  give  rise  to  serious 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  1970 

alarm  (gangrone,  tuberculosis,  coma),  but  they  are  exceptional.  Many 
patients,  with  care  and  good  hygiene,  survive  for  an  indefinite  i)eriod.  I 
have  treated  many  diabetics,  and  serious  troubles  have  appeared  to  me  to 
be  exceptional  in  those  who  are  willing  to  treat  the  disease  with  respect. 
We  must  not  base  the  prognosis  on  hospital  results,  because  most  hospital 
cases  are  far  advanced  or  are  suilering  from  severe  complication.s. 

When  we  examine  the  cases  of  diabetes  seen  in  private  practice,  we  find 
that  the  serious  ones  do  not  exceed  6  or  8  per  cent.  In  the  benign  cases, 
which  form  the  very  great  majority,  we  find  persons  who  pass  15,  20,  or 
30  grammes  of  sugar  daUy,  and  who  improve  as  long  as  they  take  care  of 
themselves.  "  Nothing  is  more  common  than  to  see  persons  in  a  state  of 
alarm  because  they  have  learnt  in  some  way  or  other  that  their  urine  con- 
tains sugar.  It  is  very  advantageous  for  the  future  of  persons  with  mild 
diabetes,  who  constitute  the  great  majority  of  cases,  and  take  care  of  them- 
selves, to  know  that  the  severe  cases  are  rare  "  (Worms).  On  the  other 
hand,  the  gravity  of  the  prognosis  is  considerable  in  pancreatic  diabetes, 
death  being  the  usual  ending. 

Pathological  Anatomy. — The  lesions  found  post  mortem  are  not  con- 
stant.    Nevertheless,  the  liver  and  the  kidney  frequently  show  changes. 

The  liver  may  show  congestion,  hypertrophy,  or  cirrhosis. 

The  lesions  of  the  kidneys  are  important.  They  have  thus  been  summed 
up  by  Straus  : 

"  As  regards  the  renal  lesions  in  diabetes,  we  find  that,  m  addition  to  the 
common  lesions,  such  as  interstitial,  parenchymatous,  or  diffuse  nephritis, 
etc.,  there  exists  a  special  alteration,  both  as  regards  its  nature  and  also  as 
regards  its  topography.  As  regards  topography,  this  change  clearly  and 
exclusively  affects  the  zona  limitans,  where  it  involves  the  straight  tubules 
of  Henle  (large  and  small),  and  also,  in  my  opinion,  some  of  the  collecting 
tubules.  This  lesion  does  not  occupy  the  whole  of  the  zona  limitans,  but 
is  confined  to  more  or  less  numerous  and  extensive  foci,  especially  in  the 
neighbourhood  of  the  capillaries.  As  regards  the  nature  of  the  lesion,  it 
presents  histologically  two  forms,  according  to  the  stains  employed.  With 
ordinary  stains,  we  find  a  hyaline  or  vitreous  change  in  the  ceUs  lining  the 
tubules.  This  lesion  was  discovered  by  Armanni.  If  we  employ,  with 
proper  precautions,  iodized  gum,  the  same  cells  are  seen  to  be  infiltrated 
with  glycogen.     This  change  was  discovered  by  Ehrlich." 

Treatment. — The  treatment  of  diabetes  has  given  rise  to  numerous 
works,  and  Robin  has  made  important  communications  on  the  subject. 
My  personal  view  of  the  matter  is  as  follows  : 

Food. — The  patient  should  abstain  completely  from  sugar.  We  may, 
nevertheless,  permit  him  to  sweeten  his  tea  or  his  coffee  with  saccharin. 
He  must  not  eat  pastry,  entremets  with  sugar,  sweet  fruits,  and,  above  all, 


1980  TEXT-BOOK  OF  MEDICINE 

raisins.  He  must  choose  wines  which  are  not  sweet.  Beer  and  milk  are 
allowed.  Milk  is,  indeed,  an  excellent  food  for  the  diabetic  (Fremont),  for 
lactose  has  nothing  to  do  with  glucose.  I  have  often  prescribed  a  milk  cure 
in  diabetics  who  also  sufiered  from  albuminuria,  and  they  did  weU. 

If  I  am  extremely  severe  on  drinks  or  foods  which  contain  sugar,  I 
am  less  so  as  regards  starchy  foods.  I  do  not  say,  of  course,  that  the 
diabetic  should  be  allowed  to  eat  bread,  potatoes,  and  farinaceous  foods 
ad  libitum,  but  I  do  say  that  it  is  a  mistake  to  suppress  them  completely. 
According  to  the  particular  case,  we  may  replace  bread  by  gluten  bread,  or 
bread  made  with  almond  meal  (Pavy's  bread) ;  but  this  is  not  a  reason  for 
prohibiting  wheaten  bread  completely,  and  the  crust  may  especially  be 
allowed.  I  also  allow  some  potatoes,  and  I  do  not  absolutely  prohibit 
sauces,  which  assist  the  alimentation. 

It  is  harmful,  in  my  opinion,  to  attempt  the  total  suppression  of  glycos- 
uria by  a  Draconian  regime.  The  diabetic,  who  has  been  robust  and 
healthy,  with  60,  80,  and  100  grammes  of  sagar  daily,  wastes  and  becomes 
feeble  if  put  on  an  absolutely  rigid  diet  with  the  object  of  suppressing  the 
glycosuria  totally  and  rapidly.  Under  the  influence  of  an  extreme  diet  the 
sugar  may  indeed  disappear  very  quickly  from  the  urine — at  least,  for  a 
time — but  the  patient  is  liable  to  complications,  such  as  albuminuria, 
wasting,  and  tuberculosis,  which  are  sometimes  formidable. 

I  often  see  diabetics  who  have  been  treated,  or  who  treat  themselves, 
with  the  greatest  severity  by  the  absolute  deprivation  of  starchy  food  until 
there  is  no  longer  any  trace  of  sugar  in  the  urine.  Many  of  them  waste, 
while  the  physician  applauds  the  result  of  the  analysis  and  the  disappearance 
of  the  sugar.  A  diabetic  submitted  to  this  extreme  regime  recently  said  to 
me  :  "  I  was  passing  2^  ounces  of  sugar,  and  was  prescribed  such  a  severe 
diet  that,  except  for  meat  without  sauce,  fish  without  sauce,  eggs,  some 
vegetables  and  gluten  bread,  no  food  was  given  me.  The  sugar  certainly 
disappeared  in  four  weeks,  but  I  have  lost  13  pounds  in  weight,  my  appetite 
has  disappeared,  and  I  feel  terribly  weak.  Give  me  back  my  sugar.  I 
really  prefer  it."     And  this  patient  was  not  wrong. 

I  have  often  noticed  the  appearance  of  albuminuria  following  upon  too 
severe  antidiabetic  treatment.  The  sugar  diminishes  or  disappears,  and 
albuminuria  makes  its  appearance. 

Lastly,  if  we  only  remember  that  tuberculosis  threatens  the  diabetic, 
we  shall  understand  that  we  must  beware  of  opening  the  door  to  it  by 
inducing,  through  too  severe  diet,  wasting,  which  the  diabetic  should  always 
avoid. 

I  cannot  too  strongly  insist  upon  these  considerations,  and  for  many 
years  I  have  done  my  best  to  spread  them  in  my  writings  and  my  teaching. 
In  diabetics  in  whom  glycosuria  is  obstinate  I  do  not  attempt  to  bring 


RHEUMATIC  AND  DVSTROPHir  DISEASES  1981 

about  the  disappearance  of  all  the  sugar,  and  I  prefer  that  tlic  diabetic 
should  have  some  sugar  rather  than  see  him  lose  in  weight. 

In  short.,  the  regime  shouhl  not  he  too  severe,  especially  at  first.  It  is 
necessary  to  know  how  to  handle  these  patients.  Starchy  foods,  potatoes, 
and  bread  should  not  he  absolutely  forhidden.  The  whole  question  depends 
on  the  severity  of  the  disease  and  the  general  condition  of  the  patient. 

The  patient  should  never  repress  his  tliirst.  He  should  drink  water  in 
sufficient  quantity,  because  he  thus  prevents  dehydration  of  the  tissues 
and  favours  elimination  of  the  sugar. 

Drugs. — The  drug  treatment  of  diabetes  is  based  on  antipyrin,  arsenical 
preparations,  and  alkaline  remedies.  Antipyrin  is,  in  such  a  case,  a 
wonderful  remedy.  It  must  not  be  given  in  large  doses  or  for  long  periods. 
My  method  is  as  follows  : 

For  the  first  week  in  the  month  the  patient  takes  twice  daily  with  meals 
a  cachet  composed  of  5  grains  of  antipyrin  and  3  grains  of  bicarbonate 
of  soda.  If  the  diabetes  is  severe,  we  may  double  or  treble  the  number  of 
cachets. 

During  the  second  week  of  the  month  the  antipyrin  is  stopped,  and 
arsenic  prescribed.  The  patient  takes  with  each  meal  a  teaspoonfvd  of  a 
solution  containing  2  ounces  of  distilled  water  and  ^  grain  of  arseniate  of 
soda.  It  is  better,  however,  to  give  a  daily  injection  of  ^  grain  of  cacodylate 
of  soda  {vide  Appendix  on  Therapeutics). 

These  two  drugs  are  continued  alternately  for  several  months,  together 
with  alkaline  solutions,  such  as  Vichy  water  (Celestins)  (8  ounces  at  each 
meal).     The  cures  at  Vichy  and  at  Carlsbad  are  very  efficacious. 

Hygiene. — Baths,  douches,  and  massage  should  be  prescribed.  Walk- 
ing or  riding,  fencing  and  swimming,  are  excellent  in  order  to  increase  the 
destruction  of  the  muscle  sugar.  Profuse  sweating  should  be  avoided,  and 
we  must  not  forget  that  symptoms  of  diabetic  coma  appear  after  fatigue, 
excess,  or  long  journeys. 

Opotherapy,  with  hepatic  extract,  appears  to  have  some  action  on  the 
glycosuria  in  some  patients  (Gilbert  and  Chassevant),  notably  in  those  who 
have  functional  insufficiency  of  the  Hver,  with  diminution  of  urea,  uro- 
bilinuria,  etc.  When  the  glycosuria  appears  to  depend  on  hepatic  hyper- 
activity, opotherapy  aggravates  the  disease.  I  have  attempted  to  ascertain 
the  possible  efficacy  of  subcutaneous  injections  of  pancreatic  juice  in 
diabetics.     I  have  not  obtained  any  satisfactory  result. 

Surgical  intervention  is  often  necessary  in  diabetics  (carbuncles,  phleg- 
mon, gangrene).  Surgeons  formerly  did  not  dare  to  operate  on  patients 
with  diabetes  for  fear  of  the  after-results.  Since  aseptic  and  antiseptic 
methods  have  been  employed,  we  have  found  that  these  fears  are  greatly 
exaggerated.     The  surgeon  may  intervene  with  excellent  results  La  diabetes. 


1982  TEXT-BOOK  OF  MEDICINE 

but  yet  we  must  not  hide  tlie  fact  that  operations  performed  under  such 
circumstances  are  not  absolutely  free  from  mishaps. 

Intoxication  is  the  more  to  be  feared  in  the  diabetic  if  the  liver  and  the 
kidneys  are  afiected.  When  the  disease  runs  a  rapid  course,  with  cachexia 
and  ascites,  the  patient  will  not  be  able  to  stand  an  operation  as  weU  as 
one  in  whom  the  disease  runs  a  slow  course,  and  scarcely  affects  the  nutri- 
tion. 

In  any  case,  we  have  to  consider  the  administration  of  chloroform ;  we 
must  remember  that  some  antiseptics  may  cause  severe  toxic  troubles 
through  imperfect  elimination  by  reason  of  the  lesions  in  the  liver  and  the 
kidney.  Lastly,  it  is  necessary  to  remember  that  the  lowered  vitality  of 
the  tissues  is  sometimes  opposed  to  the  firm  holding  of  sutures  and  to  the 
rapid  healing  of  wounds. 

In  diabetic  gangrene  remarkable  results  have  been  obtained  by  the 
application  of  superheated  air  (vide  Appendix). 

VI.  DIABETES  INSIPIDUS. 

1.  Azoturic  Diabetes  —  Azoturia. 

The  excess  of  nitrogenous  matter  in  the  urine  is  not  sufficient  to  con- 
stitute azoturic  diabetes.  Azoturia  is  a  symptom  common  to  several 
morbid  conditions,  while  azoturic  diabetes  (Demange),  like  diabetes  meUitus, 
is  a  general  disease  characterized  by  an  exaggerated  and  constant  loss  of 
nitrogenous  matter  and  by  general  symptoms — polyuria,  polydipsia,  and 
polyphagia — which  somewhat  recall  the  clinical  picture  of  diabetes  mellitus. 

Description. — The  disease  may  commence  suddenly.  It  is  ushered  in 
by  ravenous  hunger  (Bouchard),  profuse  sweats  (Eendu),  or  by  unquench- 
able thirst.  Most  frequently  it  installs  itself  insidiously.  The  thirst  and 
the  appetite  increase  progressively,  and  the  urine  becomes  very  copious. 

The  urine,  which  is  acid  and  transparent  directly  it  is  passed,  soon 
becomes  alkaline  and  turbid,  and  contains  mucus  and  sediments  (uric  acid 
and  urates),  but  no  sugar  or  albumin.  Its  density  varies  from  1002  to 
1015,  according  to  the  amount  passed.  It  is  azoturic — ^that  is  to  say,  it 
contains  an  excess  of  urea,  of  uric  acid,  and  of  nitrogenous  extractives.  In 
twenty-four  hours  the  urea  may  amount  to  100  grammes  (Bouchardat), 
instead  of  the  normal  25  grammes.  The  uric  acid  may  be  as  much  as 
9  grammes  (Bouchardat),  and  the  nitrogenous  extractives  (creatinin, 
uroxanthin)  may  exceed  70  grammes  (Bouchard).  A  similar  excess  is 
noticed  as  regards  the  chlorides  and  phosphates. 

In  cases  of  moderate  severity  the  disease  may  last  indefinitely 
without  becoming  dangerous,  but  in  grave  cases  the  muscular  power  de* 
creases,  the  patient  experiences  excessive  fatigue,  and  is  exposed  to  the 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  1983 

nervous  troubles  described  under  Diabetes  Mollitus.  He  may  suffer  from 
lippmorrhages  into  the  retina  and  the  vitreous,  wliich  are  far  from  being 
rare  in  azoturia,  just  as  in  })hosphaturia  (Trousseau).  At  a  mor<»  ad- 
vanced period  the  appetite  is  lost,  the  wasting  becomes  extreme,  and 
cachectic  oedema  apjiears.  Death  supervenes  by  reason  of  this  excessive 
de nutrition  or  of  some  complications  (haemorrhage,  gangrene,  phthisis). 
In  spite  of  the  gravity  of  the  prognosis,  definite  recovery  has  several  times 
been  recorded. 

The  diagnosis  depends  entirely  on  the  examination  of  the  urine.  The 
examination  is  the  more  important  as  in  some  cases  the  azoturia  is  exces- 
sive, while  the  polyuria  is  absent  (Bouchard).  Azoturic  diabetes  is  some- 
times associated  with  phosphaturia,  and,  indeed,  phosphaturia  may  assume 
such  importance  that  Teissier  has  described  a  separate  form  of  phosphatic 
diabetes. 

etiology — Pathogenesis. — Azoturic  diabetes  is  most  frequent  during 
the  middle  period  of  life.  It  appears  to  arise  chiefly  from  nervous  causes, 
violent  emotions,  grief,  cerebral  lesions,  traumatism,  and  syphilis. 

As  regards  the  intimate  nature  of  the  disease,  it  is  probable  that  it 
depends  upon  an  exaggerated  disassimilation  of  the  tissues.  In  this  process 
are  we  to  incriminate  chiefly  the  liver,  which,  according  to  recent  theories, 
is  the  true  source  of  urea  ?  If,  however,  the  liver  makes  urea,  it  is  at  the 
expense  of  the  albuminoid  material,  wliich  is  split  up  into  glycogen  and  urea. 
As  Demange  observes,  in  azoturic  diabetes  there  is  no  glycosuria,  and 
therefore  the  theory  is  at  fault.  Azoturia  is  a  general  disturbance  of 
nutrition,  which  probably  results  from  the  nervous  system.  At  the  moment 
our  knowledge  does  not  extend  farther. 

As  regards  treatment,  the  patient  must  be  kept  at  rest,  and  well  nourished, 
especially  with  proteid  food ;  drugs  which  appear  to  limit  the  denutrition 
should  be  prescribed — arsenic,  valerian,  and  opium  in  large  doses, 

2.  Essential  Polyuria. 

Essential  polyuria  is  often  called  diabetes  insipidus.  I  have  not  to 
describe  the  secondary  polyuria  which  is  associated  with  various  morbid 
conditions  (Bright's  disease,  hysteria),  but  I  have  only  essential  polyuria 
in  \'iew. 

Description. — Polyuria  and  polydipsia,  which  naturally  results,  form 
the  whole  disease.  Certain  individuals  drink  and  pass  10,  20,  or  30  litres 
of  water  in  the  twenty-four  hours,  and,  indeed,  these  figures  have  been 
exceeded.  The  necessity  to  pass  water  is  frequent  and  imperative,  and 
may  cause  insomnia  through  disturbing  the  night's  rest.  The  thirst  is 
excessive,  and  we  see  patients  who  swallow  1  or  2  litres  of  fluid  at  a  gulp. 
Deprivation  of  fluid  is  so  intolerable  to  them  that  they  will  drink  anything 


1984  TEXT-BOOK  OF  MEDICINE 

whicli  comes  to  hand.  They  never  go  to  bed  without  having  made  pro- 
vision for  the  night.  They  do  not  go  on  a  journey  without  taking  special 
precautions. 

This  disease  sometimes  commences  suddenly.  It  may  last  for  a  long 
while  without  compromising  health,  since  the  economy  suffers  no  loss,  and 
the  clear,  limpid  urine,  of  low  specific  gravity,  does  not  contain  more  solids 
in  the  twenty-four  hours  than  normal  urine.  Nevertheless,  says  Trousseau, 
we  must  not  rely  too  much  on  the  so-called  benignity  of  the  essential 
polyuria. 

We  do  not  see  here  the  nervous  troubles  and  the  disorders  of  nutrition 
which  are  so  characteristic  of  diabetes  meUitus.  The  intellectual  faculties 
are  intact  and  the  genital  functions  are  normal.  Pulmonary  phthisis,  which 
is  very  frequent  in  diabetes,  has  only  been  found  twice  in  seventy  cases 
(Lancereaux). 

Essential  polyuria  may  last  for  years  without  compromising  life.  The 
digestive  functions  are,  however,  often  sluggish,  and  constipation  is  very 
obstinate.     Children  do  not  stand  this  disease  so  well. 

We  know  but  little  of  the  causes  and  of  the  pathogenesis  of  essential 
polyuria.  In  some  cases  the  disease  is  .hereditary.  Many  observations 
prove  the  influence  of  nervous  causes,  acute  emotions,  head  injuries,  falls 
on  various  parts  of  the  body,  lesions  of  the  brain,  of  the  bulb,  and  of  the 
fourth  ventricle. 

As  regards  treatment,  diuretic  drinks  must,  of  course,  be  avoided. 
Saccharin  and  starchy  foods  should  be  taken  in  small  quantities. 

Opium,  valerian,  and  bromides  have  given  good  results.  Antipyrin 
appears  to  me  to  have  some  advantages.  Electricity  may  be  employed  in 
the  form  of  continuous  currents  (Le  Fort). 

If  the  polyuria  appears  to  be  associated  with  gyphilis,  mercury  and 
iodide  of  potassium  may  be  tried. 

VII.  EELATIONS  BETWEEN  INJUEY  AND  DIABETES. 

Diabetes,  diabetes  mellitus,  and  diabetes  insipidus  show  intimate  rela- 
tions with  injury.  A  shock,  a  blow,  a  fall,  a  railway  accident,  may  cause 
diabetes  in  persons  who  were  previously  in  perfect  health.  The  injury  has 
alone  been  the  cause  of  the  disease,  and  I  have  quoted  many  examples  of 
this  in  my  clinical  lecture  on  this  subject.*  I  reproduce  some  of  these  cases 
here  : 

Traumatic  Diabetes  Insipidus. — A  man,  forty-four  years  of  age,  came  under  my  care 
at  the  Hotel-Dieu  for  wasting  and  severe  thirst.    He  drank  from  10  to  12  litres  of  fluid 

*  "  Rapports  du  I^aumatisme  avec  le  Diabete  "  (Clinique  Medicale  de  V Hotel-Dieu, 
1899.  7"^  legon). 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  1985 

d'lily,  and  had  ho  nut  roatrainod  hiiusolf,  ho  would  havo  ilrunk  moro.  i£o  swallowi-d 
at  a  gulp  ft  litre  of  water  moro  easily  than  I  could  drinit  a  glassful.  He  was  therefore 
suffering  from  polydifwia — that  is  to  say,  from  constant  and  unquenchable  thirst. 
As  a  corollary  ho  liad  polyuria — that  is  to  say,  he  pas.sfd  from  10  to  12  litres  of  water 
in  the  twonty-four  hours.  The  urine  was  always  colourless,  transparent,  and  without 
the  sUghtest  deposit. 

With  these  two  sjTnptoms,  polydipsia  and  polyuria,  it  might  at  first  have  been 
supposed  that  the  man  was  suffering  from  diabetes  moilitus.  It  is  easy  to  decide  this 
point,  without  employing  the  customary  tests  for  sugar.  The  hydrometer  in  the  test- 
glass  showed  that  density  was  only  1003.  This  fact  showed  that  the  patient  was  not 
suffering  from  diabetes  mellitus,  Ixjcause  the  sugar  increases  the  specific  gravity  of  the 
urine  to  a  considerable  degree.  It  rises  from  1018,  the  normal  figure,  to  1025,  1030, 
1050,  and  even  more,  in  diabetes.  A  man  who  was  suffering  from  diabetes,  and  who 
passed  daily  10  to  12  litres  of  urine,  ought  to  pass  200  grammes  of  sugar  ;  and  therefore 
the  specific  gravity  of  his  urine  would  be  very  high.  On  the  other  hand,  the  lowering 
of  the  specific  gravity  to  1003  indicated  the  absence  of  sugar,  and,  as  a  matter  of  fact, 
the  analysis  showed  not  the  slightest  trace  of  glucose. 

Was  tliis  case,  then,  one  of  azoturic  or  of  phosphaturic  diabetes  ?  No  ;  for  in  such 
a  case  we  should  find  a  sediment  in  the  bottom  of  the  glass,  and  the  specific  gravity  of 
the  urine  would  not  be  so  low  as  1003.  I  ought  to  say,  however,  that  the  man  passed 
more  urea  and  more  phosphates  than  normal.  In  the  twenty-four  hours  the  urine 
contained  44  grammes  of  urea  and  3  grammes  of  phosphates.  This  loss  of  urea  and 
phosphates  was  not  excessive,  but  it  was  far  from  being  sufficient  to  call  the  diabetes 
azoturic  or  phosphaturic,  and  it  was  in  direct  proportion  to  the  enormous  amount  of 
urine  secreted. 

If  the  diabetes  in  this  patient  was  neither  glycosuria,  azoturic,  nor  phosphaturic, 
what  was  it  ?  It  was  a  simple  diabetes  insipidus,  also  called  polyuria,  or  simple  poly- 
dipsia. Having  made  this  point  in  diagnosis,  let  us  consider  the  history  of  the 
patient. 

The  diabetes  came  on  suddenly  in  a  few  hours.  At  one  fell  swoop  the  man  was 
taken  ill  with  intense  thirst.  This  seiziu:e  occurred  under  the  following  circumstances  : 
On  January  28,  fifteen  months  before,  he  was  working  in  a  factory,  when  the  lathe 
wheel,  which  weighed  40  kilogrammes,  broke  and  struck  him  a  severe  blow  on  the  right 
shoulder  near  the  thorax.  At  this  spot  he  had  only  a  severe  bruise,  but  the  shock 
was  so  terrible  that  the  poor  man  was  thrown  back  several  yards,  and  in  his  fall  the 
nape  of  his  neck  and  his  head  struck  against  the  block  of  a  vice.  He  remained  un- 
conscious for  five  hours,  and  was  taken  in  a  comatose  condition  to  the  Beaujon  Hospital, 
into  Lucas-Championniere's  ward.  The  wounds  were  sewn  up ;  the  scars  were  still 
visible.  It  was  not  clear  that  he  had  fractiu-ed  the  petrous  bone,  and  yet  a  serous 
and  blood-stained  discharge  flowed  from  the  right  ear,  and  from  this  time  the  sense  of 
hearing  was  lost.     This  terrible  accident  was  accompanied  by  fever  and  delirium. 

Next  day  the  patient  regained  consciousness,  and  at  once  experienced  the  urgent 
thirst  which  has  since  never  left  him.  As  it  was  not  known  at  the  moment  that  he  was 
suffering  from  polydipsia,  his  fluid  allowance  was  quite  insufficient,  so  that,  in  spite  of 
his  headache  and  vertigo, he  dragged  himself  to  the  pantry  and  anywhere  where  he  knew 
he  would  find  water,  in  order  to  satisfy  his  thirst.  "  I  would  have  drunk  anything, 
even  my  urine."  From  this  time  he  was  given  daily  15  litres  of  different  drinks — 
hops,  cocoa,  wine  and  water — and  he  took  special  care  to  provide  for  the  night.  He 
remained  about  eight  days  in  hospital,  suffering  from  violent  headache,  and  then,  as 
he  felt  better,  he  went  out,  in  order  to  resume  his  employment  as  a  mechanic.  He  had 
not  a  trace  of  glycosuria. 

A  fresh  symptom  now  appeared.  The  patient,  who  had  formerly  had  a  moderate 
appetite,  was  suddenly  seized  with  boiilimia.     He  took  four  or  five  meals  a  day,  and  goi 


1986  TEXT-BOOK  OF  MEDICINE 

up  at  niglit  in  order  to  eat  and  to  drink.  He  swallowed,  without  mastication,  enormous 
quantities  of  meat  and  bread.  The  money  which  he  earned  scarcely  served  to  feed  him, 
and  he  spent  eight  francs  a  day  on  food. 

He  was  soon  obhged  to  give  up  his  trade :  the  headache  reappeared,  he  felt  very 
weak  and  tired,  and  his  food  did  not  restore  his  strength.  He  then  came  to  the  Beaujon 
Hospital,  under  Fernet,  where  he  was  treated  with  valerian.  At  the  end  of  some  weeks, 
as  he  felt  better,  he  attempted  to  resume  his  work,  but  his  strength  failed  afresh.  He 
suffered  from  giddiness,  vertigo,  and  insomnia,  and  he  went  to  the  Charite  Hospital, 
nuder  Oulmont.  Some  weeks  of  rest  and  treatment  appeared  to  produce  improvement, 
and  he  made  a  fresh  attempt  to  work.  It  was  fruitless,  and  sis  weeks  later  he  came  to 
the  Tenon  Hospital,  under  Beclere.  Finally,  after  going  to  many  different  hospitals, 
he  came  imder  my  care. 

Apart  from  the  polydipsia  and  polyphagia,  his  condition  was  somewhat  as  follows  : 
We  found  none  of  the  usual  symptoms  of  diabetes  meUitus  ;  the  teeth  and  the  gums  were 
healthy ;  there  were  no  eruptions  of  boils  ;  the  patellar  reflexes  were  normal,  and 
the  sight  was  not  affected ;  but  the  general  condition  left  much  to  be  desired. 
The  patient  had  lost  9  kilogrammes  in  a  year,  and  was  quite  prostrated.  He  also 
suffered  from  profuse  sweating,  especially  at  night.  In  spite  of  the  bouhmia  and 
polydipsia,  he  did  not  suffer  from  dyspepsia  or  from  vomiting,  the  stomach  was  nou 
dilated,  and  the  stools  were  normal  and  regular. 

I  gave  the  man  as  much  food  and  drink  as  he  wished,  prescribed  valerian  and  opium, 
and  placed  a  seton  in  the  nape  of  the  neck.  Such  was  the  history  of  this  patient  who 
suddenly  suffered  from  polydipsia  folloTving  a  violent  injury.  His  case  will  serve 
as  a  basis  for  discussion,  but  before  treating  on  parallel  Hnes  traumatic  andnon-traumatio 
diabetes  insipidus,  I  think  it  weU  to  quote  some  other  cases.  Several  of  them  are  given 
in  Jo  dry's  thesis.     They  are  as  follows  : 

1.  A  girl,  fourteen  years  of  age,  fell  on  her  feet  after  sUding  down  an  escarpment 
4  or  5  metres  in  height.  When  she  was  picked  up  she  was  apparently  dead.  The 
condition  of  coma  lasted  for  four  hours,  with  grinding  of  the  teeth,  injection  of  the  face, 
vomiting,  dilated  pupUs,  squint,  and  haemorrhage  from  the  left  ear,  which  lasted  for 
the  greater  part  of  the  day  (July  11).  There  was  some  improvement  during  the 
nest  few  days.  On  the  19th  intelligence  was  fairly  clear,  less  squint,  peaceful  sleep, 
and  good  appetite.  On  the  20th  unquenchable  thirst  suddenly  came  on.  The  patient 
drank  6  Htres  of  fluid  in  the  twenty -four  hours,  and  passed  an  equivalent  quantity  of 
urine,  as  clear  as  water,  and  containing  no  sugar  or  albumin.  The  polyuria,  with  the 
accompanying  phenomena,  lasted  until  July  29.  On  August  4  the  thirst  ceased,  and 
the  appetite  was  great.  There  remained  only  sUght  amblyopia  and  swimming  in  the 
head,  which  disappeared  at  the  end  of  the  month.  The  patient,  who  had  lost  her  memory 
for  certain  proper  names,  recovered  it,  but  she  could  not  remember  anything  that  had 
happened  shortly  before  the  accident. 

2.  A  youth,  eighteen  years  of  age,  came  into  the  Charite  Hospital  in  January, 
1855.  He  was  suffering  from  mUd  varioloid,  which  rapidly  recovered.  Soon  after,  to  the 
great  astonishment  of  his  friends,  he  commenced  to  drink  from  8  to  10  pots  of  barley- 
water  daily.  During  the  night  he  got  up  several  times  in  order  to  drink.  His  appetite 
was  voracious.  The  polydipsia  and  boulimia  were  of  traumatic  origin,  for  the  boy 
had  been  kicked  on  the  forehead  by  a  horse  six  years  previously.  The  loss  of  con- 
sciousness had  lasted  for  only  a  few  minutes,  but  the  shock  had  been  violent,  as  a  large 
and  well-marked  cicatrix  proved.  On  the  same  day  as  the  accident  the  thirst  became 
greatly  increased,  and  had  since  this  period  never  ceased  troubling  the  patient  day 
and  night.  For  the  past  six  years  this  condition  constituted  an  inftrmity  which  was 
bearable,  and  did  not  appear  to  affect  the  patient's  health.  He  drank,  on  an  average,  • 
10  litres  in  the  twenty-four  hours.  The  quantity  of  urine  was  practically  equal  to  the 
quantity  of  fluid  ingested.     The  urine  was  clear,  colourless,  without  smell,  like  pure 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  1987 

water.  The  absonco  of  sugar  and  albuoiinuria  was  proved  oa  sevoral  occasiona.  The 
polyuria  and  tho  polydipsia  complotoly  coa.sed  during  tho  acuto  aflectioa  wliich  noces- 
Bitatod  liis  admission  to  hospital. 

3.  A  man,  twonty-soven  years  of  ago,  of  fairly  good  constitution,  fell  from  a  height 
on  Juno  18,  1859.  Ho  sustained  a  fracture,  complicated  by  a  wound,  with  Buch  cerebral 
disturbance  that  ho  remained  eleven  days  unconseious,  and  was  oltliged  to  remain 
in  hospital  for  forty  days.  He  went  out  too  soon,  his  strength  failed,  and  ho  was  obliged 
to  return.  Condition  on  August  5  :  Severe  and  almost  continuous  headache,  not  well 
defined,  andsoraotimes  more  intense  in  t  ho  noighbourhoodof  the  scar  (right  frontal  region); 
dull  and  melancholy  ;  gait  slow  and  imcortain  ;  frequent  vertigo,  gidtliness,  especially 
when  walking  or  on  making  sudden  movement ;  slight  facial  paralysis  on  tho  right  side  ; 
vision  completely  absent  on  the  right  side,  diminished  on  the  loft ;  right  arm  a  httle 
weaker  than  the  loft.  When  tho  patient  stands  up  he  always  experiences  a  backward 
movement,  just  before  he  commences  to  walk.  Digestion  good  ;  no  vomiting  ;  insomnia 
almost  constant;  great  and  continuous  thirst  since  the  accident.  During  his  first  day 
in  the  hospital  he  drank  nearly  25  litres :  urine  pale,  hmpid,  liko  water,  without  any 
traces  of  sugar.  From  the  11th  to  tho  12th  the  patient  drank  8  litres.  Two  grammes  of 
oxtrcict  of  valerian  were  prescribed,  and  next  day  2  litres  less  urine  passed.  From  the 
18th  to  the  20th  urine  fairly  abundant  and  thirst  somewhat  acute.  Extract  of  gentian 
root  prescribed,  and  a  seton  placed  in  the  nape  of  the  neck.  The  headache  diminished 
gradually,  and  disappeared  completely  during  tho  early  part  of  September.  The 
paralysis,  the  inco-ordination  of  movement,  and  the  backward  motion  also  disappeared. 
The  polyuria  and  i>olydipsia  persisted,  on  the  other  hand,  imtil  September  6.  From 
the  7th  the  quantity  of  urine  diminished  daily,  and  by  the  17th  it  had  regained  its 
normal  limit.     On  October  15  it  was  found  that  the  recovery  was  maintained. 

■i.  A  mason  fell  from  a  scaffolding  on  August  30,  1859.  After  the  fall  a  small 
contused  wound  was  found  on  the  upper  part  of  the  forehead,  but  the  frontal  bone  was 
not  laid  bare.  The  right  upper  eyelid  showed  ecchymosis,  and  blood  flowed  from  the 
left  ear.  No  fractiu-e  was  foimd  at  any  part  of  the  cranium.  Both  radii  and  the  left 
clavicle  were  fractured.  Loss  of  consciousness,  which  lasted  five  days,  during  which 
time  the  patient  passed  from  a  condition  of  stupor  to  one  of  restlessness.  On  Sep- 
tember 5  he  began  to  drink  and  to  eat  to  excess.  The  polyuria  and  the  polydipsia 
increased  progressively  from  5  to  14  litres.  The  urine  was  almost  colourless,  with  a 
slight  greenish  reflection,  but  without  any  marked  odour.  Analysis  on  two  occasions 
showed  neither  sugar  nor  albumin.  On  September  23  the  polydipsia  diminished, 
presenting  during  this  decrease  the  same  proportion  as  during  its  increase.  On 
November  10  the  patient  left  the  hospital,  completely  recovered  from  all  the  effects  of 
the  fall,  with  the  exception  of  a  slight  diminution  in  the  hearing  power  on  the  left  side. 

0.  A  youth,  eighteen  years  of  age,  who  had  always  been  in  good  health,  received 
a  blow  from  a  wooden  swM-d  on  the  right  side  of  the  head,  followed  immediately  by  loss 
of  consciousness,  violent  pain  in  the  head,  severe  fever  with  rigors,  and  acute  thirst. 
These  troubles  soon  disappeared,  and  two  days  later  he  was  able  to  resume  his  work, 
but  the  thirst  persisted.  Three  weeks  later  he  begged  for  treatment  to  relieve  the 
thirst.  He  did  not  feel  any  weaker  since  the  accident,  but  was  sure  he  had  grown  thinner. 
His  digestion  was  good,  and  his  appetite  had  not  increased.  Pulse,  70.  No  pain  in 
the  head  since  the  day  after  the  accident.  The  quantity  of  water  drunk  was  estimated 
at  more  than  30  litres  in  the  twenty -four  hours.  He  would  have  drunk  continually 
if  he  had  not  felt  his  stomach  swell  and  become  painful  when  he  drank  too  much. 
The  urine  was  proportionate  to  the  quantity  of  water  taken,  and  was  limpid,  very  sHghtly 
coloured,  and  odourless.  There  was  not  the  least  trace  of  sugar.  The  specific  gravity 
was  scarcely  higher  than  that  of  water.  After  a  futile  exhibition  of  opium,  valerian, 
in  large  doses,  was  prescribed.  Progressive  diminution  in  the  thirst  after  three  weeks' 
treatment. 


1988  TEXT-BOOK  OF  MEDICINE 

Description. — The  foregoing  cases  furnisli  material  for  tracing  the  history 
of  traumatic  diabetes  insipidus.  Although  the  disease  may  foUow  trau- 
matism affecting  any  region,  it  is  more  common  in  head  injuries.  Diabetes 
insipidus,  or  simple  polydipsia,  may  appear  some  hours  or  directly  after  the 
injury.  In  my  patient  the  shock  was  followed  by  loss  of  consciousness,  and 
on  the  next  day  the  polydipsia  was  so  great  that  10  to  12  litres  of  fluid  did 
not  satisfy  the  thirst.  In  the  youth  kicked  on  the  forehead  by.  a  horse 
(Charcot)  exaggerated  thirst  appeared  on  the  same  day  as  the  accident,  and 
from  that  time  never  ceased.  In  the  young  man  who  fell  from  a  height 
(Moutard-Martin)  the  thirst  appeared  at  the  time  of  the  accident,  and  in 
the  young  man  who  received  a  blow  on  the  head  with  a  sword  the  polydipsia 
appeared  directly  after  the  accident,  and  the  quantity  of  fluid  was  estimated 
at  more  than  30  litres  in  the  twenty-four  hours. 

These  examples  show  that  traumatic  diabetes  insipidus  may  appear 
directly  after  an  injury.  The  polydipsia  supervenes  at  once,  and  the  sur- 
prising feature  is  the  sudden  onset,  in  a  healthy  individual,  of  diabetes,  which 
may  last  for  the  remainder  of  life.  This  sudden  onset  is  not  special  to 
traumatic  polydipsia,  but  is  also  seen  in  cases  of  diabetes  insipidus  which 
are  not  traumatic. 

In  some  cases  the  polydipsia  does  not  supervene  until  some  days  after 
the  accident.  Thus,  in  the  young  girl  who  feU  upon  her  feet  (Martin)  the 
polydipsia  appeared  nine  days  after  the  accident,  and  in  the  mason  who  fell 
£rom  the  scaffolding  (Debron)  it  appeared  five  days  after  the  accident,  as 
soon  as  the  patient  recovered  consciousness. 

The  symptoms  of  diabetes  insipidus  are  identical  in  traumatic  and  in 
non-traumatic  cases.  In  those  quoted  the  patients  drank  15,  20,  and  30 
litres  of  fluid  daily,  and  even  more.  Some  have  a  thirst  which  is  truly 
unquenchable.  They  are  afraid  to  lie  down  or  to  go  to  bed  without  pro- 
viding themselves  with  an  abundant  supply  of  water.  My  patient  used  a 
siphon-tube,  so  that  he  could  satisfy  his  thirst  during  the  night  almost 
without  breaking  his  rest.  This  unbridled  thirst  is  not  special  to  traumatic 
polydipsia.  It  is  also  seen  in  non-traumatic  cases  of  polydipsia.  Thus, 
Trousseau  speaks  of  a  patient  who  drank  40  litres  daily.  Aussit  gives  the 
history  of  a  smaU  patient,  four  years  old,  who  had  such  urgent  need  for 
fluid  that  on  several  occasions  he  drank  the  contents  of  his  chamber-pot. 
On  another  occasion  he  went  down  into  a  neighbour's  cellar  and  drank  the 
beer  from  the  cask.  His  allowance  of  water  during  the  night  was  4  litres. 
Accordingly,  whether  the  polydipsia  is  traumatic  or  not,  the  need  for  drink 
is  just  as  urgent.  Perhaps,  indeed,  it  is  more  severe  in  simple  polydipsia 
than  in  diabetes  meUitus. 

The  polyuria  is  proportionate  to  the  polydipsia,  and,  according  to  the 
case,  the  patient  passes  15,  20,  or  30  litres  of  water. 


RHEUMATIC  AND  DYSTIKJPHIC  DISEASES  1980 

There  is  a  symptom  to  wliich  I  wish  to  call  attention — namely,  boulimia 
or  polyphaf!;ia — that  is  to  say,  excessive  appetite.  We  are  too  prone  to 
believe  that  i)olv][)hiigia  is  a  symptom  reserved  for  diabetes  mellitus,  but 
this  is  a  mistake.  We  see  patients  who  have  no  glycosuria,  and  who  are 
not  suffering  from  diabetes  mcllitus,  but  simply  from  polydipsia,  and  yet 
the  need  for  food  is  extreme,  and  we  may  say  that  their  hunger  is  as  great 
as  their  thirst — in  fact,  they  suffer  from  boulimia  just  as  much  as  from 
polydii)sia.  In  order  to  ascertain  the  quantity  of  food  taken  daily  by  my 
patient  in  the  Saint- Chris tophe  Ward,  liis  daily  rations  of  bread,  meat, 
vegetables,  and  fluid,  were  placed  on  a  table,  and  there  was  sufficient  to 
supply  a  whole  family  with  food  and  drink.  It  may  be  said  that  these 
patients  are  never  satisfied,  and  scarcely  is  one  meal  finished  when  they 
wish  to  start  a  second. 

Boulunia  has  been  noted  in  several  cases  of  traumatic  polydipsia. 
Trousseau  was  one  of  the  first  to  call  attention  to  it  in  persons  sufiering 
from  polydipsia  without  glycosuria,  and  he  writes  as  follows  :  "  Contrary 
to  what  you  will  find  stated  by  most  authors,  who  in  this  respect  have  only 
repeated  previous  statements,  the  appetite  as  well  as  th.e  thirst  is,  as  a  rule, 
not  only  increased,  but  very  much  exaggerated.  You  will  recall  my  patient 
in  the  Sainte- Agnes  Ward,  and  the  enormous  quantity  of  food  wliich  he  ate 
in  the  twenty-four  hours.  You  have  heard  him  say  that  he  was  the  terror 
of  proprietors  of  those  restaurants  where  bread  was  allowed  free.  As  soon 
as  he  had  taken  a  meal  or  two  in  one  of  these  establishments  he  was  offered 
money,  so  he  said,  not  to  come  back  again." 

Whether  diabetes  insipidus  is  or  is  not  traumatic,  it  may  be  said  that, 
in  spite  of  the  enormous  quantities  of  fluid  and  solids,  the  digestive  faculties 
do  not  appear  to  be  disturbed,  and  the  digestion  goes  on  as  regularly  as  in 
the  normal  condition.  The  absence  of  dilatation  is  remarkable  in  the  case 
of  a  stomach  which  for  months  and  years  receives  such  a  quantity  of  liquids 
and  solids. 

An  important  question  remains  to  be  cleared  up  :  Is  traumatic  diabetes 
insipidus  more  or  less  serious  than  the  non-traumatic  variety  ?  Let  us 
first  consider  the  prognosis  of  non-traumatic  diabetes.  "  Although  it  may 
for  a  long  while  be  compatible  with  apparent  integrity  of  health,  be  on  your 
guard,"  says  Trousseau,  "  against  thinking  that  matters  wfll  remain  for 
long  in  such  a  favourable  condition.  The  boulimia  is  soon  replaced  by  in- 
Burmountable  anorexia,  the  wasting  becomes  more  and  more  alarming,  the 
skin  ^^^the^s  and  takes  on  an  earthy  tint,  the  breath  is  foetid,  and,  just  as 
in  diabetes  mellitus,  we  see  the  symptoms  of  tubercular  phthisis  appear. 
I  have  long  believed  on  the  testimony  of  my  predecessors  that  polydipsia 
was  not  as  grave  as  glycosuria,  but  to-day  experience  has  singularly  modified 
my  ideas  in  this  respect.  AVhile  in  my  own  private  practice  and  in  my  hospital 
II-  126 


1990  TEXT-BOOK  OF  MEDICINE 

wards  I  can  record  a  large  number  of  patients  with  glycosuria  whose  health 
was  excellent  for  a  long  time,  although  I  did  not  employ  active  treatment,  I 
have,  on  the  other  hand,  had  the  misfortune  to  see  nearly  all  those  whom  I 
treated  for  polyuria  waste  rapidly,  and  come  to  the  end  of  their  lives  much 
more  quickly  than  diabetics." 

On  examining  the  cases  of  traumatic  polydipsia,  I  find  that  recovery  has 
sometimes  followed  after  a  few  weeks  or  a  few  months  of  treatment.  I  think, 
therefore,  that  traumatic  polydipsia  is  less  obstinate,  less  grave,  and  some- 
what less  rebellious  to  treatment  than  the  non-traumatic  form.  What  is 
the  treatment  ?  The  same  indications  are  applicable  to  both  varieties. 
Extract  of  valerian  in  large  doses,  extract  of  belladonna  in  daily  doses  of 
I  grain,  and  antipyrin  in  daily  doses  of  15  to  30  grains  in  the  twenty-four 
hours,  may  be  employed.  Hydrotherapy  is  also  of  service,  and  counter- 
irritation  with  the  cautery  or  with  setons  is  especially  applicable  in  trau- 
matic polydipsia.  I  applied  the  cautery  and  setons  in  my  patient.  As  a 
result,  he  showed  great  improvement :  the  nights  were  less  disturbed,  the 
thirst  was  less  acute,  the  urine  passed  only  amounted  to  6  or  7  litres  instead 
of  from  8  to  10  litres.  Although  the  therapeutic  success  was  not  complete, 
we  may  yet  admit  the  benefit  of  the  treatment. 

Traumatic  Diabetes  Mellitus. — A  shock  or  a  blow  upon  the  head  or 
some  otlier  part  of  the  body  may  bring  on  diabetes  mellitus  quite  suddenly 
in  persons  who  were  previously  in  perfect  health,  as  the  following  examples 
show : 

One  of  my  friends,  who  was  assisting  in  the  preparations  for  the  fite  on  July  14  in 
Algiers,  received  such  a  violent  blow  on  the  back  of  the  neck  that  he  lost  consciousness. 
When  he  came  to,  some  hours  later,  he  immediately  asked  for  something  to  drink,  and 
from  this  time  on  the  polydipsia  became  so  great  that  6  to  8  litres  of  fluid  a  day  scarcely 
sufficed  to  quench  his  thirst.  The  examination  of  the  urine  revealed  40  grammes  of 
sugar  in  the  twenty-four  hours  ;  the  urea  and  phosphates  were  also  increased.  In 
twenty  years  the  diabetes  has  never  completely  disappeared.  When  the  patient 
relaxes  his  diet,  the  sugar  reaches  50  and  60  grammes.  Under  the  influence  of  diet 
and  alkaline  waters,  with  arsenic  or  antipyrin,  the  sugar  falls  to  8  or  10  grammes, 
but  the  glycosuria  never  disappears  completely,  and  is  always  ready  to  show  an 
increase.  Apart  from  polydipsia  and  glycosuria,  this  traumatic  diabetes  has  never 
given  rise  to  comphcations,  and  is  not  even  accompanied  by  polyphagia.  It  comprises 
the  slight  yet  obstinate  forms  of  traumatic  diabetes.  Such  is  not  always  the  case, 
for  all  the  varieties  of  diabetes  mellitus  may  foUow  trauma.  The  following  are  cases 
taken  from  the  thesis  of  Bemstein-Kohan,  Jodry,  and  from  the  work  of  Brouardel  and 
Richardiere : 

1.  A  railway  gatekeeper,  forty-six  years  of  age,  previously  in  good  health,  received 
a  violent  blow  on  the  head.  He  remained  unconscious  for  an  hour.  After  the  accident 
he  experienced  acute  thirst  and  ravenous  hunger  and  passed  an  enormous  quantity 
of  urine.i  The  urine  was  loaded  with  sugar,  and  its  specific  gravity  was  1052.  Rest 
in  bed,  bhsters  to  the  nape  of  the  neck,  and  purgatives  caused  marked  improvement 
m  his  condition  :  the  urine  became  less  abundant,  the  specific  gravity  fell  to  1012, 
and  the  sugar  disappeared  completely.  The  man  resumed  his  work,  and  the  cure  was 
ijermanent. 


RHEUMATIC  AND  DYSTROPHIO  DISEASES  I'M)! 

2.  A  frtim-labouror,  fourteen  years  of  ago,  wHoho  health  was  usually  excolient, 
reooived  a  blow  on  the  right  occipital  region  from  a  falhng  tree  :  scalp  wound,  fracture 
of  the  cranium,  signs  of  commotio  cerebri,  loss  of  consciousness,  vomiting,  a  fofjiing  of 
heaviness  of  the  whole  body,  without  localized  paralysis.  On  the  day  following  the 
accident  the  urine  was  abundant,  and  contained  6  grammes  of  sugar  jwr  litre.  In 
the  evening  ho  was  attacked  by  irresistible  hunger,  and  ate  turnip  soup  prepartid  with 
milk.  Deat  h  followed  in  a  few  wcelcs.  The  autopsy  showed  a  fracture  of  the  occipital 
bono.     The  brain  appeared  to  be  healthy. 

3.  In  the  following  ca-so  (Frericlis)  a  young  man,  twenty-si.K  years  of  ago,  fell 
about  10  foot,  striking  his  forehead  against  the  groimd.  Ho  was  not  troubled  with 
tliirst  until  six  months  afterwards.  I'he  diabetes  became  so  severe  that  he  passed 
more  than  500  grammes  of  sugar  daily.  He  died  of  pulmonary  tuberculosis.  The 
autopsy  revealed  several  extravasations  of  blood  in  the  floor  of  the  fom-th  ventricle. 
On  the  right  side,  in  the  region  of  the  nucleus  acusticus,  there  was  a  brownish  spot  of 
the  size  of  a  lentil,  and  two  others  as  large  as  poppy  seeds,  about  3  miUimetres  fi'om  the 
median  hne.  After  hardening  the  specimens,  Frerichs  found  on  the  right  side,  at  the  level 
of  the  nucleus  acusticus,  and  immediately  outside  the  abductor  nucleus,  three  small 
hrcmorrhages,  which  could  be  followed  in  the  sections.  Another  group  was  present 
a  httle  higher  up,  6  or  7  millimetres  from  the  middle  Une  of  the  angle  of  the  floor  of  the 
fourth  ventricle.  The  larger  of  these  hsemorrhages  were  recent,  and  showed  normal 
red  blood-corpuscles.  Fi'erichs  found,  on  the  other  hand,  centres  composed  of  red 
blood-corpuscles,  which  were  completely  colourless,  and  lastly  some  scattered  masses 
of  bro\vn  pigmentary  granules. 

4.  A  boy,  sixteen  years  of  age,  who  received  a  blow  on  the  occiput  with  a  stick, 
was  taken  ill  six  days  later  with  polydipsia,  polyuria,  boulimia,  and  amblyopia.  The 
urine  showed  a  specific  gravity  of  1043,  and  contained  a  large  quantity  of 
sugar.  Recovery  took  place  in  a  fortnight,  under  the  influence  of  meat  diet  and 
alkahne  medicines,  and  yet  for  two  months  afterwards  simple  polyuria  was  still 
present. 

These  cases  deal  with  the  appearance  of  diabetes  meHitus  after  head 
injuries,  and  I  shall  now  quote  cases  in  which  diabetes  mellitus  appeared 
after  injuries  to  some  other  region  of  the  body : 

A  man,  fifty  years  of  age,  whose  previous  health  was  excellent,  was  thrown  from  his 
horse  and  fell  on  his  back.  He  soon  found  that  he  was  losing  strength,  his  thirst  became 
considerable,  and  he  passed  8  litres  of  urine  daily.  On  analysis,  72  grammes  of  sugar 
per  litre,  or  576  grammes  in  the  twenty-foTir  hours,  were  found.  Treatment  reduced 
the  sugar  in  six  months'  time  to  44  grammes  per  Utre. 

A  man,  twenty-one  years  of  age,  who  was  playing  with  one  of  his  friends,  fell  on 
a  chair  and  received  a  blow  over  the  first  two  lumbar  vertebrae.  He  did  not  sustain 
a  fracture,  but  yet,  some  days  later,  he  complained  of  very  severe  thirst  and  extreme 
weakness.  The  urine  contained  10  grammes  of  sugar  per  Utre.  He  died  some  while 
afterwards  from  coma. 

Griesinger  relates  the  case  of  a  young  man,  eighteen  years  of  age,  who  fell  from  a 
first  story  on  to  his  feet.  The  accident  was  not  followed  by  loss  of  consciousness,  but 
during  the  night  severe  diabetes  with  excessive  thirst  appeared.  The  urine  contained 
50  grammes  of  sugar  per  Utre,  or  an  amount  of  250  grammes  daily.  The  patient  was 
admitted  to  hospital  in  a  condition  of  cachexia  and  died,  covered  with  boils  and 
absces.ses. 

Children,  as  well  as  adults,  may  be  affected.  Bouvier  quotes  the  case  of  a  boy, 
eleven  years  of  age,  who  was  taken  iU  with  diabetes  following  a  blow  over  the  kidnev. 
Niedergass  reports  the  case  of  a  young  girl  who  became  diabetic  after  a  fall.     Pvossbacli 

126—2 


1992  TEXT-BOOK  OF  MEDICINE 

quotes  the  case  of  a  child,  eight  months  old,  who  fell  from  his  nurse's  arms,  and  died, 
four  months  later,  in  a  condition  of  cachexia,  with  polyuria,  glycosuria,  eczema,  and 
furimculosis  (Brouardel  and  Richardiere). 

The  foregoing  cases  prove  that  diabetes  mellitus  may  foUow  the  most 
varied  injuries,  such  as  blows  on  the  head,  on  the  nape  of  the  neck,  violent 
bruising  of  the  body,  falls  upon  the  feet,  etc.  Head  injuries,  however,  play 
the  largest  part.  Diabetes  may  appear  early  or  late  after  the  injury. 
Brouardel  and  Richardiere  give  the  following  statistics  :  "  In  twenty-five 
cases  which  state  the  precise  date  of  appearance  of  the  first  symptoms,  in 
four  diabetes  appeared  within  two  days  of  the  injury,  in  four  it  appeared 
during  the  next  week,  and  in  four  others  its  onset  was  less  rapid." 

The  symptoms  of  traumatic  diabetes  meUitus  do  not  differ  from  those 
of  the  ordinary  form,  and  in  both  the  complications,  such  as  carbuncles,  boils, 
cataract,  etc.,  may  be  seen.  They  may  both  result  in  pulmonary  phthisis  ; 
they  may  both  terminate  in  coma. 

As  regards  the  question  of  prognosis  in  both  cases,  Brouardel  and 
Richardiere  regard  the  question  in  the  following  manner  :  "  Early  traumatic 
diabetes,  which  follows  closely  upon  an  accident,  and  late  traumatic  diabetes, 
which  appears  a  long  time  after  the  accident,  have  a  somewhat  different 
prognosis.  The  differences  are  important  from  the  point  of  view  of  the 
gravity  of  the  disease,  because  in  legal  medicine  two  distinct  forms  are 
described — the  one  which  has  a  rapid  and  early  onset  is  benign ;  the  other, 
which  appears  later  and  runs  a  slower  course,  is  as  a  rule  serious.  Acute 
early  diabetes  always  ends  in  recovery.  Two  or  three  weeks,  or  perhaps 
two  or  three  months,  after  the  appearance  of  the  first  symptoms  the  patient 
feels  a  return  of  strength,  the  thirst  and  boulimia  disappear,  the  sugar  is  no 
longer  appreciable  in  the  urine,  and  plumpness  returns.  One  symptom — 
polyuria — stUl  persists,  and  becomes  even  more  severe  than  in  the  stationary 
stage  of  the  disease.  This  polyuria  may  amount  to  5  litres  daily,  and  may 
last  for  some  weeks  after  the  disappearance  of  the  glycosuria.  It  yields  at 
last,  and  as  a  rule  recovery  is  complete  two  or  three  months  after  the 
injury.  The  late  form  runs  a  very  slow  course,  lasting  for  months  and  years, 
and  usually  ending  fatally.  Death  is  caused  by  wasting  or  by  complica- 
tions, such  as  tuberculosis,  or  by  coma." 

These  considerations  regarding  the  early  and  late  forms  of  traumatic 
diabetes  are  not  absolute,  and  appear  to  me  to  include  numerous  exceptions. 

Medico-Legal  Study. — The  question  of  traumatic  diabetes  in  some 
respects  enters  the  domain  of  legal  medicine.  An  individual  becomes 
diabetic  after  a  blow  or  after  a-  railway  accident,  and  sues  for  damages  and 
costs.  How  are  we  to  decide  that  his  claim  is  genuine,  and  to  affirm  that 
the  plaintiff  was  not  diabetic  before  the  accident  ?  Here  are  two  cases  of 
this  land : 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  1003 

A  mftn,  forty-five  years  of  age,  who  had  nevor  Ijcon  ill,  was  in  the  railway 
accidtmt  of  July  18,  1884,  on  tho  lino  from  Puy  to  Saint -^itionno.  Cli— —  did 
not  lose  consciouanoss,  but  was  only  stunned.  Ho  did  not  romcinbor  how 
ho  got  out  of  tho  compartmont,  but  he  romemberod  piirfoctlv  tho  conditicm  in 
which  ho  found  the  onj;ino-drivor  and  tho  atokor.  Ho  noticed  that  ho  had  a  wound 
on    tho   loft  log,   and    he   tried    to    follow   his   travelling    coinpani(jnH.     Ho   walkml 

about   two   kilometres  to  roach   tho   nearest  station.       During   the  journey  Ch 

remarked  that  he  followed  with  dirtioulty  some  women  who  got  out  of  the  carriages  at 
the  same  time  as  he  did. 

Ch was  examined  on  three   ditTerent  occasions  by  Dr.   Vinay,  Fellow  of  tho 

University  of  Lyons.  This  physician  gave  him  three  certificates,  dated  July  30,  1884, 
December  24,  1884,  and  November  30,  1885,  and  stated  :  (1)  That  the  contused  wound 
on  the  leg  had  recovered  in  about  twenty  days  ;  (2)  that  the  lumbar  pains  which  were 
marked  on  the  first  day  persisted  and  were  very  acute  ;  and  (3)  that  the  urine,  increased 
in  quantity  from  July  30,  contained  at  the  end  of  November,  1885,  a  notable  quantity 

of  sugar.     On  February  13,  at  the  time  of  my  examination,  Ch looked  well.     The 

wound  in  tho  leg  was  healed,  and  was  represented  by  a  scar  3-5  centimetres  in  diameter. 

The  renal  pain  persisted.     It  was  absent  during  rest,  but  came  on  when  Ch tried 

to  rise,  or  to  stand  upright,  or  when  he  coughed.  It  was  not  accompanied  by  any 
appreciable  sign  of  fracture  of  the  spine.    It  was  increased  by  pressure  over  tho  lumbar 

vertebrae,  especially  on  the  loft  side.     Ch 's  vision  was  good.     He  had  no  cutaneous 

eruptions.  The  specific  gravity  of  his  urine  was  1032,  and  it  contained  47  grammes  of 
sugar  per  litre,  but  no  albumin. 

The  second  case  refers  to  a  man  forty-five  years  of  age  who  had  never  been  ill, 
but  who  wEis  hurt  in  a  railway  accident  on  August  14,  1883.  He  lost  consciousness 
after  the  accident,  and  felt  sharp  pains  all  over  his  body — notably,  above  the  right 
knee  and  in  the  left  lumbar  region.  Since  the  accident  he  had  lost  18  kilos  in  two 
years,  and  had  become  weak,  being  compelled  to  give  up  his  duties  as  a  commercial 
traveller.  He  had  also  had  haemoptysis.  At  Brouardel's  first  examination  (two 
years  after  the  accident)  the  patient  complained  of  pain  along  the  spine  :  the  pain  was 
increased  by  pressure.  The  urine,  a  detail  ignored  by  the  patient,  contained  49  grammes 
of  sugar  per  litre.     The  patient  therefore  presented  a  series  of  diabetic  symntoms. 

Speaking  generally,  the  question  of  traumatic  diabetes  is  often  difficult 
to  decide  in  legal  medicine,  because,  in  order  to  blame  the  injury,  we  must 
be  certain  that  the  plaintiff  was  free  from  diabetes  before  the  accident. 
The  question  is  the  more  difficult  to  decide  because  certain  symptoms  of 
diabetes  are  so  slight  as  to  pass  unnoticed  for  some  time.  Six  months  or 
more  may  elapse  after  the  accident  before  some  revealing  sign  attracts  our 
attention,  and  we  find  sugar  in  the  urine. 

The  medico-legal  question  may,  therefore,  be  presented  under  various 
aspects.  If  an  individual  who  has  always  enjoyed  good  health  is  suddenly 
taken  ill  with  polydipsia  following  a  blow  or  a  railway  accident,  and  if  the 
individual  shortly  after  the  injury  presents  clear  signs  of  diabetes,  including 
glycosuria,  it  is  evident  that  the  injury  must  be  held  guilty,  and  that  the 
plaintif!  has  a  right  to  damages. 

The  diagnosis  is,  however,  not  always  so  simple.  Traumatic  diabetes, 
like  the  ordinary  form,  may  be  present  for  months  and  years  without 
declaring  itself  by  the  cardinal  symptoms  of  excessive  polydipsia  or  of 


1994  TEXT-BOOK  OF  MEDICINE 

exaggerated  polyuria,  which  promptly  give  a  clue  to  the  diagnosis.  The 
patient  often  suffers  from  diabetes  without  knowing  it.  His  appetite  and 
his  thirst  are  normal,  but  yet  he  experiences  a  certain  weakness,  put  down 
to  fatigue,  complains  of  pains  called  rheumatism,  or  suffers  from  a  nervous 
condition  looked  upon  as  neurasthenia,  and  we  only  find  months  afterwards 
that  aU  these  troubles  should  have  been  put  down  to  diabetes. 

This  discussion  is  applicable  to  traumatic  diabetes,  which  may  remain 
unnoticed  for  a  long  while,  and  which  may,  for  various  reasons,  be  recog- 
nized only  at  a  late  stage.  Under  such  conditions,  how  are  we  to  ajB&rm 
that  the  injury  has  been  the  origin  of  diabetes  which  has  passed  unnoticed 
for  a  year  or  two  ?  I  think  that  in  such  a  case  the  plaintiff  will  lose  his 
case. 

Pathogenesis. — I  should  now  like  to  say  a  few  words  on  the  pathogenesis 
of  traumatic  diabetes.  It  is  at  present  a  question  of  theory.  If  we  refer 
to  the  memorable  experiments  of  Bernard,  we  find  that  puncture  of 
the  fourth  ventricle  between  the  roots  of  the  vagus  and  auditory  nerves 
determines  polyuria ;  if  the  puncture  is  slightly  higher,  glycosuria  ;  and 
higher  stiU,  albuminuria.  These  phenomena  of  an  experimental  kind  are, 
however,  transient,  and  are  in  no  way  comparable  to  the  pathological  cases, 
which  show  us  the  lasting  and  sometimes  indefinite  existence  of  diabetes 
meUitus  and  of  diabetes  insipidus. 

Furthermore,  no  lesion  of  the  fourth  ventricle  is,  as  a  rule,  present  in 
traumatic  diabetes.  A  fall  on  the  feet,  a  blow  on  the  kidneys,  or  a  violent 
shock  are  the  injuries  which  may  cause  diabetes  meUitus  or  diabetes  insipidus. 
We  might  say  that  the  thirst  or  the  hunger  may  be  caused  by  a  dynamic 
disturbance  of  the  functional  powers  of  certain  nerve  cells,  but  what  is  this 
disturbance,  and  which  are  the  cells  at  fault  ?     I  do  not  know. 

The  sudden  and  indefinite  dissociation  of  the  morbid  act  is  still  inex- 
plicable. "Why  after  a  blow,  a  faU,  or  a  bruise,  should  one  individual  suffer 
from  simple  polydipsia  without  showing  for  months  any  trace  of  sugar  in 
the  urine  ?  Why,  on  the  other  hand,  should  an  identical  injury  in  another 
person  cause  not  only  glycosuria,  but  diabetes  mellitus,  with  aU  its  train  of 
symptoms  ?  The  matter,  some  wUl  say,  is  one  of  localization,  but  I  should 
prefer  to  acknowledge  our  ignorance  on  the  point,  and  to  consider  the 
question  unanswered  at  present. 

The  treatment  of  traumatic  diabetes  mellitus  is  practically  the  same 
as  that  of  the  non-traumatic  form.  With  the  general  treatment  of  the 
disease  by  diet,  suppression  of  food  and  drink  which  contain  sugar,  and 
diminution,  but  not  suppression,  of  farinaceous  foods,  arsenical  and  alkaline 
preparations,  and  antipyrin,  we  must  also  employ  local  treatment  by 
blisters,  setons,  or  the  cautery  to  the  nape  of  the  neck,  especially  if  the 
disease  follows  a  head  injury. 


RHEUMATTO  AND  DYSTROPHIC  DISEASES  1995 

VIII.  OBESITY. 

Description. — 01)osity  is  the   pathological    condition  caused  by  the 

general  hypertrc>])lLy  of  the  adipose  tissue.  Tn  a  loss  pronounced  degree  it 
blends  with  einl)i)iipoint,  and  at  its  extreme  limit  it  takes  the  name  of 
polysarcia  or  adiposis.  Local  deposits  of  fat,  such  as  lipoma,  lipomatous 
hypertrojdiy  of  the  muscles,  and  paralytic  subcutaneous  adiposis,  must  be 
distinguished  from  obesity. 

The  distribution  of  fatty  tissue  in  the  obese  does  not  take  place  in  a 
uniform  and  identical  fashion.  The  subcutaneous  and  intermusciUar  cellular 
tissue,  the  fringes  of  the  omentum,  the  mesentery,  the  perirenal  tissue,  the 
surface  of  the  heart,  and  the  cellular  tissue  of  the  orbit,  may  be  invaded  by 
fat.  In  gross  feeders  obesity  chiefly  affects  the  abdominal  walls,  and  forms 
cutaneous  pads,  with  stretching  of  the  sldn  and  linese  comparable  to  those 
of  pregnancy.  In  some  persons  fat  accumulates  in  the  neck  (triple  chin) 
or  in  the  breasts.  Adiposis  does  not,  properly  speaking,  exist  in  the  penis 
and  the  scrotum.  The  viscera,  the  liver,  the  kidneys,  and  particularly  the 
heart,  may  be  invaded  by  fat. 

An  important  distinction  should  be  made  between  fatty  infiltration, 
which  is  compatible  with  the  life  of  the  tissue,  and  fatty  degeneration, 
which,  on  the  other  hand,  affects  the  elements  which  are  practically  dead  or 
already  necrobiotic.  The  former  belongs  to  obesity,  and  is  curable,  while 
the  latter  is  the  result  of  infections  and  intoxications,  and  is  incurable. 
^Yhen,  however,  the  polysarcia  is  extreme  and  inveterate,  it  wears  out  the 
functional  activity  of  the  organs,  and  fatty  or  fibro-fatty  degeneration  is 
often  added  to  the  fatty  infiltration.  Troubles  then  commence,  and  finally 
carry  off  the  patient. 

Obesity,  when  less  marked,  recent,  and  unaccompanied  by  a  visceral 
lesion  properly  speaking — as,  for  instance,  in  young  persons — only  causes 
slight  breathlessness  upon  movement  and  effort.  The  respiration  is  some- 
what noisy,  fatigue  comes  on  rapidly,  and  therefore  fat  persons  are  some- 
what apathetic,  and  show  but  little  inclination  for  physical  exercise. 

Digestion  is  generally  sluggish  after  meals,  sleepiness  is  felt,  but  the 
troubles  are  usually  confined  within  the  limits  of  health,  so  that  obesity 
may  be  considered  rather  as  an  infirmity  than  as  a  disease. 

On  the  contrary,  when  the  adiposis  is  excessive,  and  the  patient  is  no 
longer  young,  the  face  is  usually  deeply  coloured  and  even  cyanosed.  The 
gait  is  slow  and  halting,  and  the  breathlessness  increases  on  the  least  move- 
ment. The  act  of  walking  upstairs  becomes  especially  difficult,  speech  is 
short  and  broken,  and  the  patient,  when  saying  a  long  phrase,  is  obliged  to 
stop  and  take  breath.  The  appetite  may  be  increased  or  diminished  ;  the 
thirst  is  always  increased.     Digestion  is  troublesome ;  after  meals  the  desire 


1996  TEXT-BOOK  OF  MEDICINE 

to  sleep  is  urgent ;  tlie  aptitude  for  mental  work  is  not  always  diminished. 
This  is,  indeed,  an  interesting  peculiarity.  Examination  of  the  liver  fre- 
quently shows  enlargement  and  tenderness  of  the  organ. 

The  stools  are  often  of  a  pale  colour.  The  heart-beats  are  distant,  feeble, 
and  sometimes  irregular.  The  size  of  the  heart  is  increased,  and  the  apex- 
beat  is  difficult  to  find. 

The  skin  is  covered  with  sweat  on  the  least  exertion,  and  gives  ofi  a 
foetid  odour,  due  to  the  increase  of  the  sebaceous  secretion  and  to  the 
chemical  changes  which  this  secretion  undergoes.  The  skin  is  readily 
irritated,  and  therefore  erythema,  intertrigo,  and  eczema  are  common  in 
fat  persons. 

The  urine  presents  important  changes,  which  often  serve  as  a  guide  to 
the  pathogenesis  and  therapeutics  of  obesity. 

Without  speaking  of  polyuria,  glycosuria,  and  albuminuria,  which  are 
often  met  with  in  obese  patients,  who  are  arthritic  and  neurotic,  the  amount 
of  urea,  and  in  a  general  way  the  amount  of  the  nitrogenous  products,  have 
led  to  a  division  of  obese  patients  into  two  groups,  according  as  the  nitro- 
genous substances  in  the  urine  are  or  are  not  increased.  In  some  obese 
patients  the  proportion  of  urea  is  diminished. 

Many  patients  succumb  to  troubles  dependent  upon  visceral  degenera- 
tions, which  are  almost  always  present  at  some  time  or  other.  Progressive 
asystolia  is  a  very  frequent  mode  of  termination.  Death  also  supervenes  as 
the  result  of  some  intercurrent  disease — pneumonia,  general  bronchitis, 
erysipelas,  etc. — which  are  exceedingly  grave  in  all  fat  persons.  Other 
persons  succumb  to  some  diathetic  affection  of  which  obesity  is  only  a 
manifestation.  Here,  again,  polysarcia,  by  diminishing  the  vital  resistance 
of  the  tissues,  has  an  unfavourable  action. 

etiology  and  Pathogenesis. — Obesity  is  a  disease  of  all  ages,  though 
more  frequent  in  adults  and  rare  in  old  people,  because  of  the  general  de- 
crepitude. Women  are  more  often  sufferers  than  men.  The  disease  appears 
at  puberty,  after  marriage,  as  the  result  of  pregnancy,  and  especially  of  the 
first  pregnancy,  and  lastly  at  the  menopause.  The  genital  life  has,  there- 
fore, a  capital  importance  in  the  appearance  of  obesity. 

The  disease  is  often  hereditary,  supervening  in  certain  persons  after  an 
acute  affection  (typhoid  fever  and  pneumonia).  It  is  then  the  result  of 
profound  changes  in  nutrition. 

Obesity,  migraine,  cholelithiasis,  uric  acid,  gravel,  asthma,  articular 
rheumatism,  gout,  and  diabetes  are  all  manifestations  of  imperfect  nutrition, 
such  as  are  met  with  in  arthritic  subjects. 

It  is  also  to  the  slackening  of  nutrition  that  the  fatty  overgrowth  in  some 
diseases  of  the  nervous  system,  and  in  particular  hysteria  and  progressive 
pernicious  ansemia,  must  be  set  down. 


RHEUMATIC  AND  DYSTROPTIIO  DISEASES  1097 

Til  tlii^  iinnn;il  siato  tlic^  fiif.  Ilvrd  in  the  tissues  lias  a  douhlo  origin  — 
namely,  alimentation  and  disassimilation.  The  pathological  fat  lias  the 
same  origin.  Increase  of  fatty  food  does  not,  however,  increase  obesity 
more  surely  than  foods  containing  starch  and  sugar  and  alcoholic  drinks 
(wine,  brandy,  beer),  as  is  proved  in  the  case  of  the  Eskimos,  who  live 
almost  entirely  upon  fat,  and  who  are  not  stouter  than  the  inhabitants  of 
southern  countries.  In  order  that  these  nutritional  cau.ses  may  produce 
their  full  effect,  they  must  act  in  persons  in  whom  oxidation  is  slow  and  the 
combustion  of  these  substances  is  incomplete.  Want  of  exercise  and  the 
absorption  of  large  quantities  of  proteid-sparing  foods,  by  diminishing  the 
quantity  of  oxygen  used  up,  favour  the  deposit  of  fat  droplets  in  the  tissues. 
Increase  of  disassimilation  leads  to  the  same  result,  but  here  the  source  of 
the  fat  is  due  to  quaternary  substances.  In  the  intoxications  and  infec- 
tions the  production  of  fat  takes  place  at  the  expense  of  the  proteid 
material.  Such  is  also  the  case  in  progressive  pernicious  anaemia.  In 
these  patients  we  find  in  the  urine  an  excess  of  urea  and  an  albuminoid 
substance,  which  is  also  formed  at  the  expense  of  the  incompletely  oxidized 
proteids. 

The  study  of  the  variations  in  the  saponifying  ferment  of  the  blood  may 
perhaps  clear  up  the  pathogenesis  of  obesity.  In  one  case  Achard  and  Clerc 
have  found  exaggerated  activity  of  this  ferment. 

Treatment. — The  alimentary  regime  in  obesity  comprises  the  following 
indications  :  No  sugar,  no  starchy  foods,  fluids  taken  in  moderation  at 
meals,  avoidance  of  alcohol  and  beer.  Coffee  and  tea  are  permitted.  Mas- 
sage, dry-rubbing,  and  physical  exercise  should  be  prescribed.  We  must 
avoid  fatigue,  especially  in  elderly  persons. 

By  means  of  these  hygienic  measures  we  can  often  reduce  a  patient's 
weight  by  some  pounds.  If  this  treatment  do  not  suffice,  we  may  also 
employ  such  drugs  as  iodine  and  iodides  (iodide  of  potassium  in  small  doses). 
Tincture  of  iodide  (3  to  5  drops  in  a  teaspoonful  of  wine)  may  be  given  before 
meals.  Purgatives  and  alkaline  preparations  have  their  indications.  The 
waters  of  Marienbad,  Kissingen,  Montmirail,  and  of  Brides,  etc.,  act  both 
as  alkahnes  and  laxatives. 

The  internal  administration  of  thyroid  gland  has  been  recommended  in 
obesity,  because  the  thyroid  body  increases  denutrition.  This  treatment 
has  given  good  results.  Ten  grains  of  fresh  or  of  dried  thyroid  gland  are 
prescribed  daily.  Chaix  and  Remy's  tabloids,  which  contain  25  centi- 
grammes of  thyroid  gland,  may  be  employed,  1  or  2  grammes  being  taken 
after  each  meal. 


1998  TEXT-BOOK  OF  MEDICINE 


IX.  DIFFUSE  SYMMETRICAL  LIPOMATOSIS. 

In  tills  section  I  shall  deal  with,  the  disease  described  by  some  authorities 
under  the  name  of  diffuse  symmetrical  lipomatosis,  chiefly  affecting-  the 
neck,  and  by  Launois  and  Bensaude  under  the  name  of  sjrmmetrical  adeno- 
lipomatosis,  which  chiefly  affects  the  neck,  a  term  which  takes  the  glandular 
element  into  account.  I  shall  adopt  the  former  of  these  terms,  and  I  shaU 
give  my  reason  later. 

Here,  as  in  all  lipomata,  the  disease  consists  in  tumours  composed  of 
more  or  less  dense  fatty  tissue.  When  we  speak  of  diffuse  lipomatosis,  we 
mean  that  the  lipomatous  masses  spread  without  any  tendency  to  be  en- 
capsuled,  like  true  lipomata. 

With  few  exceptions,  this  diffuse  lipomatosis  is  a  disease  of  adult  age, 
and  is  quite  exceptional  in  women.  It  is  far  from  being  rare,  as  more  than 
a  hundred  cases  are  known.  It  is  not  directly  associated  with  obesity.  We 
see  fat  people  without  lipomata,  and  also  lipomata  in  thin  persons.  The 
real  cause  of  the  affection  is  unknown.  Heredity  has  not  been  proved,  but 
arthritism  and  alcoholism  have  often  been  suggested. 

The  onset  is  insidious,  the  lipomatous  tumours  causing  neither  dis- 
comfort, embarrassment,  nor  pain.  Symmetry  is  the  rule,  but  it  is  some- 
times apparent  only  at  more  or  less  long  intervals.  The  lipomata,  which 
are  very  small  at  first,  do  not  always  undergo  progressive  increase  in  size. 
They  may  remain  stationary  for  years,  and  may  even  recede,  although  I 
do  not  think  that  they  disappear.  In  the  long  run  they  often  reach  the 
size  of  a  nut,  an  egg,  or  of  an  orange.  They  sometimes  spread  in  various 
directions,  and  finally  acquire  a  colossal  size. 

The  first  lipomata  usually  appear  in  the  cervical  region ;  sometimes  in 
the  anterior  and  lateral  aspects  of  the  neck ;  at  other  times  in  the  nape  of 
the  neck,  which  is  often  the  first  part  to  be  invaded.  The  neck  swells,  and 
the  shirt-coUar  has  to  be  enlarged.  The  lipomatous  tumours  are  soft, 
painless,  sometimes  fused  together,  and  having  iU-defined  edges.  They  can 
be  moved  as  a  whole,  and  are  not  adherent  to  the  skin  or  painful.  Accord- 
ing to  their  disposition  and  extent,  they  form  a  coUar  or  a  collarette.  The 
lipomatous  collar  often  forms  a  complete  circle,  and  rounded  or  oval  nodules 
in  the  adipose  tissues  can  be  felt  in  the  submental,  submaxillary,  parotid, 
preauricular,  and  retromastoid  regions. 

Above  the  nape  of  the  neck  two  tumours  develop,  filling  up  in  a  sym- 
metrical manner  the  retromastoid  fossae,  and  partly  hidden  beneath  the 
hair.  Lower,  over  the  vertebra  prominens,  we  find  a  lipomatous  tumour, 
which  is  single  or  divided  into  two  symmetrical  lobes.  In  the  lateral  regions 
of  the  neck  the  lipomatous  masses  occupy  the  preauricular  and  the  parotid 
regions,  and  enlarge  the  transverse  diameter  of  the  face. 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  1099 

In  the  front  of  the  nock  thf  lipomatous  mass  may  assutac  the  form  of  a 
double  or  of  a  treble  chin  , similar  to  that  seen  in  fat  p(M){»le  (Laimois  and 
Bensaude).  "  As  the  size  of  the  neck  and  of  the  head  decreases  progres- 
sively from  below  upwards,  it  follows  that  the  ce])halic  extremity  from  the 
shoulders  to  the  summit  of  the  vertex  takes  the  form  of  a  truncated  pyramid, 
with  its  base  below  and  its  apex  above  "  (Hayem).  The  head  is  then  said 
to  be  pear-shaped. 

The  symmetrical  lipomata  may  occupy  only  the  cervical  region.  More 
often  they  develop  in  the  axillae  and  in  the  groins,  and  show  the  same 
symmetry.  In  the  axillte  they  form  soft,  painless,  mobile  tumours,  which 
run  into  one  another,  and  have  ill-defined  edges.  In  the  groin  the  sym- 
metrical lipomata  are  often  superposed  in  two  stages,  and  fonn  almost 
transverse  masses,  which  are  parallel  to  the  fold  of  the  groin,  and  which 
extend  inwards  as  far  as  the  scrotum.  From  a  distance  they  might  be 
looked  on  as  enormous  herniae.  Here,  as  elsewhere,  cutaneous  adhesions 
are  absent,  and  the  skin  preserves  its  normal  appearance. 

The  lipomata  have  not  everywhere  the  same  consistency,  being  softer 
and  more  diffuse  in  certain  part;s,  especially  in  the  region  of  the  chin.  They 
are  firmer  and  more  defined  at  the  back  of  the  neck.  Sometimes  the  lipo- 
matous mass  is  not  soft  through  its  whole  extent,  and  we  find  indurated 
nodules,  which  might  well  be  taken  for  lymphatic  glands.  I  shall  discuss 
this  question  later.  Dystrophy  has  never  been  found.  Motor  and  sensory 
troubles  are  not  seen. 

The  preceding  description  refers  to  the  symmetrical  type,  and  is  applic- 
able to  the  majority  of  cases.  It  installs  itself  insidiously,  and  for  ten, 
twelve,  or  fifteen  years,  or  even  longer,  it  runs  its  course  without  complica- 
tions. The  vessels  and  the  air-passages  are  not  compressed,  the  movements 
of  the  head  are  not  affected,  and,  as  the  condition  does  not  threaten  life,  it 
is  simply  a  deformity.  We  find  cases,  however,  which  differ  somewhat  from 
the  classical  description,  as  is  shown  by  the  following  examples  : 

In  Madelung's  case  the  lipomatosis  assumed  such  proportions  that  the  masses  of 
fat,  which  were  twenty-three  years  old,  fell  over  the  chest  and  the  back.  They  had  also 
invaded  the  mediastinum,  affecting  deglutition  and  respiration.  Launois  and  Bensaude 
quote  the  following  cases  :  In  Schmidt's  patient  the  shoulders  were  much  enlarged 
by  two  enormous  fatty  masses,  which  covered  the  deltoids  on  each  side,  and  descended 
as  far  as  the  middle  of  the  arm.  A  circular  hpomatous  mass  surrounded  the  umbihcus. 
In  Virchow  and  SchottmiiUer's  patient  the  upper  part  of  the  thighs  and  the  scrotum  as 
far  as  the  perinaeum,  were  invaded  by  a  general  fatty  infiltration.  In  Jeansehne  and 
Buinoir's  patient  the  hpomata  formed  mammae  on  the  anterior  abdominal  wall.  In 
Langer's  patient  the  beUy  and  the  back  were  padded  with  hpomata.  In  some  cases 
dyspnoea,  fatigue,  asthenia,  acceleration  of  the  pulse,  and  hypertrophy  of  the  spleen 
have  been  noted,  A  fatal  case,  probably  caused  by  compression  of  the  organs  in  the 
mediastinum,  has  been  quoted. 

Analysis  of  the  blood  shows  nothing  special.  In  one  of  my  patients,  of  whom  I 
shall  speak  later,  the  blood  examination  was  normal.     In  Pities'  patient  6,262,000 


2000  TEXT-BOOK  OF  MEDICINE 

red  corpuscles  and  10,800  white  corpuscles  were  found.  In  Demons'  patient  Sabraz&a 
found  absence  of  eosinophiles  and  increase'-of  the  polynuclear  neutrophiles.  In  Query's 
patient  the  number  of  red  corpuscles  was  normal,  and  the  number  of  white  ones  was 
slightly  increased.  ■  In  Hayem's  patient  the  number  of  red  corpuscles  was  sHghtly  in- 
creased, and  the  number  of  white  corpuscles  was  slightly  above  the  normal.  In  one  of 
Launois  and  Bensaude's  patients  the  count  showed:  red  corpuscles,  3,472,000;  and 
white  corpuscles,  6,200. 

We  have  now  to  discuss  the  nature  and  the  pathogenesis  of  symmetrical 
lipomatosis. 

Madelung  suggested  that  symmetrical  lipomatosis  might  be  dependent 
upon  disease  or  disappearance  of  the  thyroid  body.  This  hypothesis  does 
not  stand  the  test  of  analysis.  Several  authors  have  thought  that  sym- 
metrical lipomatosis  was  a  tropho-neurosis  of  myelopathic  origin.  None  of 
the  partisans  of  this  nervous  theory,  however,  "  have  succeeded  in  establishing 
any  exact  relation  between  the  nervous  system  and  the  adipose  hypertrophy. 
We  cannot,  therefore,  accept  this  theory,  unless  we  are  willing  to  place  all 
the  morbid  phenomena  of  which  we  know  not  the  nature  to  the  account  of 
the  nervous  system." 

Baker  and  Bowlby  thought  that  the  tumours  were  of  a  lymphadeno- 
matous  rather  than  of  a  fatty  nature.  Histological  examinations  have, 
however,  shown  their  fatty  character. 

According  to  Launois  and  Bensaude,  symmetrical  lipomatosis  "  is  a 
primary  disease  of  the  lymphatic  glands  and  vessels,  and  has  many  points 
of  resemblance  with  adeno-lymphocele.  Such  a  term,"  they  say,  "  does  not 
apply  to  every  periglandular  fatty  infiltration,  but  only  to  a  morbid  entity 
with  constant  characters,  and  accompanied  by  the  production  of  diffuse 
lipomata,  which  are  probably  related  to  the  lymphatic  glands  and  vessels." 

The  lymphatic  gland,  which  is  already  afiected,  may  be  surrounded  by  a 
fatty  layer,  and  simulate  a  true  lipoma,  as  in  Tuffier's  case.     This  secondary  • 
periglandular  lipomatosis  is  comparable  to  lipomatous   peritjrphlitis  and 
perinephritis,  but  it  does  not  come  under  the  heading  of  the  difiuse  and 
infiltrating  symmetrical  lipomatosis,  which  we  are  considering  in  this  section. 

Has  this  diffuse  Kpomatosis  its  origin  in  the  lymphatic  system,  and  how 
can  it  be  proved  ?  In  support  of  their  opinions,  Launois  and  Bensaude 
point  out  that  the  seat  of  election  of  the  diffuse  lipomatous  symmetrical 
tumours  is  precisely  in  the  region  where  lymphatic  glands  exist  normally. 
This  is  true,  but  the  lipomatous  tumours  are  also  found  in  regions  where 
lymphatic  glands  are  not  present.  In  the  absence  of  glands,  say  Launois 
and  Bensaude,  there  must  be  a  residue  of  lymphoid  tissue,  which  is  the  orgiin 
of  the  lipomatosis.  No  proof  exists  that  this  hypothesis  is  not  true,  but  in 
order  to  establish  it,  it  is  necessary  that  the  histological  examination  of  the 
symmetrical  lipomata  should  show  in  the  same  specimen  the  presence  of  the 
lipoma  and  the  presence  of  the  IjTnphatic  gland — or,  at  any  rate,  traces  of  it. 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  -uui 

On  reading  cases  we  see  that  the  palpation  of  the  soft  lipomatous  masses 
gives  a  sensation  of  indurated  nodules,  which  are  considered  to  be  lymphatic 
glands  embedded  in  the  fatty  tissue,  and  this  argument  is  invoked  in  favour 
of  the  adeno-lipomatous  theory,  the  gland  and  the  lipoma  being  side  by  side 
in  the  same  tumour. 

In  Pitros'  ciise  palpation  of  the  lipomatoua  tumour  gave  a  soft  and  compressible 
consistency  ;  but  small  lobulatod  masses,  which  were  firmer  and  rolled  under  the  finger, 
wore  also  felt.  These  little  masses  somewhat  resembled  hard,  glandular  nodules,  set 
in  a  lipomatous  mass.  In  Launois  and  Bensaude's  case  it  is  said  that,  on  careful  palpa- 
tion of  the  lipomata  in  the  inguinal  region,  "  hypertrophic  glandular  masses  were  found 
in  the  midst  of  the  adipose  tissue." 

When  the  value  of  the  sensation  given  by  examination  is  controlled  by 
anatomical  research,  we  find  that  the  indurated  nodules,  which  on  palpation 
are  taken  for  lymphatic  glands  included  in  the  lipoma,  are  in  reality  con- 
densed masses  of  fat,  associated  in  some  instances  with  fibrous  tissue. 

Hayem  has  published  a  case  in  which  examination  of  a  lipomatous  mass  byDelbet 
showed  small  blackish  glands  ;  but,  as  a  matter  of  fact,  in  all  the  other  cases  the  absence 
of  glands  is  carefully  noted. 

Thus,  in  Mar9ais'  case  and  in  two  of  Nelaton's  cases,  pubUshed  by  Pfestel-Mazoglu, 
the  histological  examination  did  not  reveal  any  trace  of  lymphatic  glands  in  the  fatty 
mass.  A  case  in  Query's  thesis  was  one  of  symmetrical  lipomata  of  the  cervical  type. 
The  Upomata  were  removed  by  Reclus,  and  histological  examination  was  made  in  C3omil's 
laboratory  by  Rene  Marie.  *'  On  macroscopic  section  of  the  tumours,  it  was  found  that 
they  were  composed  of  a  mass  of  soft  adipose  tissue,  which  enclosed  other  hard  masses  of 
a  fibrous  appearance,  and  very  vascular  at  their  periphery.  Rlicroscopic  examination 
showed  that  these  tumours  were  composed  of  adipose  tissue,  without  any  traces  of 
glands.  The  hard  masses  found  on  palpation  and  on  macroscopic  examination  were 
therefore  composed,  not  of  glands,  but  of  normal  adipose  tissue  much  condensed,  and 
enclosing  a  large  quantity  of  fibrous  tissue." 

Desmons,  referring  to  a  case  of  Upomatosis  on  which  he  operated,  says :  "  The 
fragments  of  the  tumour  were  examined  macroscopically  and  histologically,  and  were 
foimd  to  be  composed  of  fat  alone.  I  have  never  seen  or  touched,  much  less  removed, 
glands  or  fragments  of  tissue  of  a  glandular  appearance."  Such  statements  make  it 
impossible  to  admit  a  glandular  origin  of  symmetrical  diffuse  Upomatosis.  I  know 
that  we  may  call  in  question  the  part  of  the  lymphatic  glands,  and  more  generally  of 
the  lymphoid  tissue  in  the  evolution  of  the  fat,  and  if  we  are  wiUing  to  admit  that  diffuse 
lipomatosis  most  often  arises  in  a  region  where  glandular  tissue  abounds,  we  might 
perhaps  suppose  that  the  glandular  tissue  is  the  primum  movens  in  this  affection. 
Only  supposing  that  this  theory  were  probable,  the  genesis  of  the  fact  would  remain 
just  as  unexplicable.  Why  should  glandular  tissue  thus  lend  itself  to  the  production 
of  fatty  masses  ? 

I  have,  moreover,  seen  a  case  which  has  led  me  to  abandon  the  hypo- 
thesis of  the  association  of  fatty  and  glandular  lesions,  and  the  reader  might 
presume  this  from  the  title  of  this  section.     The  case  is  as  follows  : 

I  had  imder  my  care  in  the  Hotel-Dieu  a  man  suffering  from  classical  diffuse  lipo- 
matosis, which  gave  me  an  opportunity  for  dehveringa  clinical  lecture  on  this  affection.* 

*  Dieulafoy,  Clinique  Mcdicale  de  VHotd-Dieu,  1903,  1S°"=  lefon. 


2002  TEXT-BOOK  OF  MEDICINE 

In  this  patient,  as  in  other  similar  cases,  the  cervical  region  was  chiefly  invaded.  The 
Hpomatous  tumours  occupied  the  anterior,  lateral,  and  posterior  regions  of  the  neck. 
The  head  rested  on  a  Hpomatous  muflf.  The  fatty  masses  formed  tumours  of  various 
sizes.  They  were  not  genuinely  lobulated,  but  were  rather  spread  out  and  fused  without 
any  clear  Hne  of  demarcation.  It  was  possible  to  move  them  en  masse.  They  were 
not  painful  or  adherent  to  the  skin,  which  preserved  its  normal  appearance.  In  the 
mental  region  and  in  the  lateral  parts  of  the  neck  they  were  softer  than  behind.  At 
the  nape  of  the  neck  the  hpomatous  tumours  were  symmetrical,  and  partly  hidden  by 
the  roots  of  the  hairs.  Lower  there  was  a  large  Hpoma  at  the  level  of  the  vertebra 
prominens. 

The  patient  also  had  symmetrical  Hpomata  in  the  inguinal  regions.  They  were 
superposed  in  two  stages — in  the  form  of  prominent  pads,  which  were  parallel  to  the 
folds  of  the  groin,  and  extended  inward  as  far  as  the  scrotum.  Here,  too,  the  tumours 
were  mobile,  painless,  and  somewhat  ill-defined.  They  were  soft,  and  yet  on  kneading 
they  gave  the  feehng  of  hard  nodules,  such  as  lymphatic  glands  embedded  in  the  fatty 
mass.  Nevertheless,  guided  by  experience,  I  stated  that  these  indurated  nodules  were 
not  glands,  and  to  make  certain,  I  obtained  the  patient's  permission  to  remove  one. 
The  histological  examination  by  Jolly  confirmed  the  absence  of  any  lymphatic  tissues 
in  the  fatty  mass. 

The  patient  had  two  symmetrical  Hpomata  in  the  clavicular  regions,  and  four  others 
in  the  lumbo-sacral  region. 

The  affection  had  begun  about  twelve  years  before  in  the  cervical  region.  It  made 
slow  progress,  causing  no  discomfort  or  pain,  and  gradually  invaded  the  groins  and  other 
parts  of  the  body.     The  general  health  had  not  undergone  the  least  affection. 

Jolly  examined  the  blood,  which  was  normal.* 

The  man  left  the  hospital,  but  returned  a  year  later,  wasted,  cachectic,  and  suffering 
from  hypertrophic  alcohoHc  cirrhosis  of  the  Hver  and  tubercular  peritonitis.  The 
diflrusehpomatosis  was  still  present  in  the  same  regions,  although  the  cachectic  condition 
of  the  patient  had  caused  marked  diminution  in  its  size.  Death  followed  in  a  few  weeks. 
The  autopsy  was  especially  interesting,  because  it  is,  I  think,  the  first  time  that  we  have 
been  able  to  study  carefully  and  in  several  regions  the  hpomatous  masses,  and  to  see 
their  true  relation  to  the  Ijrnaphatic  system.     Loeper  found  the  following  results  : 

Characteristic  tubercular  peritonitis  without  adhesions  and  without  fibro-caseous 
masses  was  present.  The  Hver  showed  alcohoHc  hepatitis,  with  hypertrophy  and  fatty 
infiltration  of  the  cells.  The  spleen  weighed  12  ounces.  It  was  hard  and  fibrous. 
The  pancreas  was  large,  hard,  and  furrowed  by  fibrous  bands,  which  pushed  aside  the 
various  lobules  and  penetrated  into  the  acini.  The  intestine  showed  no  tubercular 
alceration.  Congestion  was  extremely  well  marked  in  the  kidneys,  which  were  fiUed 
vsdth  hemorrhagic  points  in  the  glomeruU  alid  tubules ;  in  the  suprarenal  capsules, 
the  vascular  network  of  which  was  very  dilated ;  in  the  thyroid  body,  which  weighed 
2  ounces ;  and  in  the  lungs,  which  showed  splenization  at  the  bases.  The  heart  was 
dilated,  and  the  auricles  were  very  distended.  The  brain  was  covered  with  large  vessels, 
and  the  Sylvian  and  Rolandic  areas  were  studded  with  typical  tubercular  granules. 
These  commonplace  lesions  were  due  to  passive  congestion  and  to  the  dissemination 
of  Koch's  baciUus.     They  had  no  relation  to  the  Hpomatosis. 

*  Red  corpuscles  per  cubic  milUmetre  . .  . .  . .  . .  4,000,000 

White  corpuscles  per  cubic  milHmetre  .  .  .  . .  . .  4,000 

Weight  of  haemoglobin  per  100  cubic  centimetres  of  blood  . .  13  grammes, 

Colour -index       ..         ..         ..         ..         ..         ..  ••  ■.  302 

'lymphocytes  . .  . .  . .  25 

Varieties  of  white  corpuscles     large  mononuclears  . .  . .       6 

per  100  leucocytes  polynuclears  . .  . .  . .  65 

eosinophiles  . .         . .  . .  . .       4 


RHEUMATiU  Ai^D  DYHTllOPinC  DISEASES  liUOJ 

Wo  ourofully  cxiuuiiiod  tho  liiJiuuatoiis  tumours  in  the  ro/^ionn  whore  fat  and  lyiii- 
pliutic  glands  are  usually  prosent,  and  also  in  tho  organs  which  auom  to  play  a  part  in  tho 
organio  oxchangos.  Those  lipomatous  masses  wore  present  bolow  tho  parotid,  along  the 
vessels  of  tho  neck,  in  tho  supraclavicular  and  axillary  hollows,  in  tho  poctoraUs  major,  in 
tho  anterior  surface  of  tho  latissimus  dorsi,  and  in  tho  inguinal  and  crural  hollows. 

Wo  also  found  masses  (which  wore  not  portuiptiblo  during  life)  in  front  of  the  iUacus 
musclo,  along  the  intercostal  space-',  under  the  pleura,  and  in  tho  spaces  themselves  ; 
and  lastly,  wo  found  them  in  front  of  tho  vertebral  oolumn  and  in  the  mesentery,  which 
was,  as  it  wore,  distended  with  fat. 

Ail  these  masses  had  tho  macroscopio  appearance  of  tho  ordinary  lipoma,  and 
sections  made  at  several  parts  of  each  of  them  showed  not  the  least  trace  ol  lymphatic 
G;Iands. 

Microscopic  examination  of  tho  axillary,  subaxillary,  inguinal,  mesenteric,  and 
intercostal  tumours  revealed  the  presence  of  typical  adipose  lobules,  traversed  by  blood- 
vessels and  capillaries,  without  any  lymphatic  glands  and  without  any  cellular  masses 
which  might  be  looked  upon  as  vestiges  or  glands.  Some  bands  of  connective  tissue, 
containing  scattered  plasma  cells  and  connective  cells,  were  situated  in  an  irregular 
fashion  in  the  fat.     Some  mastzellen  were  visible  here  and  there. 

The  organs  of  internal  secretion — i.e.,  suprarenal  capsules  and  pituitary  and  thyroid 
glands — showed,  in  addition  to  the  congestion  noted  above,  lesions  which  explain  the 
blood-stasis  and  the  infection.  We  must  note  especially  the  adenomatous  hypertrophy 
of  the  thyroid  body  and  the  large  size  (80  centigrammes)  of  the  pituitary  body.  The 
nervous  system  was  intact.     The  cells  of  the  anterior  comua  were  normal. 


X.  ADIPOSIS  DOLOROSA. 

Adiposis  dolorosa  was  described  by  Dercum,  of  Philadelphia,  in  1888. 
It  is  a  s}Tidrome  characterized  by  a  deposit  of  fat  in  the  subcutaneous 
cellular  tissue,  with  pain  in  the  fatty  neoplasms. 

Symptoms. — The  disease  generally  commences  in  a  slow  and  insidious 
manner,  with  slight  pains,  which  may  be  felt  in  any  part  of  the  body.  The 
pains  are  sometimes  continuous,  but  in  most  cases  they  are  intermittent 
and  of  variable  severity.  Patients  compare  them  to  a  feeling  of  "  hot  water 
running  along  the  arm,"  or  to  "  worms  creeping  under  the  sldn,"  to  "  a 
loosening  of  the  skin,"  or  to  "  a  constant  sensation  of  cold  in  the  knees, 
soon  followed  by  dull  pain."  We  find  at  first  slight  redness  of  the  skin, 
without  appreciable  swelling ;  later,  with  a  little  care,  we  may  discover 
small  mobile  nodules,  painful  on  pressure,  rolling  under  the  skin,  and 
varying  in  size  from  a  hazel-nut  to  a  walnut.  The  pains  may  precede  or 
may  be  contemporaneous  with  the  tumours. 

The  stationary  stage  comprises  the  cardinal  and  secondary  symptoms. 
To  the  former  belong  the  pains,  the  asthenia,  and  the  psychical  troubles. 
The  tumours  are  usually  nodular  in  form,  and  more  rarely  diffuse.  Asthenia 
is  always  marked.  It  may  be  so  severe  as  to  render  patients  incapable  of 
the  least  effort.  Among  the  psychical  troubles  let  me  mention  changes  in 
character,  cerebral  instability,  nightmares,  hallucinations,  loss  of  memory, 
and  tendency  to  melancholy  (Ballet). 


2004  TEXT-BOOK  OF  MEDICINE 

To  the  secondary  symptoms  belong  various  hsemorrliages,  vasomotor, 
motor,  and  sensory  troubles,  with  zones  of  anagsthesia  or  of  hjrperaesthesia, 
disturbance  of  the  special  senses,  and  trophic  troubles  (arthropathies, 
muscular  atrophy). 

The  disease  lasts  for  years,  and  the  patient  succumbs  to  cachexia  or  to 
some  intercurrent  disease.     Recovery  is  exceptional. 

The  diagnosis  must  be  made  from  nervous  oedema,  diffuse  lipomatosis, 
neuro-fibromatosis,  and  symmetrical  lipomata. 

Pathological  Anatomy. — The  neuro-fibromatous  lesions  and  the  svm- 
metrical  lipomata  affect  the  connective  tissue  and  the  viscera.  The  con- 
nective tissue  undergoes  an  oedematous  swelling,  which  is  characterized  by 
the  presence  of  large  fusiform  cells,  without  fatty  cells,  and  by  embryonic 
connective  tissue.  The  adiposis  then  appears,  and  gives  place  to  a  final 
fibrosis.  In  a  biopsy  by  Renon  it  was  easy  to  see  the  fatty  change  in  the 
connective  cells.  The  "^asceral  lesions  are  but  little  known.  Observers  have 
found  changes  in  the  thyroid  body  and  in  the  pituitary  gland,  atrophy  of 
Goll's  column,  and  the  presence  of  myeline  fibres  in  the  pia  mater,  covering 
the  posterior  columns  of  the  spinal  cord. 

etiology. — We  do  not  exactly  know  the  setiology  and  the  pathogenesis 
of  adiposis  dolorosa.  It  is,  however,  chiefly  seen  in  women  during  the 
mature-  age  and  after  injuries.  Sellerin  thinks  that  the  disease  may  be  due 
"  in  some  cases  to  a  simple  dynamogenous  trouble  in  the  nervous  system," 
since  "  the  psychical  condition  of  certain  patients,  as  well  as  their  rapid 
recovery,  can  only  be  set  down  to  the  possibility  of  troubles  which  are 
purely  functional  and  of  nervous  origin,  nob  to  say  hysterical,"  The 
lipasic  ferment  of  the  blood-serum  is  normal  in  amount. 

As  regards  treatment,  extu'pation  of  the  fatty  masses,  hydrotherapy, 
salicylate  of  soda,  arsenic,  strychnine,  and  thyroid  extract  have  so  far  been 
employed  with  varying  results. 

XI.  MYXCEDEMA. 

General  and  Historical  Considerations. — Myxcedema,  which  was  practically  unknown 
until  thirty  years  ago,  now  forms  one  of  the  most  complete  diseases  which  it  is  possible 
to  study  in  pathology.  Its  pathogenesis  has  been  rapidly  elucidated,  and  the  siirgeon, 
while  operating  upon  the  thyroid  gland,  has  often  reproduced  in  man  the  characteristic 
syndrome  with  all  the  exactness  of  an  experiment.  Lastly,  we  possess  for  myxcedema 
the  most  rational  and  specific  treatment  at  present  known.  It  is,  then,  a  disease 
which,  though  rare,  should  be  reported  in  detail. 

Myxcedema  was  first  described  in  an  adult  woman  by  Gull  in  1873.  It  was  after- 
wards studied  by  Ord,  who  named  it,  and  by  Charcot,  who  called  it  pachydermic 
cachexia. 

In  1880  Boumeville  showed  that  the  syndrome  of  myxcedema  may  also  appear  m 
idiots,  and  described  the  clinical  type  of  myxoedematous  idiocy. 

In   1882  Reverdin  observed,  after  total  extirpation  of  the  thyroid  body,  mucous 


RnEUMATIC  AND  DYSTFlOP[[[r  DISEASES  2005 

radomii  similar  to  t  li;i(  (l(>3cribod  by  (lull  hikI  Orel,      llo  theroforo  tlohoribod  an  oponiti  ve 
myxcBdonia  wbicb  KoL^hor  oallod  ciichoxia  strumipriva  or  thyroipriva. 

Expc^riniontal  nwoarohos  soon  showed  that  rayxfjodoma  could  bo  produced  in  animals 
by  extirpation  of  the  thyroid  b(Kly,  and  the  identity  of  apontanooua  myxocdoma  in  the 
adult,  of  cachoxiii  strumipriva,  and  of  myxtodematous  idiocy,  was  speedily  established. 
Clinical  observation  hiw  shown  that  wo  may  go  farther,  and  that,  in  addition  to  these 
types  of  myxoedema,  other  myxcodoraatous  conditions  may  supervene,  as  an  accessory 
syndrome,  in  cretins  and  in  certain  imbeciles.  The  discovery  of  the  specific  treatment 
by  injection  of  thyroid  extract  was  the  corollary  of  these  researches. 

etiology. — Myxoedema  is  only  a  syndrome  consecutive  to  the  surgical 
extirpation  or  to  various  changes  of  the  thyroid  gland.  We  are  ignorant  of 
the  reason  for  the  congenital  absence  of  the  gland  which  causes  myxoede- 
matous  idiocy,  and  we  have  scarcely  more  information  as  to  the  causes  of 
myxoedema  in  the  adult.  Writers  have  incriminated,  though  without  cer- 
tainty, various  acute  or  chronic  infectious  diseases  which  are  said  to  cause 
thyroiditis,  ending  silently  in  sclerosis  and  atrophy  of  the  organ. 

Pathological  Anatomy. — If  myxoedema  is  the  result  of  the  functional 
suppression  of  the  thyroid  gland,  which  are  the  changes  that  may  give  rise 
to  it  ? 

Operative  myxoedema  necessitates  the  total  removal  of  the  gland.  The 
appearance  of  the  syndrome  is  exceptional  after  partial  thyroidectomy. 
Cachexia  does  not  appear  if  a  third  of  the  gland  be  left. 

Congenital  myxoedema  almost  always  results  from  the  absence  of  the 
thyroid  body. 

Acquired  myxoedema  depends  on  an  inflammation  of  the  thyroid  body, 
ending  in  atrophy  and  fibrosis.  The  fibrosis  of  the  organ  may  be  complete, 
but  more  often  we  find,  especially  at  the  onset,  masses  of  round  cells  in  the 
walls  of  the  vesicles — that  is  to  say,  proliferation  of  the  epithelium.  The 
inflammation  of  the  gland  must,  therefore,  be  both  interstitial  and  parenchy- 
matous. 

Any  lesion  of  the  thjTxoid  body  ending  in  suppression  of  its  function  may 
be  a  cause  of  myxoedema. 

The  infiltration  of  the  subcutaneous  cellular  tissue  by  a  mucinoid  sub- 
stance is  the  most  constant  and  best-known  secondary  lesion.  Cases  of 
true  lipomatosis  have  also  been  cited.  Compensatory  hypertrophy  of  the 
pituitary  gland  has  been  found. 

Operative  Myxoedema. — The  first  symptoms  of  operative  myxoedema 
generally  appear  three  or  four  months  after  removal  of  the  gland.  Sensa- 
tions of  weakness  and  of  coldness  in  the  limbs,  mucous  infiltration,  and 
decoloration  of  the  skin,  suppression  of  the  sweat,  and  cerebral  torpor  are 
the  symptoms  which  gradually  appear,  and  which  we  shall  find  complete  in 
spontaneous  myxoedema. 

Operative  myxoedema  may  be  slight  and  curable.  In  these  cases  the 
U.  127 


2006  TEXT-BOOK  OF  MEDICINE 

extirpation  of  the  gland  has  doubtless  been  only  partial.  If  the  myxoedema 
results  from  the  removal  of  the  thyroid  body,  or  in  a  child  with  goitre,  we 
see  arrest  of  development  and  grave  intellectual  troubles,  which  are  com- 
parable to  those  of  the  congenital  disease. 

Spontaneous  Myxoedema  in  Adults. — The  onset  is  generally  insidious, 
and  the  disease  shows  three  periods.  The  first  period  is  marked  by  the 
mucoid  infiltration  of  the  skin.  The  derma  and  the  subcutaneous  tissue 
are  infiltrated  with  colloid  substance.  The  skin  is  swollen,  elastic,  and 
loses  its  suppleness.  It  is  of  a  yellowish- white  colour.  The  pressure  of  the 
finger  does  not  cause  pitting.  The  lips  are  thickened,  the  nose  is  enlarged, 
and  the  face  has  a  full-moon  appearance.  The  hands  and  feet  are  swollen, 
and  become  pachydermic.  The  epidermis  is  dry ;  the  sweat  is  diminished ; 
the  hair,  eyebrows,  eyelashes,  and  the  beard  become  thin.  The  tongue  and 
the  mucous  membrane  of  the  mouth  and  pharynx  are  thickened. 

At  the  end  of  a  few  months  the  stationary  stage  is  characterized  by 
profound  muscular  weakness  and  psychical  troubles,  which  are  ushered  in 
by  dulness,  very  marked  intellectual  torpor,  and  absolute  indifference.  The 
pulse  becomes  slow ;  the  temperature  falls  to  95°  or  96°  F.  The  patient  is 
very  sensitive  to  cold;  the  urine  diminishes,  and  the  voice  is  rough  and 
monotonous.  In  fact,  as  Brissaud  says,  in  the  patient  with  myxoedema 
the  entire  body  appears  to  be  asleep.  At  this  period  atrophy  of  the  thyroid 
body  is  the  rule,  and  hypertrophy  is  the  exception.  If  specific  treatment 
be  not  employed,  the  patient  passes  into  a  state  of  pachydermic  cachexia, 
and  death,  is  the  ending  of  the  third  phase.  Specific  treatment  wiU  prevent 
the  onset  of  this  last  period. 

Congenital  Myxoedema— Myxoedematous  Idiocy.— Congenital  myx- 
oedema may  appear  before  the  age  of  two  years.  Absence  of  the  thyroid 
body  and  infiltration  of  the  skin  are  seen  in  children,  just  as  in  adults. 
Arrest  of  mental  and  physical  development  characterizes  myxoedematous 
idiocy.  "  It  does  not  run  a  course  characterized  by  successive  periods,  and 
does  not  end  in  cachexia.  It  remains  the  same  from  the  first  to  the  last 
day,  and  life  is  not  compromised.  The  general  nutrition,  which  is  at  a  very 
low  ebb,  when  it  should  be  at  its  maximum,  is  in  keeping  with  a  duU,  indo- 
lent, and  passive  state  of  existence,  without  initiative,  without  needs,  and 
almost  without  instinct.  The  heart  beats,  the  lungs  breathe,  but  the  brain 
remains  plunged  in  its  foetal  torpor,  and  nothing  awakens  it."  Such  is  the 
striking  picture  of  myxoedematous  idiocy  painted  by  Brissaud.  The  Pacha 
of  Bicetre,  whose  height  was  only  3  feet  at  twenty  years  old,  is  a  striking 
example.  The  physical  and  intellectual  condition  remains  practically  in 
the  same  state  as  when  the  individual  was  afiected,  and  "  he  is  con- 
demned to  perpetual  infancy  "  (Brissaud). 

Myxoedematous  idiocy,  as  we  have  already  said,  is  reproduced  experi- 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  2007 

mentally  in  young  children  in  whom  the  thyroid  body  is  extirpated.  The 
myxccdenia  is  really  a  trophic  trouble  following  extirpation  of  the  thyroid 
body,  and  its  effects  vary  according  to  the  ago  of  the  patient. 

Cretins  with  goitre  are  most  often  myxoedematous,  and  their  history 
closely  resembles  that  of  myxa'dematous  idiots.  In  the  cretin  the  thyroid 
body  is  almost  always  hypertrophied,  but  cystic  degeneration,  just  as  much 
as  the  atrophy,  deprives  the  thyroid  gland  of  its  functions. 

Brissaud  distinguishes  thyroid  from  parathyroid  myxoedema.  The 
latter  disease  is  said  to  be  in  man  the  analogue  of  the  experimental  myx- 
oedema which  follows  the  extirpation  of  the  parathyroid  glands  in  animals 
(Gley).  Myxoedema,  properly  speaking,  is  not  complicated  by  intellectual 
apathy.  Parathyroid  myxoedema,  which  results  from  a  complete  and  total 
change  in  all  the  parts  of  the  gland,  is  characterized  by  "  cretinoid  idiocy 
and  the  brutishness  of  cachexia  strumipriva,"  in  addition  to  the  iD.filtration 
of  the  skin  (Brissaud). 

Diagnosis. — We  shall  not  dwell  on  the  diagnosis  of  myxoedema,  as  it  is 
always  easy  to  difEerentiate  it  from  various  forms  of  soft  oedema  in  cardiac 
and  renal  diseases,  from  lipomatosis,  or  from  acromegaly.  Let  us  only 
remember  the  relations  which  exophthalmic  goitre  and  myxoedema  may 
present  in  exceptional  cases.  Hyperthyroidation  may  gradually  give  place 
to  hypothyroidation. 

Cretinism  is  special  to  certain  regions,  and  the  goitre  from  which  the 
patient  suffers  is  nearly  always  hereditary. 

Pathogenesis. — Physiologists  have  shown  that  extirpation  of  the  thyroid 
body  in  animals  causes  trophic  troubles  similar  to  those  of  human  myxoedema. 
Horsley  experimented  upon  the  monkey.  One  question  remains  to  be 
elucidated  :  How  does  functional  insufficiency  of  the  thyroid  body  lead  to 
myxoedema  ? 

SchifE,  in  order  to  answer  the  question,  has  stated  the  following  pro- 
positions :  Either  the  thyroid  body  elaborates  by  internal  secretion  a  sub- 
stance which  is  indispensable  to  the  proper  action  of  the  nerve  centres,  or 
else  in  the  normal  condition  it  has  an  iahibitory  action  on  certain  toxic 
substances  which  are  produced  in  the  economy,  and  which  can  freely  exer- 
cise their  harmful  powers  after  the  annihilation  of  the  gland.  In  spite  of 
experiments  reported  by  physiologists  in  favour  of  the  second  proposition, 
clinical  facts  appear  to  be  in  favour  of  the  first  one.  Do  not  the  mar- 
vellous therapeutic  results  obtained  by  the  injection  of  thyroid  extract 
appear  to  indicate  that  the  gland  secretes  a  substance  useful  to  the  proper 
function  of  the  organs  ?  Besides,  we  are  commencing  to  recognize  the 
intimate  nature  of  the  active  principles  of  the  thyroid  juice.  Baumann  has 
discovered  thyroidin,  an  organic  substance  consisting  of  proteid  matter  and 
iodine  in  intimate  combination.     This  substance,  which  is  a  very  active 

127—2 


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extract  of  the  thyroid  body,  cures  myxoedema,  as  very  clear  cases  have 
proved. 

From  the  practical  point  of  view,  we  must  always  assure  ourselves  of  its 
existence  in  the  extracts  used  therapeutically,  and  the  iodine  which  it  con- 
tains renders  its  discovery  easy.  Frankel  of  Vienna,  has  recently  isolated 
a  crystallizable  substance  called  thyro-antitoxin,  which  does  not  contain 
iodine.  In  animals  it  lessens  the  symptoms  caused  by  extirpation  of  the 
thyreoid  body.  Chemistry  has,  without  doubt,  not  said  its  last  word  as  to 
the'  nature  of  the  substances  in  the  thyroid  juice. 

Treatment. — The  specific  treatment  of  myxoedema  consists  in  supplving 
the  economy  with  thyroid  substances,  the  absence  of  which  causes  the  disease. 

G-rafting  the  thyroid  body  of  animals  and  hypodermic  injections  of 
thyroid  extract  were  the  first  methods  employed,  but  they  have  been 
abandoned. 

Howitz  was  the  first  to  institute  the  treatment  of  myxoedema  with 
thyroid  tabloids.  This  method  is  the  only  one  employed  to-day.  We  can 
procure  ready-made  tabloids  of  the  thpoid  extract,  but  the  best  prepara- 
tion is  the  home-made  one  prepared  from  the  thyroid  body  of  the  sheep ; 
it  must  be  administered  by  lobes  mth  the  greatest  care  in  order  to  avoid 
the  troubles  of  hyperthyroidation,  which  may  even  simulate  the  symtoms 
of  Basedow's  disease,  and  which  are  most  frequently  ushered  in  by  head- 
ache, syncope,  albuminuria,  etc. 

Under  the  influence  of  the  thyroid  juice  the  central  temperature  is  raised, 
rapid  demyxcedemization  occurs,  the  cerebral  torpor  disappears,  and  the 
patients  rapidly  regain  their  health.     Eecovery  is  only  maintained  by  con- 
tinuous treatment,  and  one  or  two  lobes  weekly  must  be  given  for  the  rest 
of  the  patient's  life. 

Such  are  the  principles  of  this  treatment,  which  is,  it  must  be  said,  one 
of  the  greatest  conquests  of  contemporary  medicine. 

The  employment  of  Bayer's  thyro-iodine  has  also  been  advised  in  doses 
of  from  50  centigrammes  to  1  gramme.  The  results  produced  by  this  drug 
are  most  favourable. 

Pierre  Marie  and  Crouzon  treated  a  man  suffering  from  operative  myxcedema, 
and  found  that  the  patient's  weight  fell  from  99  to  88  kilos  in  three  months.  Further, 
the  urine,  which  contained  1-10  grammes  of  albumin  per  htre  before  treatment,  did 
not  contain  a  trace  at  the  end  of  sis  weeks.  These  authors  hare  not  obtained  the  same 
results  with  capsules  of  fresh  thyroid.  The  weight  remains  high,  and  the  patient  does 
not  experience  the  same  benefit  as  with  iodothyrin. 

XII.  SCEOFULA— LYMPHATISM. 

If  we  refer  to  the  descriptions  which  have  been  rendered  classical  by  the  authority 
of  our  predecessors;  we  shaU  see  that  scrofula  "  is  a  constitutional  dystrophy  of  which 
the  manifestations  are,  for  the  most  part,  of  an  inflammatory  nature,  and  infect  the 


RHEUMATIC  AND  DYSTROPHTO  DISEASES  2009 

lymphatio   glands,    tho  skin,    mucous  mombranos,   cellular   tiasuo,    tho    j.stoo- fibrous 
tissues,  and  tho  viscera  "  (Jaccoud). 

There  is,  said  Bazin,  in  tho  appearance  of  these  multiple  manifestations  a  kind  of 
regularity  which,  although  not  absolute,  yet  has  some  value.  Thus,  the  skin  and  tho 
IjTnphatic  glands  are  the  first  alTocted  oven  in  youth  ;  later  tho  mucous  mombranos 
and  the  connective  tissues  suffer  ;  in  tho  third  place  wo  find  the  lesions  of  tho  bones  and 
of  tho  joints  ;  and,  lastly,  changes  in  the  viscera. 

According  to  tho  old  description,  scrofula  commences  in  the  first  year  of  life. 
Children  at  the  breast,  or  when  approacliing  dentition,  present  impetiginous  eruptions 
on  the  head  or  on  the  face  (milk  crusts).  Later,  we  find  chronic  blepharitis,  impetigo, 
crusts,  discharges  from  the  nose  and  ears,  and  chilblains,  which  become  ulcerated. 

The  glandular  enlargements  often  appear  about  the  second  dentition  (lymphatic 
temperament).  Scrofulous  adenitis  takes  place  in  successive  attacks.  It  is  often 
limited  to  the  glands  of  the  neck,  but  it  sometimes  attacks  the  bronchial  and  me.senteric 
glands  (tabes  mesenterica).  Cervical  adenitis  may  be  isolated  or  multiple  ;  it  may  end 
in  resolution  or  in  suppuration,  which  is  sometimes  interminable,  and  leaves  indelible 
scars. 

The  look  of  the  patient  is  characteristic.  The  upper  lip  is  enlarged  and  projecting, 
the  nose  is  swoUen,  the  chin  is  flattened,  the  tonsils  are  large,  and  the  child  is  subject 
to  sore-throats  and  colds. 

At  a  more  advanced  age  we  find  scrotolides  or  dermatoses,  which  have  their  seat  of 
election  on  the  head  and  face.  These  lesions  are  chiefly  erythematous,  vesicular,  and 
pustular.     They  often  have  a  violet  tint,  and  do  not  cause  pain  or  itching. 

The  later  manifestations  of  scrofula  are  chronic  and  ulcerative  coryza,  with  or 
without  ozaena,  ulcerative  scrofuhdes  of  the  throat  and  lupus,  ulcerative  or  tubercular 
dermatitis,  which  especially  attacks  the  nose  and  cheeks. 

At  the  same  time  cold  abscesses,  articular  and  bony  lesions,  such  as  periostitis, 
caries,  fungous  arthritis,  and  white  swelling  appear  ;  and,  finally,  the  last  period, 
according  to  Bazin,  comprises  scrofula  affecting  the  testis,  the  genito-urinary  organs, 
the  breast,  or  the  brain,  and  bronchial  or  pulmonary  phthisis. 

Scrofula,  which  is  a  diathetic  or  acquired  disease,  may  be  arrested  at  any  point  in 
its  evolution.  It  rai'ely  commences  after  the  age  of  puberty,  but  often  presents  long 
remissions,  and  an  adult  may  suffer  from  scrofulous  lesions,  although  he  has  had  no  trace 
since  infancy. 

This  general  survey  of  scrofula  answers  to  the  classical  picture  which  has  been 
handed  down  to  us. 

But  what  remains  of  this  picture  to-day  ?  Practically  nothing.  The  dismember- 
ment of  scrofula  has  profited  tuberculosis  and,  to  a  slight  extent,  syphilis.  Scrofula 
has  therefore  lost  its  autonomy.  In  many  cases  scrofulo-tuberoulosis  has  replaced 
the  old  scrofula. 

Some  part  of  the  old  scrofula  must,  however,  be  preserved.  Thus  the  impetiginous 
eruptions  on  the  face  and  on  the  head  which  supervene  during  lactation  and  the  approach 
of  dentition  ;  the  milk  crusts  and  the  scabs,  as  they  are  vulgarly  called,  which  persist 
and  recur  with  obstinacy ;  the  erythemata  and  the  discharges  from  the  nose  and  the 
ears,  form  a  clinical  picture  which  corresponds  to  the  views  held,  if  not  of  scrofula, 
at  least  of  lymphatism.  It  may  be  said  that  children  subject  to  such  manifestations 
are  more  hable  than  others  to  become  scrofulo-tubercular.  We  shall  discuss  later 
this  question,  which  proves,  in  any  case,  the  affinity  of  these  various  conditions,  but  not 
their  identity. 

It  is  certain  that  in  the  so-caUed  lymphatic  persons  resolution  is  imperfect  in  con- 
gested or  inflamed  parts,  and  it  appears  as  though  the  lymphatic  circulation  were  in- 
terrupted. Catarrhs  of  the  nasal,  ocular,  and  pharyngeal  mucous  membranes  persist 
indefinitely;  the  alse  nasi  and  the  upper  Up  remain  indurated  and  thickened;  the 


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blepharitis  seems  everiasting  ;  coryza  and  angina  occur  on  the  least  opportunity ;  the 
lymphatic  glands  readily  suffer  from  the  shock ;  the  tonsils  are  hypertrophied  and 
remain  large.  These  various  lesions  give  a  characteristic  appearance  to  the  lymphatic 
patient. 

It  is  also  undeniable  that  these  "  lymphatic  "  subjects  are  less  armed  for  defence  ; 
the  "  soil "  is  in  their  case  of  inferior  quahty ;  the  skin  and  the  mucous  membranes 
are  readily  invaded  by  the  pyogenic  and  saprophytic  microbes  which  usually  hve  on 
these  surfaces,  and  hence  the  frequency  of  impetigo,  of  boils,  and  of  cutaneous  suppura- 
tions, with  or  without  consecutive  adenitis.  This  attenuated  scrofula,  or  "  lymphatic 
temperament,"  if  we  prefer  to  preserve  an  ancient  term,  deserves  a  place  in  our  patho- 
logical descriptions,  but  all  the  remainder  of  the  old  scrofula  should  be  transported 
elsewhere. 

Thus  tuberculosis  and  syphilis  must  claim  the  ulcero-crustaeeous  scrofulides,  the 
so-caUed  scrofulous  adenitis,  the  scrofulides  of  the  mucous  membranes,  and  the  king's 
evU.  Most  cases  of  adenitis  which  were  regarded  as  scrofulous  are  reaUy  tubercular. 
Their  tubercular  nature  is  proved  by  pathological  anatomy  and  by  experimental  research, 
for  their  substance  produces  tuberculosis  on  inoculation.  These  cases  of  adenitis 
often  supervene  in  persons  who  have  not  had  any  scrofulous  trouble.  They  may 
persist  for  a  long  while  in  the  condition  of  local  tuberculosis.  They  improve,  become 
worse,  and  are  followed  by  tuberculosis  of  the  bronchial  glands,  by  suspicious  bron- 
chitis, and  by  pulmonary  phthisis.  Their  course  is  sometimes  very  slow.  It  may  last 
for  a  great  number  of  years,  and  yet  in  some  cases  the  march  of  events  is  much  more 
rapid.  An  individual  (the  case  is  common  in  soldiers)  who  has  never  had  any  past 
history  of  scrofula  is  taken  ill  with  bronchitis,  or  with  pleurisy,  or  perchance  has  a 
cold  abscess,  caries  of  a  bone,  without  any  trace  of  pulmonary  phthisis ;  and  yet  his 
health  declines,  adenitis  appears,  and  is  really  tubercular,  though  apparently  scrofulous. 
Acute  pulmonary  tuberculosis,  which  proves  fatal,  soon  follows. 

Syphilis  in  the  tertiary  period  gives  rise  to  glandular  gummata  (Foumier).  These 
gummata  are  seated  chiefly  in  the  inguinal,  submaxillary,  and  cervical  regions.  At 
first  they  are  hard  and  painless,  but  later  they  soften,  ulcerate  in  the  form  of  a  crater, 
and  give  exit  to  thick,  viscid,  and  purulent  matter.  The  analogy  is  sometimes  so  great 
between  these  syphilitic  adenopathies  and  those  which  were  formerly  called  scrofulous 
that  treatment  alone  can  decide  the  diagnosis.  We  can  therefore  ehminate  the  group 
of  so-caUed  scrofulous  adenopathies. 

The  group  of  malignant  scrofulous  anginse  must  also  be  struck  out ;  and  these  anginse 
are  due  to  acquired  or  to  hereditary  syphihs,  or  are  of  tubercular  origin. 

Lupus  of  the  skin  and  mucous  membrane  is  also  a  lesion  of  scrofulo -tubercular 
origin.     The  description  of  lupus  has  already  been  given. 

Cold  abscesses,  which  we  are  too  ready  to  caU  scrofulous,  must  be  referred  to  tuber- 
culosis.    Tubercles  and  baciUi  have  been  found  in  their  walls. 

Scrofula,  according  to  old  descriptions,  affected  the  joints  and  the  bones,  causing 
white  tumours,  caries  with  suppuration,  and  fistulous  tracts,  from  which  spHnters  of 
bone  came  out.  On  closer  inspection,  however,  it  has  been  found  that  these  so-called 
scrofulous  lesions  (chronic  arthritis,  fungous  arthritis,  and  white  swelling)  are  anatomi- 
cally and  chnicaUy  tubercular  in  nature. 

Fungous  tubercular  arthritis  rarely  commences  in  the  synovial  membrane ;  it 
almost  always  has  its  origin  in  tuberculosis  of  the  bone.  A  tubercular  focus  develops 
in  the  epiphysis,  softens,  causes  osteitis,  caries,  necrosis,  and  the  joint  is  then 
invaded. 

In  some  cases  these  lesions  represent  a  local  tuberculosis,  which  may  recover  with  or 
without  ankylosis — coxalgia,  white  swelling  of  the  knee  (Lannelongue's  treatment) — 
but  sometimes  tuberculization  of  the  joint  is  followed  at  a  more  or  less  lengthy  interval 
by  pulmonary  phthisis,  and  reports  prove  that  apumtation  may  cause  an  outburst 


RHEUMATIC  AND  DYSTROPHIC  DISEASES  2011 

of  acute  pulmonary  tuboroulosis  (Vornouil).     In  other  oaHos  the  tuboroular  lesions  in 
the  joints  and  bonoa  dovolop  at  ( lio  saiuo  t  irao  as  a  raoro  or  I(3S.h  latent  phthisis. 

Other  bony  lesions  which  have  the  apijoaranco  of  scrofula  aro  syphilitic  in  nature. 
Lastly,  others  arise  in  an  old  ostoomyohtis,  which  has  probably  fallen  short  <jf  complete 
recovery  (Lannelonguo).  All  these  changes  must  bo  abstracted  from  the  hst  of 
scrofula. 

Visceral  Lesions. — Many  visceral  lesions  which  wore  formerly  regarded  as  scrofula 
must  be  put  under  the  head  of  tuberculosis.  We  aro  not  sufliciently  familiar  with  the 
course  of  those  local  forms  of  tuberculosis ;  we  aro  not  yet  sufficiently  free  from  the 
famous  law  of  Louis,  wliich  states  that  pulmonary  tuberculosis  must  accompany 
tuberculosis  of  other  regions  or  of  other  organs.  Local  or  localized  tuberculosis  may 
appear  primarily  in  a  region  or  in  an  organ,  where  it  remains  locaUzod  and  ends  in 
recovery.  It  has  not  the  same  gravity  in  all  organs,  its  evolution  does  not  run  the 
same  course,  and  its  tendenc}'  to  become  general  is  different. 

Certain  changes  in  the  testis,  characterized  by  chronic  orchitis,  with  induration 
of  the  epididymis,  softening,  suppuration,  and  fistulae,  have  long  been  called  scrofulous. 
These  changes  are  really  tubercular.  Not  only  does  the  lesion  recover  Uke  a  local 
tuberculosis,  but  in  ten  cases  out  of  thirty  tuberculosis  of  the  testis  has  no  tendency 
to  become  general  (Reclus).  I  would  say  the  same  of  tuberculosis  of  the  uterine  mucosa, 
of  the  ovary,of  the  bladder,  of  the  kidney,  and  of  the  breast— lesions  formerly  considered 
by  Bazin  as  scrofulous  in  nature. 

As  regards  the  changes  in  the  lung,  we  know  that  the  tubercle  and  the  caseous 
products  are  of  the  same  nature  (Laennec's  work) ;  the  so-called  scrofulous  phthisis 
and  tubercular  phthisis  belong  to  one  single  morbid  process,  and  clinically  the  differ- 
ences in  their  symptomatology  are  most  often  reduced  to  a  question  of  degree. 

The  foregoing  comparative  and  analytical  study  proves  that  scrofula  no  longer 
exists  as  a  morbid  entity  ;  some  of  its  changes  belong  to  syphilis,  and  a  still  larger  share 
belongs  to  tuberculosis.  One  thing  remains  :  I  mean  "  the  lymphatic  temperament,"  on 
wliich  I  have  dwelt  above,  and  which  constitutes  a  weakness  on  the  part  of  the  in- 
dividual. This  weakness,  which  we  call  lymphatic  or  scrofulo-lymphatic,  may  be 
acquired  or  hereditary. 

It  may  be  caused  at  the  most  tender  age  by  defective  or  insufficient  nourishment, 
and  it  may  depend,  at  a  somewhat  more  advanced  age,  on  faulty  hygienic  conditions, 
such  as  damp,  dark,  and  airless  dweUings,  or  bad  nourishment.  It  may,  lastly  and 
chiefly,  be  hereditary  when  the  child  is  bom  of  arthritic,  syphilitic,  alcoholic,  or  of 
tubercular  parents,  or  when  the  fcetus  has  been  conceived  under  adverse  conditions 
(advanced  age  of  the  father,  ill-health  of  the  mother). 

Are  we  to  consider  lymphatism  as  the  first  stage  of  tuberculosis  ?     I  do  not  think  so. 

It  is  indisputable  that  lymphatic  persons  are  specially  predisposed  to  scrofulo- 
tubercular  changes  and  to  pulmonary  phthisis,  but  this  doM  not  prove  the  identity 
of  the  two  processes ;  it  proves,  rather,  at  most,  that  the  scrofulo-lymphatic  person 
offers  a  soil  favourable  to  the  development  of  tuberculosis. 

The  treatment  of  scrofulo-lymphatism  is  as  follows :  Residence,  as  far  as  possible, 
in  the  open  air,  in  the  coimtry,  or  at  the  seaside  ;  physical  exercises,  riding,  and  gymnas- 
tics. The  food  should  be  carefully  chosen,  and  should  consist  of  meats,  fresh  vegetables, 
fat  and  oily  foods,  such  as  caviare,  sardines  in  oil,  tunny-fish,  and  pate  de  foie  gra-s.  Cod- 
liver  oil  in  large  doses,  preparations  of  iodine,  phosphates,  and  arsenic  are  the  chief 
drugs.  Hydrotherapy,  sea-baths,  saline,  sulphur,  and  bromine  waters  should  be 
advised  (Kreuznach). 


PART  IX 

PARASITIC   INFECTIONS 

I.  TEICHINOSIS. 

Trichinosis  is  the  disease  produced  by  tiie  entrance  of  a  large  number  of 
trichinae  into  the  organism,  and  especially  into  the  striated  muscles. 

iEtiology  —  Pathogenesis. — The  trichina — Trichina  spiralis  (Owen), 
Trichindla  spiralis  (Raillet) — is  a  helminth  of  the  order  of  the  Nematodes 
and  of  the  tribe  of  the  TrichotracheHdes  (Blanchard). 

The  male,  which  is  1*5  millimetres  in  length,  of  a  cylindro-conical  form, 
and  pointed  in  front,  presents  at  its  posterior  part  two  appendages — "  a 
kind  of  copulatory  pouch "  (Blanchard).  The  female,  which  is  from 
3  to  4  millimetres  long,  only  attains  these  dimensions  after  pairing,  when  it 
is  filled  with  eggs.  The  hatching  of  the  latter  takes  place  in  the  oviduct 
at  the  end  of  six  or  of  seven  days,  the  trichina  being  "  ovoviviparous." 
The  embryos  are  set  free  alive,  and  each  female  may  give  rise  to  many 
thousands  of  small  trichinse. 

In  man  the  trichinee  contained  in  measly  pork  make  their  way  out  of 
the  muscular  cysts  into  the  intestine,  where  they  pair,  and  beget  an  immense 
number  of  embryos.  The  greater  part  passes  into  the  striated  muscles — 
"  their  normal  habitat "  (Brouardel).  The  paths  of  this  migration  are 
still  under  discussion.  According  to  some  authorities,  the  fecundated 
females  perforate  the  wall  of  the  intestine,  and  give  ofE  the  embryos  during 
their  passage.  The  latter  penetrate  into  the  lymphatic  network  of  the 
lacteals,  pass  into  the  venous  circulation,  and  then  into  the  general  circula- 
tion, in  order  to  make  their  way  through  the  capillaries,  and  to  be  arrested 
in  the  muscles  (Cerfontaine).  According  to  other  authors,  the  young 
trichinse,  having  come  from  the  villi  of  the  mucosa,  invade  the  lymphatic 
tracts,  and  reach  the  blood-current  after  passing  through  the  thoracic  duct 
(Askanazy).  In  the  striated  muscles  the  embryo  increases  in  size,  becomes 
encysted,  and  commences  a  latent  life. 

Man  contracts  trichinosis  by  eating  contaminated  pork  which  has  not 
been  cooked.     Severe  epidemics  of  trichinosis  have  been  noted,  especially 

2012 


PARASTTir  r?iFF/TfONS  2013 

in  tho  North  of  Germany  and  in  America.  Among  the  great  epidemics  in 
Germany,  I  may  quote  those  of  Emersleben,  Dccnsdorf,  Groeningen,  and 
Nienhagen  in  1883,  studied  on  the  spot  by  Brouardel  and  Grancher.  The 
ingestion  of  raw  pork  which  contains  trichinae  is  the  chief  cause  of  the  disease. 
Cooking,  however  slight,  removes  all  danger.  Salting  has  also  a  beneficial 
influence,  and  salted  meats  appear  to  be  less  harmful  than  others. 

Pathological  Anatomy. — If  the  patient  dies  during  the  first  few  weeks 
we  find  catarrhal  iutlammation  of  the  gastro-intestinal  mucous  membrane  ; 
if  death  occurs  later,  the  lesions  in  the  digestive  system  are  no  longer  present, 
but  we  find  congestion,  inflammation,  and  oedema  of  the  lung,  and  some- 
times a  general  oedema,  without  other  special  changes. 

The  specific  lesions  affect  the  striated  muscles.  All  the  muscles  may  be 
affected.  The  diaphragm,  the  intercostal  muscles,  the  muscles  of  the 
pharynx,  and  those  of  the  neck  and  eye,  are,  however,  the  most  liable.  The 
changes  are  also  more  frequent  in  the  neighbourhood  of  the  tendons.  The 
muscles  are  riddled  with  cysts  containing  the  larvae.  The  cyst  contains  the 
trichina  in  its  centre,  and  is  enveloped  by  an  external  layer  of  myolemma, 
which  is  softened  and  converted  into  a  cellular  sheath  (Grancher).  Pro- 
gressive atrophy  of  the  muscle  fibre  is  often  present.  The  cysts  finally 
undergo  calcareous  infiltration.  The  trichinae  become  impregnated  with 
chalk,  and  the  cystic  coverings  with  phosphate  of  calcium.  The  adult  cysts, 
wliich  vary  from  0*3  to  O'S  millimetre  in  length,  generally  contain  a  single 
larva.  In  exceptional  cases  we  may  find  as  many  as  six  or  seven  larvae 
in  the  same  cyst  (Owen,  Chatin).  According  to  Soudake witch,  the  larva 
causes  phagocytic  phenomena,  wliich  tend  to  prevent  the  invasion  of  the 
parasite. 

Symptoms. — Following  Brouardel,  we  may  describe  three  periods  in  the 
clinical  study  of  tricliinosis  : 

1.  Intestinal  or  Gholeriform  Phase. — This  period  commences  three  or 
four  days  after  the  ingestion  of  the  infected  food  with  signs  of  indigestion. 
The  patient  suffers  from  nausea,  which  is  soon  followed  by  abundant  and 
repeated  vomiting.  The  diarrhoea  is  profuse  and  choleriform.  It  is  accom- 
panied by  rigors  and  fever,  which  may  reach  as  high  as  104°  F.  At  the  end 
of  a  few  days  these  alarming  symptoms  become  less  severe,  and  about  the 
end  of  the  first  week  we  notice  the  appearance  of  considerable  but  transient 
oedema  of  the  face,  whence  the  name  of  epidemics  of  big  heads  given  to  the 
German  epidemics.  We  sometimes  find  pains  in  the  limbs,  but  they  are 
less  acute  than  those  of  the  second  period. 

2.  Rheumatic  and  Typhoid  PJiase. — About  the  eighth  or  ninth  day 
pains  appear  in  the  muscles.  The  movements  are  painful  and  difficult,  and 
cause  the  patient  to  cry  out.  Sometimes  the  muscles  are  rigid  and  con- 
tracted.    If  the  diaphragm  is  affected,  respiration  is  rendered  difficult. 


2014  TEXT-BOOK  OF  MEDICINE 

The  involvement  of  the  muscles  of  the  eye  gives  the  patient  a  fixed  look, 
as  in  total  ophthalmoplegia.  The  adynamia  is  profound,  and  is  sometimes 
followed  by  violent  delirium.  Auscultation  often  yields  signs  of  oedema 
and  of  pulmonary  congestion. 

3.  Cachectic  Phase. — It  is  characterized  by  enormous  oedema  of  the 
legs,  of  the  abdomen,  and  sometimes  of  the  upper  limbs.  The  face  is  wasted, 
the  eye  is  dull,  and  the  voice  is  broken  (Grancher). 

Slight  cases  of  trichinosis  recover  after  a  few  weeks.  Severe  cases  may 
last  two  and  three  months,  and  generally  end  in  death.  The  fatal  termina- 
tion, which  is  rare  before  the  third  or  the  fourth  week,  is  due  to  the  pro- 
gressive course  of  the  disease,  but  especially  to  pulmonary  oedema,  to 
secondary  pneumonia,  and  to  ulcerative  infections  vrith  cachexia. 

The  prognosis  varies  directly  with  the  duration  of  the  afiection,  and  in 
prolonged  cases  is  often  fatal. 

The  diagnosis  is  very  simple  during  an  epidemic.  The  first  few  and 
isolated  cases  are  much  more  difl&cult  to  recognize.  They  may  simulate 
cholera,  typhoid  fever,  and  renal  or  cardiac  cachexia.  Bacteriological 
examination  of  the  stools  will  decide  the  question  of  cholera,  and  sero- 
diagnosis  will  eliminate  typhoid  fever.  If  we  find  no  reason  for  the  con- 
dition of  cachexia  in  any  organ,  we  may  perhaps  by  a  biopsy  of  the  painful 
muscle  bundles  discover  the  trichinae,  and  also  trace  them  in  the  suspected 
foods. 

Treatment. — Rigorous  prophylaxis  will  tend  to  prevent  contamination 
by  food.  Cooking  of  doubtful  meat  is  one  of  the  best  measures.  Thera- 
peutics have  but  little  effect  when  the  disease  is  present.  We  may  attempt 
by  anthelmintics  (calomel  or  santonin)  and  purgatives  to  sweep  the  trichinae 
out  of  the  intestine.  This  treatment  is  absolutely  powerless  when  the 
parasites  have  already  passed  into  the  lymphatic  tracts  of  the  muscles. 
General  treatment  must  be  employed  for  the  cachexia. 


II.  FILARIASIS. 

The  name  fliariasis  is  applied  to  an  affection  which  follows  the  invasion 
of  the  human  organism  by  the  Filaria  sanguinis  hominis  of  Lewis,  and  by 
the  F.  nocturna  of  Patrick  Manson.  The  troubles  caused  by  the  F.  medi- 
nensis  (subcutaneous  collections  of  pus,  destruction  of  the  skin,  centres  of 
gangrene,  etc.)  should  be  separated  from  this  description,  and  described 
under  the  heading  of  dracuneulosis. 

etiology — Pathogenesis. — Filariasis  is  a  disease  of  hot  countries. 
While  it  is  endemic  in  practically  all  intertropical  regions,  it  is  found  chiefly 
in  Lower  India,  China,  Japan,  Australia,  Lower  Egypt,  Mauritius,  Reunion, 
Madagascar,  on  the  West  Coast  of  Africa,  in  Brazil,  Cuba,  Guadeloupe,  and 


PARASITIC  INFECTIONS  2015 

in  tlie  South  of  the  United  States.     It  is  exceptional  in  Earope,  nw]  is  found 
only  in  persons  who  have  lived  in  hot  countries. 

The  F.  nocturna  is  a  helminth  of  the  order  of  Nomatoch's  and  of  the 
genus  Filaria.  Demarquay  was  the  first  to  find  the  embryos  of  the  filaria 
in  the  fluid  from  a  chylous  hydrocele,  in  1863. 

The  adult  worm  is  found  in  the  lymphatic  vessels  of  man.  The  male  is 
colourless,  and  measures  83  millimetres  in  length ;  the  female,  of  a  darker 
colour,  is  larger  and  longer,  and  measures  from  88  to  155  millimetres.  The 
embryos,  which  are  present  in  great  numbers  in  the  lymphatic  vessels,  pass 
through  the  thoracic  duct  or  through  the  large  lymphatic  vein,  and  reach 
the  blood-stream.  The  embryos  of  the  filaria  are  found  in  the  peripheral 
circulation  only  during  the  evening  and  the  night,  appearing  about  five  or 
six  o'clock  in  the  evening,  and  disappearing  about  eight  or  nine  o'clock  in 
the  morning.  If  during  this  time  we  prick  the  finger,  we  fiind  in  the  drop 
of  blood  a  considerable  number  of  filaria  embryos.  Their  length  is  from 
125  to  300  fi,  and  their  breadth  from  7  to  11  /tt.  They  make  very  rapid 
movements,  and  push  the  red  and  white  corpuscles  in  their  passage.  They 
are  surrounded  by  a  transparent  sheath,  which  they  perforate  in  order  to 
become  free.  They  do  not  possess  a  digestive  tube  or  a  reproductive 
system. 

In  human  blood  the  filaria  embryos  carm.ot  pass  into  the  larval  state. 
This  transformation  is  effected  by  an  intermediate  host,  the  mosquito 
(Manson).  The  female  mosquito  sucks  the  human  blood,  and  swallows  the 
filaria  embryos,  which  lose  their  sheath,  perforate  the  digestive  tube  of  the 
mosquito,  and  lodge  in  its  thoracic  muscles.  When  the  mosquito  lays  its 
eggs,  falling  into  water  and  dying,  the  larvae  are  set  free  from  the  dead 
insect.  Until  recently  it  was  admitted  that  the  larvae  were  ingested  by 
man  in  drinking  water.  The  recent  researches  of  Manson  show  that  the 
mechanism  is  quite  different.  The  embryos,  taken  into  the  stomach  of  the 
female  mosquito,  together  with  the  human  blood,  lose  their  enveloping 
membrane,  pass  through  the  waU  of  the  stomach,  and  reach  the  muscles  of 
the  thorax,  where  they  grow  and  develop.  About  the  fifth  day  the  larvae 
proceed  towards  the  prothorax,  collect  in  the  head,  and  accumulate  below 
the  mouth  and  enter  the  proboscis.  If  the  female  mosquito  bites  a  man  at 
this  time  she  inoculates  him  with  the  filaria  larvae,  which  will  become  adult. 
The  pathogenic  mosquito  is  the  Cidex  cUiaris.  The  Anopheles  which  trans- 
mits malaria  does  not  transmit  filariasis. 

Symptoms. — FUariasis  may  show  no  symptom.  As  a  rule,  this  is  not 
the  case,  and  the  troubles  provoked  by  the  parasite  are  very  varied. 

As  regards  the  skin,  the  complications  depend  upon  the  more  or  less 
complete  mechanical  obstruction  of  the  lymphatic  vessels  by  the  filariae. 
We  find  lymphatic  varices,  especially  in  Scarpa's  triangle,  the  scrotal  region, 


2016  TEXT-BOOK  OF  MEDICINE 

the  inguinal  region,  and  the  lower  limbs.  The  lymphatic  vessels  stand  out 
under  the  skin,  and  form  large  varicose  networks,  and  the  glands  are  much 
enlarged.  AU  these  parts  are  of  a  soft  and  fatty  consistency.  Lymphatic 
thrombosis  foUows  the  development  of  the  varices,  and  oedema  appears. 
The  swelling  is  considerable.  The  skin  is  white,  wrinkled,  and  covered  by 
small  warty  or  gelatinous  projections,  which  preserve  the  imprint  of  the 
finger.  The  lymphatic  oedema,  though  most  often  transient,  is  very  subject 
to  relapses,  and  is  at  length  accompanied  by  a  thickening  of  all  the  layers 
of  the  skin  and  of  the  subcutaneous  tissue,  which  produces  elephantiasis 
of  the  legs.  The  scrotum  is  often  affected  by  elephantiasis,  and  the  swelling 
may  reach  the  size  of  an  adult  head.  The  penis  disappears  completely,  and 
the  meatus  is  represented  by  a  smaU  depressed  slit  on  the  surface  of  the 
tumour  (Marie).  Ulcerations  and  injuries  of  the  skin  affect  the  distended 
lymphatic  tracts,  and  give  rise  to  a  flow  of  viscid  greyish-white  lymph, 
which  forms  crusts. 

As  regards  the  viscera,  filariasis  produces  lymphatic  effusions  in  the 
various  serous  cavities  and  in  the  urinary  system. 

Chylous  hydrocele  is  characterized  by  a  milky  effusion  into  the  tunica 
vaginalis.  Puncture  gives  exit  to  a  milky  fluid  composed  of  fine  fatty 
granules  and  abundant  white  corpuscles.  The  filaria  embryos  are  present 
in  great  numbers,  and  it  was  here  that  Demarquay  discovered  them.  Chylous 
hydrocele  may  supervene  during  the  onset  of  filariasis  or  at  a  later  period. 
It  is  sometimes  preceded  by  sharp  testicular  pains,  which  may  resemble 
renal  colic  (Audain).  These  crises  were  very  marked  in  one  of  Renon's 
cases,  and  supervened  on  an  average  twice  a  year,  without  any  prodromata. 
The  patient  was  awakened  in  the  morning  with  pain  in  the  right  testis, 
sometimes  accompanied  by  fever,  and  radiating  into  the  right  iliac  fossa  as 
far  as  the  lumbar  region.  The  attack  resembled  the  sjnnptom- complex  of 
renal  colic,  with  sharp  pain  and  vomiting.  The  only  differences  were  the 
onset  with  testicular  congestion  and  the  complete  absence  of  changes  in  the 
urine.  The  crisis  yielded  at  the  end  of  twenty-four  or  thirty-six  hours, 
and  it  was  only  after  eight  years  of  these  attacks  that  the  hydrocele  appeared. 
The  patient  was  not  troubled  by  oedema  of  the  scrotum  or  of  the  legs,  or  by 
chyluria.  The  filariasis  was  practically  confined  during  this  time  to  these 
crises.  It  is  necessary  to  remember  these  facts,  for  I  cannot  too  strongly 
insist  upon  the  difficulty  of  diagnosis. 

Chylous  ascites  is  rare.  It  cannot  be  distinguished  from  ascites  of  other 
origin  except  by  pimcture. 

Chylothorax  is  exceptional.  As  a  rule,  only  one  of  the  pleural  cavities 
is  affected. 

The  chyluria  may  be  pure.  Generally  we  see  an  admixture  of  blood. 
The  urine  is  of  an  opaque  and  yeUowish-white  colour.     When  it  contains 


PARASITIC  INFECTIONS  2017 

blooJ,  the  colour  becomes  like  that  of  cafe-au-lait,  chocolate,  or  of  dark  beer, 
etc.  The  urine  contains  serin,  globulin,  peptones,  red  corpuscles,  white 
corpuscles,  fine  fatty  granulations,  and  filaria  embryos.  The  passage  of 
chylous  urine  takes  place  suddenly,  without  great  pain,  following  excessive 
fatigue.  It  ceases  at  the  end  of  a  few  days,  to  reappear  after  fatigue, 
injury,  or  excess. 

The  general  health  is  but  little  affected,  and  the  course  of  the  disease  is 
very  slow.  Filariasis  is  characterized  by  acute  attacks,  which  are  followed 
by  periods  of  calm.  It  may  last  fifteen,  twenty,  thirty,  and  even  fifty  years. 
Recovery  is  sometimes  spontaneous.  It  follows  the  death  of  the  adult 
filaria.  The  obstruction  of  the  lymphatic  channels  ceases,  and  causes  pro- 
gressive disappearance  of  the  signs  of  the  disease.  Death  results  from  severe 
visceral  complications  and  from  secondary  infection. 

Diagnosis. — The  presence  of  the  embryo  in  the  blood  and  in  the  patho- 
logical fluids  (ascites,  effusions,  and  oedema)  will  at  once  make  the  diagnosis 
certain.  The  search  for  the  embryos  in  the  blood  should  be  made  at  night. 
The  exudate  is  centrifugalized,  and  the  deposit  is  examined.  We  can  thus 
see  the  living  embryos  or  stain  them  after  having  fixed  the  preparation. 
The  methodis  as  follows  :  Gibbs's  borated  carmine  is  employed,  followed  by 
washing  with  hydrochloric  alcohol,  and  then  staining  with  methylene  blue. 
The  embryo  is  stained  a  blue  colour,  and  its  cuticle  is  a  rose-red  (De  Nabias 
and  Sabrazes).  The  symptoms  of  filariasis  may  be  confused  with  many 
affections,  and  I  cannot  enumerate  them  aU.  Haematochyluria  is  readily 
distinguished  from  hsematuria  and  from  hsemoglobinuria.  The  haematuria 
caused  by  the  Bilharzia  hcematobia  is  accompanied  by  the  presence  of  the 
oval  eggs  of  the  parasite  in  the  urine.  We  should  always  think  of  filariasis 
in  any  abnormal  case  of  renal  colic  which  is  complicated  by  early  and 
pronounced  congestion  of  the  testis. 

Treatment. — The  employment  of  boiled  and  filtered  water  and  protec- 
tion against  the  mosquitoes  of  the  genus  Cvlex  ciliaris  are  the  only  pro- 
phylactic measures  which  are  efficacious  against  the  disease.  Parasiticide 
treatment  of  filariasis  by  mercury  and  iodine  has  not  given  good  resiJts. 
On  the  other  hand,  we  may  remove  the  local  troubles  by  puncture  of  the 
chylous  effusions  or  by  dissection  of  the  lymphatic  varices  of  the  invaded 
regions,  but  we  cannot  expect  a  radical  cure  unless  there  is  a  chance  of 
removing  the  adult  filaria. 


PART  X 

DISEASES  AFFECTING  THE  LOCOMOTOR  SYSTEM 

I.  RICKETS. 

iEtioIogy. — Rickets  is  a  disease  of  infancy,  characterized  by  faulty 
nutrition  and  growth,  of  the  tissues  which  are  concerned  in  ossification.  It 
is  probable  that  the  absence  of  calcification  in  the  rachitic  bones  or  the  delay 
in  this  calcification  arises  from  the  fact  that  the  organism  does  not  receive 
or  does  not  assimilate  in  sufficient  quantity  the  materials  which  form  phos- 
phate of  lime.  In  other  cases,  however,  the  absence  of  calcification  concerns 
only  one  side  of  the  question,  and  cannot  explain  the  extreme  overgrowth 
of  the  tissues.  We  may,  therefore,  say  that  the  pathogenesis  of  rickets  is 
as  yet  obscure. 

This  disease  has  been  for  some  years  the  object  of  much  research.  Beneke 
and  Bouchard  hold  it  to  be  a  disease  caused  by  faulty  nutrition,  and  con- 
secutive to  the  non-absorption  of  the  phosphate  of  lime  which  is  necessary 
for  the  formation  of  the  bones.  In  the  normal  condition  the  phosphate  of 
lime  is  not  absorbed  ;  it  is  split  up.  The  chalk  combines  with  hydrpchloric 
acid  to  form  chloride  of  calcium,  while  the  nascent  phosphoric  acid  com- 
bines with  the  glycerine  produced  by  the  action  of  the  pancreatic  juice  on 
tjie  fats  in  order  to  produce  glycero-phosphoric  acid.  If  the  contents  of  the 
iiitestine  become  alkaline,  or  if  the  acidity  of  the  contents  is  due  to  lactic 
acid,  as  occurs  in  rickets,  the  sphtting  up  does  not  take  place,  and  the 
absorption  of  the  phosphate  of  lime  becomes  insufficient.  On  the  other 
hand,  the  excess  of  lactic  acid  passes  into  the  blood,  impregnates  the  tissues, 
and  dissolves  the  phosphate  of  lime  which  is  already  fixed.  Such,  then,  is 
the  primary  cause  of  rickets,  according  to  the  two  authorities  just  quoted. 

Rickets  often  coexists  with  dyspeptic  troubles,  which  are  accompanied 
by  dilatation  of  the  stomach.  Comby  looks  upon  this  dilatation  as  the  real 
cause  of  rickets,  in  consequence  of  the  imperfect  elaboration  of  the  food. 

According  to  certain  authors  (Parrot),  rickets  is  one  of  the  manifestations 
of  hereditary  syphilis,  but  this  view  has  not  been  generally  adopted. 

Since  the  publication  of  Parrot's  monograph  the  bony  lesions  of  heredi- 

2018 


DISEASES  AFFECTING  THE  LOCOMOTOR  SYSTEM       2019 

tary  syphilis  have  been  more  carefully  studied  (Fournier,  Lannelongue), 
and  it  has  been  shown  that  radical  differences  exist  between  the  changes  in 
the  bones  caused  by  syphilis  and  those  which  are  attributable  to  rickets 
(Berne).  On  the  other  hand,  Galliard  has  published  the  case  of  a  rachitic 
child  born  of  parents  who  were  not  syphilitic,  although  they  contracted 
syphilis  several  years  after  the  birth  of  the  child  ;  and  Giraudeau  has  re- 
ported four  cases  of  rachitic  persons  who  contracted  syphilis.  These  facts 
do  not  agree,  if  we  admit  that  rickets  is  syphilitic  in  origin. 

Gley  and  Charrin  have  been  able  to  reproduce  experimentally  in  animals 
by  the  injection  of  toxines  into  the  parents  lesions  which  resemble  those  of 
human  rickets,  and  Mircoli  has  been  the  defender  of  an  infectious  theory  of 
rickets.  I  merely  state  these  researches,  without  being  able  as  yet  to  draw 
conclusions  from  them. 

Pathological  Anatomy. — In  the  first  period  the  affected  bones  are  not 
deformed  ;  in  the  second  period  the  deformities  are  considerable  ;  the  third 
period  corresponds  to  the  consolidation  of  the  affected  bones.  The  parts 
concerned  in  the  growth  of  the  bone — that  is  to  say,  the  epiphyseal  cartilage 
and  the  periosteum  of  the  diaphyses — are  the  initial  seat  of  the  lesion. 

In  the  normal  condition,  when  we  study  the  epiphyseal  end  of  a  bone  in 
process  of  growth,  we  find  in  the  deep  parts  of  the  epiphyseal  cartilage  a 
translucent  and  bluish  layer,  in  which  the  phenomena  of  proliferation  go  on 
and  converge  towards  the  points  of  ossification.  Below  this  cartilaginous 
layer  we  find  another  layer,  "  formed  by  areolar  tissue,  in  which  the  rows 
are  composed  of  a  ground  substance  of  cartilage  infiltrated  with  calcareous 
salts  "  (Corral  and  Ranvier).  It  is  below  this  ossiform  layer  that  the  true 
bone  is  formed. 

In  rickets  the  lesions  affect  the  deep  layer  of  the  cartilage  and  the  ossiform 
layer.  The  bluish  cartilaginous  layer,  which  is  normally  1  millimetre  or 
1^  millimetres  in  thickness,  becomes  several  centimetres  thick.  This  tissue 
has  been  named  chondroid — a  faulty  term,  because  we  are  dealing  with  a 
true  cartilage. 

At  the  level  of  the  ossiform  tissue  we  find  the  spongy  tissue  so  called, 
which  is  very  vascular,  and  which  may  encroach  upon  the  diaphysis  of  the 
bone.  The  overgrowth  and  the  persistence  of  these  tissues  is  the  cause  of  the 
swelling  of  the  epiphyses.  The  rachitic  tissues  do  not  end  in  the  formation 
of  bone,  the  osteoblasts  do  not  ossify,  the  soft  and  little  resistant  epiphysis 
allows  itself  to  be  deformed  by  muscular  contraction,  and  a  node  is  formed. 

We  also  find  a  spongy  layer  in  the  periosteum.  In  the  interior  of  the 
bone  the  marrow  is  much  congested,  its  peripheral  layers  are  organized  as 
in  young  connective  tissue,  and  the  medullary  cavity  is  narrowed  or  filled 
up  by  the  curves  and  deformities  of  the  bone. 

As  the  result  of  these  lesions,  the  skeleton  offers  but  little  resistance,  the 


2020  TEXT-BOOK  OF  MEDICINE 

epiphyses  become  swollen,  and  tlie  nodes  may  even  afiect  the  extremity  of 
bones  which  have  not  an  epiphysis.  The  shaft  of  the  long  bones  is  curved, 
deformed,  and  sometimes  fractured.  The  weight  of  the  body,  the  tonic 
action  of  the  muscles,  the  laxity  of  the  ligaments,  and  other  external  causes, 
contribute  to  cause  the  deformities  of  rickets. 

We  can  thus  explain  the  curves  of  the  vertebral  column,  the  deformity 
and  narrowing  of  the  pelvis,  the  persistence  of  the  fontanelles  and  the  size 
of  the  head,  the  lateral  flattening  of  the  chest  and  its  projection  forwards 
(chicken  breast),  the  curves  of  the  legs  outwards  or  inwards,  and  the  de- 
formities of  the  arms.  The  deformities  of  the  legs  occur  in  an  order  which 
differs  according  to  the  age  of  the  patients.  They  commence  in  the  legs  of 
children  who  are  walking,  but  in  those  who  have  not  begun  to  walk  the 
arms  are  the  first  to  show  deformity,  because  they  play  a  more  active  part. 

Rickets  may  recover  without  any  great  deformity  when  it  is  slight,  but, 
as  a  rule,  after  the  period  of  consolidation  of  the  bones  the  patient  preserves 
the  deformities,  which  are  in  part  due  to  the  too  rapid  ossification  of  the 
epiphyseal  cartUages.  The  growth  of  the  bone  is  arrested,  the  rachitic 
person  remains  small  and  more  or  less  deformed,  and  as  the  ossification  of 
the  bones  of  the  cranium  occurs  late,  the  head  is  usually  large. 

Description. — Rickets  usually  commences  about  the  end  of  the  first 
year  or  in  the  first  half  of  the  second  year.  The  bony  deformities  are  some- 
times preceded  by  precursory  signs — the  child  becomes  sad  and  peevish, 
and  dreads  every  movement  because  of  the  pain  which  results. 

The  child  who  has  been  walking  or  trying  to  stand  upright  is  now 
content  to  lie  down  ;  the  child  who  loved  to  sit  in  the  arms  of  his  nurse  no 
longer  does  so,  and  weeps  when  he  is  taken  up  from  his  cot,  because  of  the 
acute  pain  on  movement.  In  some  patients  the  disease  commences  with 
an  intestinal  catarrh ;  in  others  the  fontanelles  remain  open  beyond  the 
normal  term,  and  dentition  is  delayed  or  is  arrested  if  it  has  commenced 
(Trousseau).  A  little  later  nodes  or  deformities  appear  at  various  points. 
The  nodular  prominences  appear  at  the  junction  of  the  ribs  and  the  costal 
cartilages  (rachitic  rosary) ;  the  chest  is  flattened  laterally,  bulges  in  the 
sternal  region,  and  is  enlarged  in  the  region  of  the  lower  ribs.  In  conse- 
quence of  these  deformities  the  costal  respiration  is  embarrassed,  the 
diaphragmatic  respiration  is  exaggerated,  the  abdominal  organs  are  pushed 
down,  and  the  beUy  becomes  prominent.  The  joint  swellings  are  marked, 
the  deformities  of  the  legs  and  of  the  arms  become  exaggerated,  and  the 
disease  is  then  complete.  The  articular  deformities  are  the  more  striking 
if  the  child  is  emaciated. 

The  general  symptoms  increase  in  severity,  the  appetite  is  lost,  the  skin 
is  covered  with  abundant  sweat,  diarrhcsa  is  frequent,  and  the  urine  contains 
a  fairly  large  quantity  of  earthy  phosphates. 


DISEASES  AFFECTING  THE  L(K;()M()T()R  SYSTEM       JOl^L 

Rickets  usually  runs  its  course  in  six  or  in  cij^ht  months,  and  then 
renuiins  stationary  for  one  or  two  years.  Consolidation  of  the  bones  next 
occurs,  and  the  patient  recovers  at  the  exjjense  of  the  deformities  previously 
mentioned.  In  several  instances,  however,  the  disease  terminates  in  death, 
due  either  to  the  severity  of  the  disease  itself  or  to  intercurrent  complications, 
such  as  bronchitis  or  pneumonia. 

Acute  rickets  with  paralysis  of  the  limbs,  subperiosteal  swelling  of  the 
dia]ilivses  of  the  bones,  fever,  marasma,  and  haemorrhages  from  the  gums  or 
from  the  nose,  etc.,  should  be  distinguished  from  true  rickets  (Barlow).  It 
is  really  infantile  scurvy  (Comby),  which  recovers  when  the  child  is  fed  on 
fresh  milk,  meat- juice,  and  orange  or  citron  juice. 

Cod-liver  oil,  butter,  with  iodide  of  potassium  and  chloride  of  sodium, 
preparations  of  the  phosphates,  and  milk  of  good  quality,  form  the  basis  of 
treatment.     Salt  baths  or  sea  baths  render  great  service. 

11.  OSTEOMALACIA. 

etiology. — Between  rickets  and  osteomalacia  there  is  this  essential 
diflerence — that  in  the  former  the  bone  does  not  reach  its  complete  state  of 
development,  becaase,  as  the  result  of  vicious  nutrition,  the  elements  of 
calcification  are  wanting,  and  the  normal  evolution  of  the  bone  is  interrupted. 
In  osteomalacia,  on  the  other  hand,  the  bone  is  perfectly  formed,  and  the 
fault  in  nutrition  consists  in  a  disassimilation  of  the  elements  of  calcification. 
The  bone  becomes  decalcified.  Rickets  is  a  disease  of  gro\vth,  osteomalacia 
is  a  disease  of  the  adult,  in  which  the  destruction  of  the  calcareous  salts 
induces  softening  of  the  skeleton. 

The  primary  cause  of  this  destruction  of  the  calcareous  salts  is  scarcely 
understood,  and  the  theories  formulated  do  not  aptly  give  the  reason. 
Osteomalacia  is  extremely  rare  in  man.  It  is  a  disease  of  women  between 
the  ages  of  thirty  and  fifty  years,  and  pregnancy  forms  its  starting-point  in 
about  half  the  cases.  Osteomalacia  is  more  frequent  in  certain  countries — 
■^or  example,  in  Bavaria. 

Pathological  Anatomy. — During  the  first  period  the  bones  are  not  as 
yet  rarefied,  although  they  can  be  more  easily  cut  with  the  knife.  We  find 
under  the  microscope  that  the  edges  of  the  bony  arches  no  longer  contain 
calcareous  salts,  which  are  still  found  in  the  centre.  The  vessels  of  the 
marrow  are  turgid,  and  haemorrhages  occur  both  into  the  marrow  and 
under  the  periosteum.  During  the  second  period  the  bones  become  rarefied 
and  softened.  They  change  their  shape,  diminishing  in  size,  and  readily 
breaking.  The  bony  arches  are  in  part  decalcified  and  in  part  absorbed. 
Ossein,  which  is  the  fundamental  substance  of  the  bony  lamellae,  becomes 
fibrillary.  It  loses  its  properties,  and  can  no  longer  be  converted  into  gelatin. 
n.  128 


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Fractures  rarely  unite  firmly,  and  if  callus  forms,  it  has  in  its  turn  a  ten- 
dency to  Tmdergo  the  changes  of  osteomalacia  (Bouley). 

The  bones  become  flexible  and  deformed.  The  vertebrae  become  weak 
and  flattened,  and  the  bones  of  the  pelvis  undergo  changes  which  are  of  the 
greatest  importance  in  pregnancy  and  labour.  The  deformities  of  the 
thorax  resemble  those  of  rickets.  The  bones  of  the  limbs  are  often  frac- 
tured. 

Description. — Osteomalacia  commences  with  pains  in  the  vertebral 
column,  pelvis,  and  limbs.  These  pains  sometimes  come  on  in  the  form  of 
attacks,  and  are  increased  by  movement,  pressure,  walking,  and  sitting. 
We  find,  in  addition  to  the  pains,  feebleness  and  a  sensation  of  fatigue,  which 
prevent  the  patient  from  moving. 

The  softening  of  the  bones  shows  itself  by  the  deformities  which  I  have 
previously  enumerated — the  patient  is  bent  and  shrunken,  and  the  thorax 
is  deformed.  We  often  see  painful  contractions.  Attacks  of  fever  some- 
times appear.  The  general  functions,  which  were  normal  during  the  first 
part  of  the  disease,  commence  to  fail,  the  appetite  diminishes,  and  the 
patient  complains  of  palpitation,  dyspnoea,  giddiness,  and  formication  of 
the  lower  limbs.     Fractures  are  frequent. 

Osteomalacia  does  not  always  run  a  continuous  course.  Remissions  and 
paroxysms  occur  in  some  cases.  The  urine  may  contain  an  excess  of  phos- 
phates and  carbonates  of  lime,  and  always  of  albuminose.  After  several 
years  the  disease  passes  into  a  cachectic  condition.  Diarrhoea  is  the  rule, 
wasting  is  extreme,  and  the  patient  dies  from  marasmus,  unless  carried  off 
by  some  intercurrent  disease.     Cases  of  recovery  are  quite  exceptional. 

The  diagnosis  of  osteomalacia  is,  therefore,  difficult  at  the  onset,  before 
the  period  of  deformities.  In  syphilitics  fractures  may  easily  occur  by 
reason  of  the  fragility  of  the  bones.  In  such  cases  the  deformities  of  osteo- 
malacia are  absent. 

Treatment  with  phosphorus  is  naturally  indicated.  Castration  gives 
encouraging  results  (Fehling),  and  total  extirpation  of  the  uterus  and  of  the 
ovaries  has  been  advised  at  the  commencement  of  pregnancy  (Chroback). 
Utero-ovarian  amputation  (Neumann)  or  Caesarian  section  has  been  advised 
at  the  termination  of  pregnancy.  The  beneficial  influence  of  extirpa- 
tion of  the  internal  genital  organs  upon  the  evolution  of  osteomalacia  is 
undoubted,  although  its  action  is  stfll  obscure  (Polgar). 

III.  ACROMEGALY. 

Description. — Acromegaly  (a«/909,  extremity ;  yLteya?,  large),  described 
for  the  first  time  by  Marie  in  1885,  presents  as  its  cardinal  sjrmptoms  : 
(1)  Considerable  hypertrophy  of  the  hands,  of  the  feet,  and  of  certain  parts 


DISEASES  AFFECTlNCr  THE  L()C(JMOT()K  SYSTEM       20:^:5 

of  the  face,  and  especially  of  the  lower  jaw  ;  (2)  cer  vice -dorsal  kyphosis  ; 
(3)  visual  troubles,  which  are  very  frequent ;  (1)  in  women,  almost  constant 
amenorrhoia. 

The  disease  generally  commences  in  the  hands,  which  become  hyper- 
trophied  as  a  wliole.  Their  breadth  and  thickness  are  considerably  increased, 
whence  the  names  of  "  mutton  fist "  or  "  padded  hand."  Their  length  is 
practically  normal.  The  increase  in  size  affects  all  the  tissues.  The  folds 
of  the  skin  are  deeper  than  normal ;  the  thenar  and  hypothenar  eminences 
arc  remarkable  for  the  thickness  of  their  fleshy  mass  ;  the  metacarpus  is 
enlarged  and  massive  ;  the  fingers,  which  are  short  and  thick,  are  swollen 
at  the  level  of  the  phalanges.  The  nails,  encased  by  fleshy  tabs,  are  narrow, 
flattened,  often  atrophied,  and  striated  in  a  longitudinal  direction. 

The  functions  of  the  hands  are  preserved.  The  fingers  remain  apt  in 
performing  delicate  tasks,  and  are  not  the  seat  of  any  abnormal  sensation. 

The  other  segments  of  the  upper  limb,  except  the  wrist  in  some  cases, 
are  normal  in  size. 

The  feet  are  enormous,  being  increased  in  breadth  and  in  thickness, 
though  as  a  rule  they  preserve  their  normal  length.  The  hypertrophy 
assumes  the  same  appearance  as  in  the  upper  limbs.  "  We  find  here  the 
same  deep  furrows,  and  especially  the  digito-palmar  folds,  which  separate 
the  same  fleshy  pads  "  (Souza-Leite).  The  heel  is  hypertrophied  (Ver- 
straeten)  ;  the  instep  is  often  large  ;  the  big  toes  and  the  nails  show  changes 
similar  to  those  of  the  fingers.  The  upper  parts  of  the  lower  limb  are 
normal. 

The  deformity  of  the  face  is  characteristic,  and  the  acromegalic  fades 
sometimes  carries  the  diagnosis  with  it.  The  deformity  chiefly  afiects  the 
lower  jaw.  The  chin  is  prominent  and  enlarged,  and  instead  of  representing 
the  axis  of  an  oval  with  its  normal  extremity  above,  as  it  does  in  the  normal 
condition,  it  becomes  the  axis  of  an  ellipse.  The  upper  jaw  takes  but  little 
part  in  the  hypertrophy,  and  as  a  result  the  dental  arches  do  not  correspond, 
the  lower  arch  standing  out  in  front  of  the  upper  one.  This  prognathism  is 
accompanied  by  thickening  of  the  lower  lip,  which  is  prominent  and  everted. 
The  tongue  is  enormous,  so  enlarged  and  thickened  as  to  hinder  swallowing 
and  the  pronunciation  of  the  Unguals. 

The  vault  and  the  velum  palati  are  usually  enlarged  ;  the  tonsils  and 
the  uvula  are  hypertrophied.     The  nose  is  splayed  out  and  hypertrophied. 

The  cheeks  and  the  internal  apophyses  of  the  orbit  are  prominent. 
These  prominences  depend  on  the  dilatation  of  the  maxillary  and  frontal 
sinuses.  The  ears  are  hypertrophied,  thickened,  and  elongated.  The 
skin  as  well  as  the  cartilages  participates  in  this  hypertrophy.  The  forehead 
appears  low,  and  is  not  in  proportion  with  the  exaggerated  dimensions  of 
the  face.     The  cranium  preserves  its  normal  size.     The  eyes,  which  are  aa 

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2024  TEXT-BOOK  OF  MEDICINE 

a  rule  small  and  deep-set,  are  sometimes  more  prominent.  The  penis,  the 
labia  majbra,  and  the  clitoris  are  often  increased  in  size. 

Cervico- dorsal  kyphosis  is  found  in  nearly  all  cases.  It  is  sometimes 
accompanied  by  lumbar  lordosis  or  scoHosis,  with  a  variable  degree  of 
inclination.  In  the  antero-inferior  part  of  the  thorax  a  compensatory 
bulging  is  often  found.  The  clavicle,  the  ribs,  and  the  sternum  are  generally 
thickened,  and  the  hjrpertrophy  of  the  costal  cartilages  frequently  hampers 
the  breathing,  which  then  assumes  the  inferior  thoracic  and  abdominal  type. 

The  early  and  almost  constant  amenorrhoea  helps  in  certain  cases  to 
support  the  diagnosis  at  the  onset  of  the  disease. 

The  following  phenomena  have  been  noticed  fairly  often  :  Bistre  colour 
of  the  skin,  profuse  sweating,  elevation  of  the  peripheral  temperature, 
enlargement  of  glands,  diminution  in  the  size  of  the  thyroid  body  (Bury), 
hypertrophy  of  the  thymus  characterized  by  a  zone  of  retrosternal  dullness 
(Erb),  asymmetry  of  the  two  halves  of  the  body,  amyotrophy,  creaking  in 
the  joints,  erratic  pains,  increased  sensibility  to  cold,  and  a  sensation  of 
dead  fingers. 

A  separate  place  must  be  reserved  for  the  visual  troubles,  which  may 
vary  from  slight  amblyopia  to  complete  blindness.  The  narrowing  of  the 
visual  field,  the  hemianopsia,  the  prominence  of  the  eyeballs,  which  is 
accompanied  by  a  certain  degree  of  paresis  in  the  extrinsic  muscles  of  the 
eye,  and  the  congestion  of  the  disc,  may  be  explained  by  the  hypertrophy 
of  the  pituitary  body,  which  is  so  frequent  in  this  disease. 

The  larynx  sometimes  participates  in  the  hypertrophy  of  the  extremities, 
and  the  voice  then  assmnes  a  deep  tone,  which  is  especially  striking  in 
women.  The  dilatation  of  the  sinuses  of  the  face  also  contributes  to  the 
echoing  of  the  voice  (Marie). 

Polyuria  (Balzer),  slight  albuminuria,  peptonuria,  slight  glycosuria, 
and  phosphaturia  have  been  noted  in  some  patients.  Palpitation  and 
hypertrophy  of  the  heart  are  also  seen,  the  latter  almost  always  associated 
with  arterio-sclerosis. 

The  intelligence  is  usually  intact,  but  changes  in  character  are  frequent 
(sadness,  irascibility,  and  uncertain  temper).  This,  indeed,  is  not  sur- 
prising, considering  the  profound  impression  which  the  disease  produces  on 
the  sufferers. 

Acromegaly  commences  between  the  ages  of  twenty  and  twenty-six 
years.  Its  course  is  progressive,  as  can  readily  be  proved  by  making  a 
comparative  examination  of  photographs  of  patients  taken  at  long  intervals. 
Periods  of  arrest,  followed  by  active  progress,  are  frequent.  The  duration 
of  the  disease  is  generally  from  twenty  to  thirty  years.  Death  comes  from 
slow  cachexia,  or  from  some  intercurrent  disease.  The  patient  sometimes 
dies  suddenly,  and  the  autopsy  reveals  no  lesions  to  explain  this  result. 


DISEASES  AFFECTINO  THK  LociJMuToli  SYSTEM       2n'2r, 

etiology.-- Tlio  .rtidloo:)'  of  acromcifiily  is  quite  unknown.  All  wo  can 
say  is  that  it  is  ncitluT  hereditary  nor  congenital,  and  that  it  difTers  in  these 
two  respects  from  most  dystrophic  diseases.  Cold,  sypliilis,  grief,  injury, 
alcoholism,  rheumatism,  etc.,  have  all  been  found  in  the  antecedents  of 
patients,  but  they  are  absent  in  such  a  large  number  of  cases  that  there  really 
exists  no  definite  relation  between  these  pretended  causes  and  acromegaly. 

Pathological  Anatomy. — Hypertrophy  of  the  pituitary  body  has  been 
found  by  Marie,  and'  since  then  by  a  very  large  number  of  authors,  who 
would  seek  to  make  this  lesion  the  anatomical  substratum  of  acromegaly. 
The  tumour  varies  in  size  from  a  pigeon's  egg  to  a  hen's  egg.  It  dilates  the 
sella  turcica,  separates  the  cUnoid  processes,  and  lodges  itself  at  the  base 
of  the  cranium  in  a  cavity  which  depends  on  its  size.  Compression  of  the 
optic  chiasma  and  of  the  ocular  vessels  accounts  for  the  visual  troubles. 
Histologically,  the  lesion  is  rather  a  simple  hypertrophy  than  a  new  growth. 

Persistence  and  reviviscence  of  the  th}Tnus ;  increase  in  the  size  of  the 
heart  and  of  the  vessels  (Klebs) ;  hjrpertrophy  of  the  ganglia  and  cords  of 
the  great  s}Tnpathetic  have  been  mentioned. 

The  lesions  of  the  skeleton  are  constant.  In  the  limbs  "  the  hypertrophy 
chiefly  affects  the  bones  of  the  extremities  and  the  extremities  of  the  bones  " 
(Marie).  It  consists  in  an  increase  of  the  spongy  tissue,  in  dilatation  of  the 
vascular  orifices  of  the  bones,  and  in  enlargement  of  the  canals  for  the 
passage  of  the  arteries.  Histologically,  the  alveoli  are  enlarged,  and  repre- 
sent very  dilated  Haversian  canals  with  thin  walls.  The  marrow  contains 
neither  osteoblasts  nor  myeloplaxes  (Renaut). 

The  bones  of  the  other  parts  of  the  body,  and  particularly  those  of  the 
face,  present  similar  changes.  The  lower  jaw,  compared  with  that  of  a  man 
of  the  same  stature,  appears  enormous,  and  the  various  sinuses  are  markedly 
enlarged.  The  osteopathies  of  acromegaly  have  been  studied  on  the  living 
patient  with  the  Rontgen  rays. 

Diagnosis. — The  diagnosis  of  acromegaly  is  generally  easy,  especially 
at  an  advanced  stage  of  the  disease.  It  has,  however,  been  confounded  with 
myxoedema  in  a  certain  number  of  cases.  The  error  is  easily  avoided,  since 
the  "  fuU-moon  "  face  seen  in  cases  of  m}Tcoedema  does  not  resemble  the 
prognathism  seen  in  acromegaly.  In  mj'xoedema  the  hypertrophy  affects 
the  soft  parts  alone.  The  skin  is  stretched  and  cannot  be  displaced,  the 
thyroid  body  is  atrophied,  mental  troubles  are  frequent,  and  kyphosis  is 
always  absent. 

Paget's  osteitis  deformans  is  characterized  by  "  considerable  overgrowth 
of  the  long  bones  of  the  legs,  and  also  of  the  trunk  and  of  the  head.  The 
femur  and  the  tibiae  present  a  marked  anterior  curve,  the  legs  are  separated, 
the  trunk  and  the  neck  are  bent  forwards  by  the  curve  of  the  spine,  the 
breathing  is  laboured,  and  assumes  the  diaphragmatic  type,  because  of  the 


2026  TEXT-BOOK  OF  MEDICINE 

hypertropliy  and  welding  of  the  ribs.  Fairly  often  at  the  onset,  or  in  the 
course  of  the  disease,  severe  pains,  somewhat  analogous  to  lightning  pains, 
may  be  present  "  (Marie). 

Giants  have  enormous  hands  and  feet,  but  in  gigantism  the  difierent 
parts  of  the  body  are  in  proportion  to  their  abnormal  development.  The 
increase  in  growth  occurs  in  a  regular  fashion  both  in  length  and  in  breadth, 
and  is,  therefore,  unlike  the  growth  which  takes  place  in  acromegaly. 
Gigantism  and  acromegaly  are,  therefore,  two  difierent  conditions,  and  yet 
writers  have  published  cases  in  which  these  two  conditions  were  found 
together.  The  most  remarkable  of  these  cases  is  that  of  the  giant  of  Mon- 
tastruc. 

This  giant  was  at  the  same  time  acromegalic.  He  had  the  stature  of  a  giant,  but 
the  hands,  face,  feet,  and  torso  of  the  acromegalic.  He  was  an  example  of  "  these 
two  kiads  of  exuberant  dystrophy  in  the  human  body."  But  how  are  we  to  interpret 
the  association  of  these  two  dystrophies  ?  Is  their  association  independent,  or  is  it 
dependent  on  the  same  cause  ?  Brissaud  and  Meige  come  to  the  following  conclusions  : 
"  Gigantism  and  acromegaly  are  one  and  the  same  disease.  If  the  period  during 
which  the  increase  in  the  skeleton  takes  place  belongs  to  adolescence  or  to  youth, 
the  result  is  gigantism  and  not  acromegaly.  If  this  period  belongs  to  adult  age — ^that 
is  to  say,  to  a  time  of  Kfe  when  the  stature  is  already  fixed — the  result  is  acromegaly. 
Acromegaly  is  gigantism  of  the  adult,  and  gigantism  is  acromegaly  of  the  adolescent. 
If  the  process  of  increase  in  the  skeleton  commences  during  youth,  at  an  age  when  the 
stature  is  stiU  increasing  and  encroaches  upon  the  age  of  manhood,  the  result  is  the 
combination  of  acromegaly  and  gigantism." 

Hypertrophic  pulmonary  osteo-arthropathy  is  met  with  in  persons  suffer- 
ing from  old  pulmonary  lesions,  and  also  in  some  cardiac  cases.  The  hands 
are  enormous,  but  the  hypertrophy  chiefly  affects  the  fingers,  which,  instead 
of  being  short  and  cylindrical,  as  in  acromegaly,  are  long,  flattened,  and 
clubbed  at  their  tips.  The  thumb  has  been  compared  by  most  writers  to 
the  "  clapper  of  a  bell  "  (Rauzier). 

The  metacarpus,  on  the  other  hand,  is  scarcely  altered.  It  does  not 
present  either  the  prominences  or  the  fleshy  pads  of  acromegaly.  The  size 
of  the  wrist  is,  on  the  contrary,  slightly  increased.  The  hypertrophy  chiefly 
affects  the  skeleton,  and  spares  the  soft  parts.  The  nails  are  enlarged,  and 
curved  both  in  length  and  breadth.  In  the  feet  the  same  deformities  are 
seen,  but  the  big  toes,  and  especially  their  free  extremity,  attract  attention, 
while  the  metatarsus  is  much  less  affected.  The  face  is  always  spared,  and 
in  the  vertebral  column  the  cervico-dorsal  kyphosis  of  acromegaly  is  replaced 
by  a  dorso-lumbar  kyphosis,  which  is  often  accompanied  by  scoliosis, 
depending  on  the  coexisting  pleuro-pulmonary  lesions. 

The  treatment  of  acromegaly  is  purely  symptomatic.  Some  attempts 
have,  however,  been  made  at  attacking  the  cause  of  the  disease.  Three 
patients  suffering  from  acromegaly  were  treated  by  Marinesco  with  tabloids 
of  pituitary  body.    Notable  improvement  appeared  in  the  general  symptoms. 


DISEASES  AFFECTINO  THE  LOCOMOTOR  SYSTEM       2027 

TV.  PAGET'S  DISEASE— PROGRESSIVE  OSTEITIS  DEFORMANS. 

In  tliis  section  I  shall  describe  the  affection  to  which  the  name  of  Paget's 
osteitis  deformans  has  been  given.  Sir  James  Paget's  first  memoir  was 
•j)ul)lisluMl  in  1877  in  the  Medico-Chirurgical  Transaclions.  Its  title  is 
"  Chronic  Inflammation  of  the  Bones,"  and  its  subtitle  "  Osteitis  Deformans." 
In  a  later  work,  published  in  1882,  Paget  calls  the  affection  by  the 
name  of  osteitis  deformans.  The  five  cases  in  the  first  monograph  are  not 
all  of  equal  value,  but  some  of  them  are  so  characteristic,  especially  the 
first  one,  that  they  have  led  to  the  acceptance  of  the  morbid  entity  described 
by  the  author. 

I  have  devoted  a  clinical  lecture  to  this  disease,*  and  shall  give  here  the 
notes  of  the  case  : 

A  man,  fifty-two  years  of  age,  came  into  one  of  my  wards  with  somewhat  marked 
intellectual  decay  ;  his  memory  was  often  at  fault,  and  we  had  therefore  to  send  for  his 
wife,  in  order  to  obtain  the  desired  information. 

The  onset  of  the  disease  dated  back  some  twelve  years.  The  patient's  health  had 
previously  been  excellent.  At  this  time  he  remarked  that  walking  became  diflBcult 
and  painful ;  his  legs  could  scarcely  support  the  weight  of  his  body,  and  appeared  to 
be  growing  soft,  while,  at  the  same  time,  they  became  deformed  and  bowed.  This 
inward  bowing  of  the  legs  gradually  became  well  marked ;  the  knees  were  thrown 
outwards,  and,  as  the  legs  curved  inwards,  they  became  so  much  the  shorter.  It 
was  therefore  necessary  to  cut  down  his  trousers,  which  had  become  too  long.  About 
the  same  time  the  head  began  to  increase  in  size,  and  his  hat  became  too  small. 

At  length  the  neck  subsided,  the  head  seemed  to  sink  between  the  shoulders  and 
was  bent  forwards,  the  chest  was  hunched  up,  the  back  became  bent,  the  height 
diminished,  the  arms  appeared  too  long,  the  hands  reached  as  far  down  as  the  knees, 
walking  became  more  and  more  difficult,  and  could  only  be  carried  out  with  the  aid  of 
a  stick.     The  cerebral  activity  left  much  to  be  desired. 

Later  the  respiration  became  embarrassed,  breathlessness  was  frequent  and  accom- 
panied by  palpitation,  the  appetite  diminished,  and  the  patient  grew  thin. 

The  thighs  and  the  legs,  showed  an  anterior  curve.  This  curve  was  especially  well 
marked  in  the  leg,  where  the  tibia,  with  its  thickened  crest,  somewhat  recalled  the 
"  scabbard  deformity  "  seen  in  syphihs.  On  palpation,  we  found  enormous  thickening 
of  the  bone,  but  did  not  discover  any  osteo-periosteal  tumour,  apart  from  some  slight 
roughness  ;  the  hypertrophy  of  the  bone  appeared  to  be  uniform.  A  radiograph  taken 
by  LacaiUe  showed  that  the  femur  and  the  fibula  were  much  less  affected  than  the 
tibia.  The  bones  of  the  feet  appeared  to  be  normal,  with  the  exception,  of  the  cal- 
caneum,  which  was  markedly  hypertrophied. 

The  patient's  skuU  was  enormous,  and  measured  22  inches  in  circumference  just 
above  the  ears.  It  was  neither  deformed  nor  nodular.  The  thickening  of  the  cranial 
bones  was  general,  uniform,  and  considerable,  as  shown  in  the  radiograph.  The  bones 
of  the  face  were  not  hypertrophied  to  the  same  extent,  and  yet,  as  the  radiograph 
showed,  the  upper  and  lower  jaws  were  relatively  large.  The  clavicles  were  enormous, 
and  their  curves  were  exaggerated.  The  spine  of  the  scapula  participated  in  the 
bony  hypertrophy.  The  radiograph  showed  that  the  pelvis  was  narrowed  below  and 
spread  out  above. 

*  Dieulafoy,"  Maladie  Osseuse  de  Paget  "  (Clinique  Medicah  de  V Hotd-Dieu,  1903, 
ITtiieje^on). 


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The  patient's  attitude  was  remarkable  :  The  shoulders  were  prominent  and  carried 
forwards  ;  the  head  appeared  to  lie  between  the  shoulders  and  to  bend  towards  the 
sternum,  and  this  was  due  to  the  pressing  together  of  the  vertebrae.  The  thorax  had 
undergone  similar  compression,  the  ribs  were  enlarged  and  close  together,  and  the 
result  was  that  the  height  of  the  thoracic  cavity  was  notably  diminished.  The  shorten- 
ing of  the  trunk  made  the  arms  appear  much  too  long — they  were  deformed,  slightly 
curved  inwards,  and  the  size  of  the  bones  was  increased.  The  hands  were  not  larger 
than  normal,  contrary  to  what  is  seen  in  acromegaly.  Some  bones  of  the  carpus,  as 
our  radiograph  showed,  were,  however,  affected  by  hypertrophic  osteitis.  In  short, 
in  about  twelve  years  the  greater  part  of  the  skeleton  had  been  progressively  affected 
by  bony  lesions  of  a  deforming  and  hypertrophic  character. 

The  skeleton  was  not  alone  affected.  The  patient  gradually  became  cachectic. 
Moreover,  he  was  breathless.  The  dyspnoea  was  in  part  due  to  the  bony  lesions,  which 
had  narrowed  the  chest,  and  also  depended  on  a  cardiac  lesion.  Auscultation  of  the 
heart  gave  a  systoUc  murmur,  with  reduphcation  of  the  second  sound.  The  lesion  was 
mitral. 

From  this  time  the  intellectual  troubles  became  more  marked.  The  patient  lost 
his  memory,  did  not  finish  sentences  or  words,  he  stammered  while  speaking,  and 
at  times  his  pronunciation  recalled  that  of  general  paralysis.  It  might  be  asked  if 
these  cerebral  troubles  were  due  to  compression  of  the  brain  by  the  hypertrophied 
cranium,  but  this  was  not  the  reason,  since  the  bony  hypertrophy  was  not  concentric 
and  did  not  encroach  upon  the  cranial  cavity.  Accordingly,  the  cause  of  these  cerebral 
troubles  had  to  be  looked  for  in  a  meningeal  or  in  a  cerebral  lesion. 

The  patient  died  from  progressive  cachexia.  JoUy  made  the  autopsy  and  the  histo- 
logical examination,  and  furnished  the  foUowing  notes  as  to  the  condition  of  the  skele- 
ton and  of  the  organs  :  In  the  lungs,  emphysema,  and  congestion  of  both  bases  with 
hepatization ;  pleurae  normal ;  larynx,  trachea,  ahmentary  canal,  and  peritoneum  normal. 
The  Uver  was  engorged  with  blood,  and  was  of  the  nutmeg  variety,  without  cirrhosis. 
It  weighed  40  ounces.  The  spleen  was  small  and  sclerous  ;  it  weighed  3  ounces.  Kid- 
neys, suprarenal  capsules,  pancreas,  genital  organs,  and  thyroid  gland  normal. 

■  The  heart  was  soft  and  flabby.  The  mitral  orifice  was  somewhat  incompetent. 
We  found  at  the  mitral  and  at  the  tricuspid  valve  fibrous  thickening  of  the  walls,  with 
nodules  which  were  as  large  as  a  pea.  The  pulmonary  valves  were  not  affected,  but  the 
aortic  valves  were  indurated,  though  calcification  was  absent.  Some  points  of  atheroma 
were  present  in  the  aorta.     The  heart,  without  clots,  weighed  9  ounces. 

In  the  cranial  cavity  there  were  no  adhesions  between  the  dura  mater  and  the  soft 
meninges,  but  the  adherence  between  the  dura  mater  and  the  cranium  was  complete. 
On  the  surface  of  the  brain,  especially  the  convex  parts  and  the  base,  thickenings  of  the 
pia  mater  were  found.  Nothing  of  importance  was  to  be  noticed  in  the  sections  of  the 
cerebrum,  cerebellum  ar.d  bulb. 

Histological  examination  of  the  cortex  of  the  brain,  at  the  points  where  the  meninges 
were  thickened,  showed  the  following  lesions  :  The  cerebral  substance  was  covered  by 
a  relatively  thick  layer  (1  milUmetre  to  IJ  millimetres)  of  loose  connective  tissue,  which 
contained  a  large  number  of  congested  vessels.  This  tissue  was  infiltrated  with  numerous 
round  lymphoid  cells  with  a  rounded  nucleus,  scattered  in  an  irregular  manner. 
The  lesion  was  therefore  chronic  meningitis.     There  was  nothing  in  the  spinal  cord. 

Let  us  pass  on  to  the  lesions  of  the  skeleton.  At  the  autopsy  we  were  able  to  verify 
the  bony  changes  which  were  so  clear  in  the  radiographs.  Speaking  generally,  these 
changes  consisted  in  hypertrophy  with  deformity  of  the  bone,  and  in  modification 
of  structure.     The  hypertrophy  was  considerable  and  somewhat  regular. 

The  two  tibiae  were  enormously  hypertrophied  and  curved.  Some  slight  roughnesses 
were  present  on  the  surface  of  the  bone.  One  tibia  was  incised,  in  order  to  show  the 
thickness  of  the  bony  wall,  which  in  front  was  nearly  an  inch. 


DISEASES  AFFECTINO  THE  LOCO.MoTolt  SYSTEM       I'Ol'^i 

Most  of  t!m  riha  took  part  in  the  hypcrtropliy.  In  the  upper  limbs  tho  liyportrophy 
and  (Icforinity  of  the  bonus  woro  Ions  nuirkod  than  in  tlio  lowor  hmbs.  Thf>  humoruH 
and  tlio  radius  were,  however,  hirtjo  and  curved.  Tho  two  clavicles  were  enormously 
hypcrtrophied  and  vory  muoh  ctirvf^l. 


Fig.  8y. — Normal  and  Diseased  Tiei^ 

At  some  points  the  bones  of  the  skull  were  treble  their  normal  thickness,  but  the 
cranial  cavity  was  not  encroached  upon. 

The  structure  of  the  hypcrtrophied  bones  was  modified.      We  know  that  in  the 


Fig.  89. — Normal  and  Diseased  Clavicles. 

normal  condition  at  the  diaphj-ses  the  wall  of  tho  medullary  canal  is  formed  of 
compact  tissue,  with  peripheral  lamella  and  Haversian  systems,  which  are  parallel  to 
tho  axis  of  tho  diaphysis.       In  this  patient,  a  transverse  section  of  the  diaphysis  of 


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the  tibia  showed  that  the  tissue  of  the  bony  wall  was  much  less  dense  ;  the  Haversian 
canals  were  large  and  irregular,  running  in  all  directions,  and  giving  the  bony  tissue  a 
structure  resembling  that  of  the  diplog. 


Fig.  90. — ^Normal  Skull. 


Fig.  91.— Diseased  Sktjll. 


Description. — Osteitis  deformans  is  a  disease  of  both  sexes  and  of  adult 
age.  It  is  a  trophic  trouble  which  diminishes  the  resistance  of  the  bones, 
while  it  provokes  overgrowth  of  tissue.     The  bones,  which  become  less 


^\::'-^-^   ■■■■■■- 


;V''-       -Vi:,  .    ]'-f.:S  '^K 


:  .  -       ■  % 


"S^i'l''    ''^'-i%    '  -^ 


t; 


Fig.  92. — Tkansverse  Section  of  Diaphysis  of  Tibia. 


resistant,  bend  and  are  deformed.  The  bony  deformities,  which  are  usually 
symmetrical,  are  generally  an  accentuation  of  the  normal  curves,  and  seem 
to   indicate   softening   of   the   bone   with   hypertrophying   osteitis.     This 


DISEASES  AFFECTING  THE  LOCOMOTOR  SYSTEM       20^1 

softening  is,  however,  very  slight,  for  the  bones  are  not  brittle,  and  fractures 
are  exceptional 

The  bones  of  the  lower  limbs  are  often  the  first  to  be  attacked.  The 
deformities  are  most  marked  in  this  situation,  doubtless  because  these  bones 
have  to  support  the  weight  of  the  body.  The  legs  form  two  arcs,  with  a 
double  concavity  inwards  and  baclcwards.  In  this  new  situation  the  heels 
may  come  in  contact,  but  the  knees  project  outwards,  and  cannot  be  brought 
together,  being  separated  from  one  another  by  an  interval  of  6  or  7  inches. 
The  legs  sometimes  show  a  tendency  to  become  crossed  during  walking. 
The  bending  of  the  legs  causes  a  diminution  in  the  stature  of  the  patient, 
and,  therefore,  dresses  and  trousers  become  too  long ;  one  child  said  to  its 
grandmother  :  "  Grandmother,  you  are  shrinking."  The  crest  of  the  tibia, 
which  is  broad  and  hypertrophied,  forms  a  wide  curved  edge  like  a  scabbard. 

In  Hudelo  and  Heitz's  cases  the  bones  of  the  right  leg,  which  were 
hypertrophied  and  curved,  were  completely  joined  in  their  lower  two-thirds. 
The  bones  of  the  feet,  in  contradistinction  to  what  is  seen  in  acromegaly, 
do  not  participate,  or  only  to  a  small  extent,  in  the  process  of  the  hyper- 
trophpng  osteitis.     In  my  patient  the  calcaneum  was  large. 

The  disease  sometimes  sets  in  without  pain  ;  at  other  times  the  pains  are 
sharp,  continuous  or  paroxysmal,  and  simulate  rheumatism  or  tabes. 

Hypertrophy  of  the  cranial  bones  is  practically  constant  in  osteitis 
deformans.  It  is  rarely  the  earliest  to  appear,  and  it  follows  closely  the 
bony  lesions  of  the  lower  limbs.  The  head  becomes  enormous,  and,  conse- 
quently, the  hats  become  too  small.  The  story  of  larger  hats  is  found  in 
most  cases,  and  is  comparable  to  the  story  of  the  trousers  or  of  the  dresses, 
which  have  to  be  shortened.  The  circumference  of  the  head,  taken  above 
the  ears,  measured  22  inches  in  my  patient,  and  24  inches  in  Gilles  de  la 
Tourette  and  Magdelaine's  patient.  In  its  general  shape  the  hypertrophied 
head  is  often  asymmetrical,  the  parietal  eminences  stand  out,  the  parietal 
fossae  are  filled  up,  and  the  forehead  assumes,  as  in  my  patient,  the  appear- 
ance of  the  Olympian  brow.  On  anatomical  examination  of  the  cranium, 
we  find  disappearance  of  the  sutures,  prominences  and  elevations  on  the 
external  surface,  and  levelling  of  the  inner  surface.  The  bones  of  the  base 
of  the  skull  (petrous  and  sphenoid)  sometimes  participate  in  the  hyper- 
trophy. 

Although  the  hypertrophy  of  the  cranial  bones  is  very  frequent,  thev  have 
sometimes  been  found  unaffected  post  mortem,  as  in  the  cases  of  Hudelo  and 
Heitz,  Thibierge,  Martel,  and  Moizard  and  Bourges. 

The  enormous  size  of  the  cranium  contrasts  with  the  condition  of  the 
face,  which  remains  normal.  Hypertrophy  of  the  inferior  maxUla  and  of 
the  malar  bones  has  been  noted.  In  my  patient  the  lower  and  upper  jaws 
were  enlarged.     In  a  case  reported  by  Joncheray  the  inferior  maxilla  was 


2032  TEXT-BOOK  OF  MEDICINE 

much  elongated,  and  the  lower  incisors  projected  in  front  of  the  upper  ones. 
In  the  superior  maxilla  the  alveolar  border  was  much  thickened.  In  Gilles 
de  la  Tourette  and  Magdelaine's  patient  the  inferior  maxilla  was  hyper- 
trophied.  It  would,  therefore,  be  an  error  to  think  that  the  bones  of  the 
face  are  free  in  Paget's  disease.  The  condition  is,  however,  not  comparable 
to  that  seen  in  acromegaly. 

The  neck  is  short  and  bent  forward,  so  that  the  head  has  the  appearance 
of  emerging  between  the  two  shoulders,  while  the  chLu  approaches  the 
sternum.  The  spine  is  curved  forwards,  and  the  patient  is  bent.  The  ribs 
are  hypertrophied,  and  sometimes  ankylosed.  As  a  whole,  the  thorax  is 
short,  and,  as  it  were,  cramped  together.  It  has  the  appearance  of  being 
"  pushed  into  the  abdomen,  like  an  opera-glass,"  so  that  the  play  of  the 
diaphragm  and  the  free  activity  of  the  intrathoracic  organs  are  often  ham- 
pered (Cadet).  This  is  one  of  the  causes  of  the  respiratory  distress  noted  in 
several  cases.  The  clavicles  and  the  scapulae  are  often  enormous,  as  in  my 
patient.     The  double  incurvation  of  the  former  is  characteristic. 

The  shoulders  project  forwards.  In  consequence  of  the  cramping  and 
bending  of  the  trunk,  which  has  diminished  in  height,  the  upper  limbs 
appear  elongated,  and  the  hands  reach  below  the  loiees.  The  arms  are  less 
deformed  than  the  legs.  The  ulna  and  the  radius,  however,  are  hyper- 
trophied and  curved  inwards,  contrary  to  what  is  seen  in  acromegaly. 
They  do  not,  however,  escape  the  hypertrophying  osteitis  completely. 
Thus,  in  my  patient  some  of  the  bones  of  the  carpus  were  afiected ;  in 
Gnies  de  la  Tourette  and  Magdelaine's  patient  the  second  and  third  meta- 
carpal bones  of  the  right  hand  were  very  large.  Sometimes,  as  in  Marie's 
patient,  the  iliac  crests  are  much  hypertrophied,  and  form  large  projections 
into  the  flank,  "  so  that  the  hip-bones  as  a  whole  assume  the  form  of  a 
vase,  which  receives  into  its  opening  the  thorax,  which  is  too  small  for  its 
aperture."  In  short,  when  Paget's  disease  is  complete  and  confirmed,  the 
attitude  of  the  patient  is  characteristic.  Large  cranium ;  head  deeply  set 
between  the  shoulders  and  flexed  on  the  chest ;  back  bent ;  thorax  com- 
pressed and  shortened ;  deformities  of  the  bones  as  regards  their  normal 
curves  ;  arms  deformed  and  apparently  too  long  ;  legs  bent  and  curved  in  the 
form  of  bows ;  difficulty  in  walking,  which  requires  the  aid  of  one  or  of  two 
sticks  ;  bony  hypertrophy,  affecting  chiefly  the  tibiae,  the  cranium,  and  the 
clavicle,  make  up  the  clinical  picture  known  as  Paget's  osteitis  deformans. 

I  have  described  above  the  lesions  found  on  histological  examina- 
tion of  the  bones.  In  Hudelo  and  Heitz's  case  there  was  a  mixture 
of  rarefying  and  condensing  osteitis.  The  most  characteristic  feature  was 
"  the  complete  derangement  of  the  whole  organization  of  the  lamellar 
systems,  the  loss  of  the  circular  disposition  of  the  bony  arches  around  the 
Haversian   canals,   and  the  architectural  structure  of  the  whole  bone." 


DISEASES  AFFECTIN(!  Till':  LOCOMOTOR  SYSTEM       iiOuli 

Gombaiilt  liiis  notod  rarofactioii  of  tlic  bony  tissue,  without  foriuatifdi  of 
now  l)()iu'.  Tiiiltii^Tge  has  found  iu  four  cases  zones  of  rarefying  »».sleitia 
alongside  those  of  osteitis  neofornians. 

The  chC'Tuical  composition  of  tlic  bone  is  modititMl,  but  tiiese  niodiiica- 
tiojis  have  not  much  pathological  value,  since  they  are  variable  in  diflerent 
cases.  Thus,  in  Hudelo  and  Ilcitz's  case  there  was  an  increase  in  the 
organic  materials  and  a  diminution  in  the  mineral  salts,  while  in  (iillcs  de 
la  Tourette  and  Magdelaine's  case  there  was  a  diminution  in  the  amount  of 
organic  matter  and  an  increase  in  the  salts. 

Although  the  attention  is  chiefly  directed  to  the  bony  system,  other 
lesions  and  systems  must  also  be  considered.  Thus,  lesions  of  the  heart 
and  of  the  aorta  are  so  frequent  that  we  cannot  consider  them  as  a  remark- 
able coincidence,  and  I  look  upon  them  as  forming  part  of  the  morbid 
process. 

On  auscultating  my  patient,  we  found  signs  of  a  mitral  lesion,  which  was  confirmed 
post  mortem.  Paget  found  in  his  first  patient  signs  of  a  mitral  insuflSciency,  and  at 
the  autopsy  the  mitral  valve  was  narrowed  and  atheromatous,  with  calcareous  deposits. 
The  aortic  valves  and  the  first  portion  of  the  aorta  showed  some  patches  of  atheroma. 
In  Levy's  patient  mitral  insufficiency'  and  hard  arteries  were  found.  The  autopsy 
showed  that  the  heart  was  enlarged,  the  pericardium  adherent,  the  mitral  valve  tliick- 
ened,  retracted,  and  wrinkled,  the  aortic  valves  calcified  in  places,  and  the  aorta  athero- 
matous. Gilles  de  la  Tourette  and  Magdelaine's  patient  had  had  several  attacks  of 
asystole,  and  the  autopsy  showed  that  the  heart  was  hypertrophied  and  dilated  with 
atheromatous  patches  on  the  inner  surface  of  the  aorta.  Moizard  and  Bourges'  patient 
had  atheromatous  patches  on  the  mitral  and  aortic  valves.  Marie's  patient  had  all 
the  symptoms  of  a  mitral  lesion — \-iz.,  breat  hlcssness,  palpitation,  intermittent  pulse, 
systoUc  murmur,  and  oedema  of  the  lower  limbs.  Bomiier's  patient  had  a  mitral  and 
aortic  murmur,  and  died  suddenly.  Gaillard's  patient  had  signs  of  mitral  stenosis. 
In  See's  case  there  was  hy|)ertrophy  of  the  left  ventricle  and  atheromatous  lesions. 
In  short,  in  nearly  every  case  the  heart,  the  aorta,  and  the  arteries  are  affected  by 
atheroma  or  by  sclerosis. 

I  do  not  know  if  the  lesions  of  chronic  meningitis  in  my  patient  form  a 
direct  part  of  Paget's  disease.  It  is  certain  that  meningeal  lesions  have 
been  fomid  in  several  cases.  In  one  of  the  cases  in  Richard's  thesis  it  is 
said  that  the  patient  became  deaf  in  the  right  ear,  and  that  his  memory 
failed,  so  that  he  often  forgot  the  names  of  the  most  common  objects.  He 
also  sufiered  from  vertigo.  At  the  post-mortem  examination  patches  of 
softening  were  found. 

In  short,  Paget's  osteitis  deformans  is  a  morbid  entity  which  must  be 
clearly  distinguished  from  other  affections  of  the  bony  system.  From  the 
ill-classified  group  in  which  multiple  hyperostoses  were  formerly  included 
Paget's  osteitis  and  Marie's  acromegaly  stand  out  as  well-defined  morbid 
types. 

Paget's  osteitis  deformans  has  certain  characters  which  permit  of  a 
diagnosis,  even  though  the  affection  is  not  far  advanced.     They  are  as 


2034  TEXT-BOOK  OF  MEDICINE 

follows  :  The  osteitis  chiefly  affects  the  tibiae,  the  cranium,  and  the  clavicles, 
while  the  bones  of  the  hands,  the  feet,  and  the  face  are  practically  free. 
The  bony  lesion  is  uniform,  and  affects  the  diaphyses  of  the  long  bones. 
The  deformities  of  osteitis  deformans  are  only  an  exaggeration  of  the  normal 
curves  of  the  bones.  The  evolution  of  osteitis  deformans  is  slow,  some- 
times painful,  and  usually  s}Tnmetrical.  It  must  not  be  confounded  with 
osteomalacia  and  with  rickets,  which  in  the  time  of  their  appearance  and 
in  the  lesions  produced  differ  so  clearly  from  Paget's  disease  that  furthei 
mention  is  needless.  In  acromegaly  the  tibise,  the  cla^-icles,  the  cranium, 
etc.,  are-  not  affected.  The  feet  and  the  hands  become  enormous,  and  the 
"  hypertrophy  shows  itself  chiefly  in  the  bones  of  the  extremities  and  in  the 
extremities  of  the  bones  "  (Marie).  Without  comiting  the  other,  charac- 
teristic signs,  this  distinction  alone  would  suffice  to  differentiate  acromegaly 
from  Paget's  disease. 

When  we  consider  the  course  of  Paget's  disease,  we  find  a  progressive 
trophic  change  in  the  bony  system.  The  trophic  trouble  causes  diminished 
resistance  in  the  bone  and  overgrowth  of  its  tissue.  The  bone,  which  has 
grown  less  resistant,  becomes  bent,  curved,  and  deformed.  Although 
certain,  bones,  and  notably  those  of  the  hands,  feet,  and  face,  are  less  affected, 
or  are  even  spared,  and  other  bones,  such  as  the  tibise,  the  cranium,  and 
the  clavicle,  form  the  seat  of  election  in  osteitis  deformans,  it  is  none 
the  less  true  that  the  skeleton  as  a  whole  participates  more  or  less  in  the 
lesions,  which  run  a  slow  but  progressive  course,  extending  over  many  years. 
The  patient  at  length  grows  cachectic,  but  this  cachexia,  which  terminates 
in  death,  does  not  depend  upon  the  bony  lesion,  properly  speaking.  It 
depends  upon  a  complex  of  troubles  and  lesions  which  are  directly  or  in- 
directly associated  with  the  bony  dystrophy — cardiac,  aortic,  cerebral, 
pulmonary  lesions,  etc. 

It  is  certain  that  Paget's  disease  is  a  systematic  and  progressive  dystrophy. 
By  its  course  it  approaches  the  group  of  affections  which  Vulpian  called 
"  systematic,"  and  which  Duchenne  of  Boulogne  named  "  progressive  " — 
progressive  muscular  atrophy,  progressive  locomotor  ataxia,  and  progressive 
general  paralysis.  Paget's  disease  is  systematic,  for  it  invades  almost  the 
whole  skeleton  systematically,  showing  itself  by  lesions  which  are  identical ; 
it  is  progressive,  because,  like  the  so-called  progressive  diseases,  it  pursues 
unchecked  its  fatal  course.  Accordingly,  in  the  subheading  of  this  section 
I  have  added  a  word  to  the  term  osteitis  deformans,  and  have  called  the 
disease  progressive  osteitis  deformans. 

As  regards  the  primary  cause  of  the  lesions,  we  can  only  conjecture. 
The  hypothesis  of  an  initial  medullary  lesion  had  been  advanced  by  GiUfcs  de 
la  Tourette  and  Marinesco,  who  in  two  cases  found  changes  in  the  posterior 
column  of  the  spinal  cord.     Le^d,  however,  who  studied  these  lesions  in 


DISEASES  Al^FECTING  THE  L<JCOMUT()R  SYSTEM       2035 

another  case,  considers  them  to  be  senile  lesions  of  vascniliir  origin.  Huflclo 
ami  ITeitz  agree  with  the  conclusions  of  Levi,  and  think  also  that  these 
raedullaTy  lesions,  when  they  are  found,  cannot  explain  the  bony  lesions. 
My  ])atient  had  no  medullary  lesion. 

The  other  hypotheses,  such  as  a  lesion  of  the  vascular  system,  atheroma 
of  the  nutrient  arteries  of  the  bones  (Beclere),  interstitial  neuritis  of  the 
nutrient  nerve  of  the  bone,  do  not  appear  to  be  sufficient,  and  I  conclude 
with  Hudelo  and  Heitz  that  we  do  not  know  the  causative  lesion  of  the 
bony  malformations  in  Paget's  disease. 

According  to  Lannelongue  (who  has  made  a  profound  study  of  syphilis  of 
the  bones),  Paget's  disease  is  syphilitic  in  nature.  Fournier  shares  this  opinion. 

IJenou,  in  a  recent  case,  has  obtained  a  positive  Wassermann's  reaction 
on  two  occasions,  and  abundant  lymphocytosis  of  the  cerebro-spinal  fluid. 

V.  THOMSEN'S  DISEASE. 

Description. — The  description  of  Thomsen's  disease  is  of  recent  date. 
It  was  in  1876  that  a  physician  named  Kappeln  (Schles^vig)  pubUshed  the 
history  of  the  affection  from  which  he  suffered,  and  which  had  also  attacked 
several  members  of  his  family.  He  spoke  of  it  in  the  following  terms  : 
"  Tonic  spasms  in  the  voluntary  muscles,  in  consequence  of  an  hereditary 
psychical  disposition."  This  term  has  not  been  preserved,  any  more  than 
that  of  muscular  spasms  at  the  onset  of  voluntary  movement  proposed  by 
Ballet  and  Marie.  This  latter  term  has,  however,  the  merit  of  showing  the 
essential  character  of  the  affection. 

When  the  patient  begins  to  execute  any  movement,  he  experiences 
suddenly  in  the  muscles  of  the  region  put  into  action  a  peculiar  rigidity, 
which  for  some  moments  opposes  this  movement.  Thus,  if  he  wishes  to 
walk,  or  to  catch  hold  of  some  object,  or  to  strike  a  blow,  the  muscles  of  the 
leg,  hand,  and  arm  suddenly  enter  into  contraction,  and  remain  j&xed.  If 
he  wishes  to  shake  hands,  he  cannot  for  some  moments  loosen  the  hand 
which  he  has  just  seized.  The  same  troubles  may  affect  the  muscles  of  the 
neck,  of  the  jaw,  of  the  eyes,  and  of  the  tongue.  In  the  latter  case  speech 
and  pronunciation  are  much  affected.  It  is  on  the  occasion  of  sudden 
movements  at  a  word  of  command,  as  in  military  ser\-ice,  that  the  spasms 
reach  their  maximum.  At  the  end  of  a  few  seconds  the  rigidity  ceases, 
and  the  movements  gradually  regain  their  freedom. ;  but  on  the  occasion  of 
a  fresh  cause,  which  may  be  insignificant,  similar  troubles  appear,  and 
disappear  a  few  moments  afterwards. 

On  examining  the  muscles  when  they  are  contracted,  we  find  that  they 
are  hard  and  very  prominent.  The  size  of  the  limbs  is  larger  than  in  the 
normal  condition,  but  in  spite  of  this  apparent  hypertrophy,  the  muscular 
power  is  sometimes  diminished.     Patients  are  easily  fatigued,  and  although 


203a  TEXT-BOOK  OF  MEDICINE 

the  ajSection  is  not  in  an  advanced  stage,  they  are  incapable  of  work  requiring 
even  a  moderate  degree  of  force. 

AU  the  striated  muscles  may  be  affected,  but  the  smooth  muscles  are 
usually  free. 

The  mechanical  excitability  of  the  muscles  is  much  increased  (Erb).  The 
least  pressure  or  the  least  blow  with  a  percussor  or  with  the  end  of  the  finger 
causes  spasm  in  the  muscle  fibres.  The  faradic  and  galvanic  excitabihty 
is  also  increased.  At  the  commencement  of  the  excitation  the  muscle 
contracts  energetically,  and  then,  as  the  current  continues  to  pass,  the 
muscle  relaxes  gradually,  and  behaves  towards  the  electrical  stimulus  like 
an  ordinary  muscle. 

The  electrical  and  mechanical  excitability  of  the  nerves  is  practically 
normal.  Isolated  stimuli  cause  short  and  transient  contractions ;  accumu- 
lated stimuli  cause  tonic  contractions,  which  are  persistent.  This  symptom- 
complex,  furnished  by  the  examination  of  the  nerves  and  muscles,  con- 
stitutes Erb's  myotonic  reaction. 

In  addition  to  the  severe  and  moderate  cases,  we  also  find  slight  and 
defaced  forms. 

Thomsen's  disease  usually  begins  in  infancy  or  in  youth.  Sometimes  it 
has  a  very  slow  progressive  course,  but  it  usually  remains  stationary,  and 
it  may  even  recede.  It  is  often  accompanied  by  changes  in  character,  such 
as  melancholia  and  hypochondria,  which  led  Thomsen  to  look  upon  the 
trouble  as  a  psychosis.  It  is  frequently  hereditary,  and  coincides  with 
mental,  arthritic,  and  hysteriform  manifestations  in  other  members  of  the 
family. 

The  diagnosis  is  usually  easy,  given  the  mode  of  the  appearance  and 
the  disappearance  of  the  spasms  which  characterize  it.  In  spasmodic 
tabes  dorsalis  the  spasms  are  continuous  ;  they  are  completely  absent  in 
pseudo-hypertrophic  paralysis ;  they  are  painful  in  tetany ;  they  may 
appear  in  hysteria,  but  in  the  latter  case  the  question  is  rather  one  of  a 
true  "  diathesis  of  contracture,"  and  the  hysterical  stigmata  are  hardly 
ever  wanting. 

All  the  treatment  employed  in  Thomsen's  disease  has  been  inefficient. 
Massage  and  gymnastics  are  the  most  useful  measures. 

The  pathological  anatomy  is  very  incomplete,  for  no  histological 
examination  of  the  nerves  and  of  the  nerve  centres  has  as  yet  been  made. 

Erb's  researches  upon  fragments  of  the  muscles  removed  from  hving 
subjects  have  shown  hypertrophy  of  the  muscular  bundles,  rounding  off  of 
their  angles,  and  multipUcation  of  their  nuclei,  with  a  watered  appearance 
and  a  vacuolated  condition  of  certain  muscle  fibres.  The  primary  bundles 
which  form  the  secondary  bundle,  instead  of  being  straight  and  parallel,  as 
in  the  normal  condition,  are  wavy.     Lastly,  the  interstitial  connective  tissue 


DISEASES  AFFECTING  THE  LOCOMOTOR  SYSTEM       -'0:;7 

is  usually  more  abundant  than  in  the  normal  condition,  though  much  less 
tiian  in  psoudo-hvpertrophic  paralysis.  Theso  characters,  which  wen;  found 
by  chance  in  the  muscles  of  a  cadaver,  led  Erb  to  make  a  retrospective 
diagnosis. 

VI.  PROGRESSIVE  MUSCULAR  DYSTROPHIES. 

Discussion. — In  describing  the  diseases  of  the  spinal  cord,  I  have  already 
said,  when  referring  to  progressive  muscular  atrophy,  that  the  troubles  and 
the  changes  which  affect  the  muscular  system  must  be  divided  into  two 
great  classes.  We  have  studied  the  first  class  in  connection  with  the 
diseases  of  the  nervous  system,  and  we  have  seen  that  the  muscular  atrophies 
associated  with  lesions  of  the  anterior  cornua  of  the  spinal  cord  (myelopathic 
amyotrophies)  have  sometimes  only  the  value  of  an  epiphenomenon ;  in 
other  cases  they  form  a  morbid  entity. 

At  the  present  moment  we  shall  deal  with  the  primary  diseases  of  the 
muscular  system — that  is  to  say,  diseases  which  appear  to  affect  the  muscle 
alone,  and  not  the  nervous  system.  Among  these  diseases  we  find  pseudo- 
hypertrophic muscular  paralysis  (Duchenne's  type)  and  progressive  atrophic 
myopathy  (Landouzy  and  Dejerine  type).  I  say  that  these  diseases  appear 
to  be  independent  of  lesions  of  the  nervous  centres,  and  yet,  when  we  note 
the  symmetry,  the  progressive  course,  and  the  almost  systematic  evolution 
of  the  muscular  lesion,  we  cannot  but  formulate  hypotheses  regarding  the 
existence  of  lesions  in  the  nervous  system.  With  Vulpian,  we  may  ask  if 
these  so-called  primary  myopathies  are  not  comparable  ynth.  the  reflex 
muscular  atrophies  of  articular  origin,  with  apparent  integrity  of  the  nervous 
system,  and  whether  "  the  weakening  and  disappearance  of  the  trophic 
power  of  the  motor  cells  of  the  spinal  cord  do  not  exist  in  all  these  cases  as 
the  instigating  cause  of  the  morbid  process  situated  in  the  muscles"  (Vulpian). 
We  must  not  strain,  says  Raymond,  at  drawing  conclusions  from  negative 
facts,  and  say  that  the  nervous  system  is  healthy  because  we  find  no  trace 
of  myelitis  or  of  cellular  atrophy.  It  seems  more  reasonable  to  suppose  that 
some  trouble  has  perhaps  existed  at  the  time  when  the  central  nervous 
system  is  complete  and  perfect,  and  has  caused  an  obstacle  in  its  regular 
evolution,  producing  a  deviation  of  structure  in  proportion  as  the  patient's 
age  increases. 

The  expectations  of  Raymond  have  been  completely  realized,  and,  as  I 
have  indicated  in  Diseases  of  the  Spinal  Cord,  "  no  insurmountable  line  of 
demarcation  exists  between  the  familiar  progressive  amyotrophies  and  the 
progressive  muscular  atrophies  of  the  Aran-Duchenne  type.  The  various 
types  of  progressive  muscular  atrophy  are  only  variants  of  the  same  morbid 
entity  "  (Raymond). 

n.  129 


2038  TEXT-BOOK  OF  MEDICINE 

However  this  may  be,  let  us  still  consider  as  primary  the  myopathies 
which  we  are  now  about  to  describe. 

By  the  side  of  progressive  muscular  atrophy  (Aran-Duchenne  type) 
Leyden  was  the  first  to  describe  a  form  of  muscular  atrophy  which  com- 
mences in  the  lower  limbs,  reaches  the  arms,  and  is  often  accompanied  by 
pseudo-hypertrophy — amyotrophy  of  family  origin,  very  probably  due  to  a 
lesion  of  the  muscles  themselves.  Since  this  time  other  analogous  cases 
have  multiplied.  Moebius  insists  on  the  cases  observed  by  Leyden,  and 
Eichorst  describes  a  case  of  muscular  atrophy  of  myopathic  origin  com- 
mencing in  the  femoro-tibial  region,  but  without  pseudo -hypertrophy. 
Zimmerlin  describes  a  case  of  family  muscular  atrophy  of  myopathic  origin, 
which  commenced  in  the  shoulder  and  reached  the  lower  limbs.  In  1884 
Erb  collected  all  these  varieties  in  a  single  group,  regarding  the  pseudo- 
hypertrophy as  a  contiDgent  phenomenon  which  may  be  present  or  absent, 
and  he  added  that  the  onset  of  the  disease  in  difEerent  parts  of  the  body  is 
not  sufiicient  to  stamp  these  amyotrophies  as  so  many  distinct  diseases. 
Lastly,  Erb  insists  on  the  early  appearance  of  muscular  atrophies,  to  which 
he  gives  the  term  of  juvenile  form.  In  the  following  year  Landouzy  and 
Dejerine  published  a  memoir  on  progressive  atrophic  myopathy  com- 
mencing in  the  face  (facio-scapulo-humeral  type),  but  they  refused  to 
consider  it  as  a  variety  of  Erb's  juvenile  form.  In  their  opinion,  the  disease 
is  distinct,  and  may  sometimes  appear  in  adult  life. 

Lastly,  there  are  transitional  forms,  which  present  a  family  origin,  as  in 
the  preceding  muscular  atrophies,  but  which  commence  in  the  feet,  spread 
to  the  legs,  and  then  to  the  hands,  and  are  accompanied  by  fibrillary  tremors 
and  reaction  of  degeneration.  This  is  the  Charcot-Marie  type.  These 
authors  believe  that  the  disease  is  not  a  primary  myopathy,  but  a  medullary 
afiection  or  a  neuritis.  The  same  may  be  said  of  the  hereditary  femoral 
form,  with  "  claw-foot,"  described  by  Brossard.  It  must  not,  however,  be 
held  that  in  these  latter  cases  the  muscular  atrophy  may  never  be  accom- 
panied by  pseudo-hypertrophy,  for  Bidard  and  Eemond  in  1892  published 
a  case  in  which  certain  muscles  were  manifestly  enlarged. 

In  1891  Erb  reopened  this  question,  and  united  aH  the  cases  under  the 
name  of  progressive  muscular  dystrophy.  He  has  shown  that  in  this 
respect  the  histological  process  is  the  same,  whether. hypertrophy  is  present 
or  absent.  Moreover,  in  the  same  muscle  we  may  find  hypertrophic  and 
atrophic  lesions,  so  that  the  volume  of  the  muscle  may  be  normal,  although 
the  whole  structure  is  really  diseased.  Whatever  be  the  variety  of  the 
progressive  muscular  dystrophy  in  question,  the  lesions,  says  Erb,  always 
run  the  same  course.  In  the  first  degree  we  find  hypertrophy  of  the  mus- 
cular fibres  with  proliferation  of  the  nuclei ;  the  fibres  then  divide  and 
break  up,  while  the  interstitial  connective  tissue  presents  some  signs  of 


DISEASES  AFFECTING  THE  LOCOMOTOR  SYSTEM       L'O.JO 

irritation.  Tlic  second  degree  is  characterized  by  atrophy  of  the  muscle 
fibres,  which  gradually  disappear.  At  this  moment  the  connective  tissue 
proliferates  freely,  and  the  walls  of  the  vessels  become  thickened.  Lastly, 
in  the  third  period  the  connective  tissue  is  infiltrated  with  fat,  so  that  at  a 
given  moment  the  muscle  is  replaced  by  fibrous  tissue  more  or  less  loaded 
with  fat.     Then  apparent  atrophy  or  hypertrophy  of  the  muscle  appears. 

These  lesions,  as  we  see,  are  absolutely  distinct  from  the  progressive 
muscular  atrophy  of  myelopathic  origin,  and  should  keep  the  distinction 
which  has  been  established  between  these  two  groups  of  muscular  atrophy. 
On  the  other  hand,  the  different  varieties  of  muscular  atrophy  of  myopathic 
origin  which  I  have  just  re\'iewed  are  related  by  such  close  ties  that,  from 
the  nosographic  point  of  view,  there  is  reason  to  unite  them  under  the  term 
proposed  by  Erb— progressive  muscular  dystrophy. 

Cases  published  in  1891  and  in  1893  by  Werndig  and  J,  Hoffmann,  how- 
ever, appear  to  show  a  clear  relation  between  the  two  great  classes  of  pro- 
gressive muscular  atrophies,  and  to  admit  the  existence  of  a  progressive 
muscular  atrophy  which  at  the  same  time  is  of  a  myelopathic  and  family 
form.  This  variety  commences  in  early  infancy,  most  often  during  the 
first  year  of  life,  in  an  insidious  manner,  without  convulsions  and  without 
fever.  The  power  and  the  extent  of  the  movements  of  the  lower  limbs 
diminish,  and  the  muscles  of  the  back  are  affected  by  motor  paresis.  The 
upper  limbs,  the  muscles  of  the  nape  of  the  neck  and  of  the  neck  are  invaded 
secondarily  months  and  years  afterwards.  Death  takes  place  after  four  or 
five  years,  and  is  caused  by  some  intercurrent  respiratory  affection.  The 
autopsy  reveals  "  the  existence  of  atrophy  of  the  ganglion  cells  in  the 
anterior  comua,  along  the  whole  extent  of  the  neuron,  with  its  maximum 
in  the  cervical  and  lumbar  enlargements,  and  with  very  pronounced  atrophy 
of  the  anterior  roots  ;  similar  degeneration,  but  much  less  severe,  of  the 
fibres  of  the  mixed  motor  sensory  nerves  ;  lastly,  correlative  atrophy  of  the 
muscles,  and  an  interstitial  deposit  of  fat,  without  hypertrophy,  and  with- 
out pseudo-hypertrophy  of  the  muscular  fibres  "  (Raymond). 

Clinically,  however,  two  varieties  stand  out  prominently  :  (1)  pseudo- 
hypertrophic paralysis ;  and  (2)  progressive  atrophic  myopathy  (Landouzy 
and  Dejerine  type). 

VII.  PSEUDO-HYPERTROPHIG  ilUSCULAR  PARALYSIS. 

iEtiology. — Pseudo-hypertrophic  muscular  paralysis  is  a  disease  of 
infancy,  which  may  commence  before  the  child  has  begun  to  walk  or  during 
the  early  years  of  life.  It  may  be  asked  whether  this  is  not  an  apparent 
onset,  and  whether  the  real  onset  does  not  date  from  the  intra-uterine 
existence.     In  some  cases  the  disease  appears  at  a  more  advanced  age,  as 

129—2 


2040  TEXT-BOOK  OF  MEDICINE 

from  six  to  eight,  and  even  from  fourteen  to  fifteen  years,  though  rarely 
later.  It  is  more  common  in  boys  than  in  girls,  and  it  is  not  rare  to  see 
several  children  in  the  same  family  suiTering  from  this  disease. 

Pathological  Anatomy. — The  hypertrophy  of  the  muscular  system  is 
only  apparent,  as  the  muscular  fibres  disappear,  and  are  replaced  by  con- 
nective and  fatty  tissue.  Histological  examination  of  the  muscles  has  been 
made  on  the  living  patient  with  small  pieces  of  muscles  removed  by  means 
of  a  harpoon.  This  examination  shows  that  the  muscle  fibre  has  almost 
completely  disappeared,  and  is  replaced  by  cellulo-fatty  tissue.  As  we 
have  said  above,  the  muscular  lesion  runs  the  following  course :  hyperplasia 
of  the  interstitial  connective  tissue,  accumulation  of  interstitial  adipose  cells, 
and  simple  atrophy  of  the  muscle  fibres.  Adipose  tissue  is  substituted  for 
muscle  fibre,  and  the  muscular  tissue  undergoes  granulo-fatty  degeneration 
only  in  exceptional  cases.  In  its  first  stage  the  lesion  is  rather  fibrous  ;  in 
its  second  stage  it  is  chiefly  fatty. 

The  medullary  lesions  which  have  been  noted  up  to  the  present  appear 
to  be  secondary  or  independent.  They  do  not  affect  the  autonomy  of  the 
muscular  lesions. 

The  apparent  hypertrophy  of  the  muscle  contrasts  in  a  singular  way  with 
the  small  size  of  the  tendons.  While  some  muscles  stand  out  in  relief, 
others  are  atrophied. 

Description. — The  characteristic  features  of  this  disease  are  :  (1)  An 
exaggerated  growth  in  the  size  of  certain  muscles,  which  appear  hyper- 
trophied,  when  really  they  are  not  so ;  (2)  a  gradual  diminution  of  the 
power  of  voluntary  contraction,  which  ends  in  complete  abolition  of  move- 
ment. It  must,  however,  not  be  thought  that  these  two  symptoms  are 
absolutely  associated,  and  that  the  muscular  weakness  increases  with  the 
size  of  the  muscle — in  fact,  the  diminution  of  movement  is  proportional  to 
the  number  of  fibres  which  have  disappeared  ;  but,  while  the  muscular  fibres 
disappear,  the  size  of  the  muscle  may  undergo  every  possible  variation. 
It  is  often  increased  by  the  addition  of  foreign  elements,  but  it  is  sometimes 
wasted. 

The  disease  nearly  always  commences  in  the  muscles  of  the  calf,  which 
stand  out  in  marked  relief ;  then  in  its  ascending  and  symmetrical  course 
the  lesion  attacks  in  succession  the  sacro-lumbar  muscles,  the  deltoid,  the 
glutei,  the  quadratus  lumborum,  the  tensor  vaginse  femoris,  the  serratus 
magnus,  the  muscles  of  the  abdomen  and  of  the  scapula,  the  adductors  and 
the  flexors  of  the  thigh,  etc.  The  child  appears  to  have  the  musculature  of 
an  athlete. 

The  muscles  which  are  increased  in  size  are  sometimes  firm  and  some- 
times soft,  depending  upon  the  predominance  of  fibrous  or  of  adipose 
tissue. 


DISEASES  AFFECTI\(J    rilK  LOCOMOTOR  SYSTEM       2041 

The  increastMl  size  of  tho  musrlea  aff«!C<('(l  by  sclerolipomatosis  is  in 
Ringulur  contrast  with  the  atro]>hied  miisdes.  The  atrophy  may  supervene 
at  an  advanced  ])eriod  in  muscles  which  were  formerly  very  large  ;  it  may 
also  attack  from  the  first  certain  muscles,  especially  the  latissimus  dorsi, 
the  pectonilis  major,  and  the  muscles  of  the  arm. 

Lastly,  the  disease  may  exist  in  a  functional  form,  in  which  it  is  im- 
possible to  recognize  either  hypertrophy  or  atrophy  of  the  muscles.  Pseudo- 
hy])ertr(»phy  is  not,  then,  the  characteristic  and  pathognomonic  symptom 
of  this  disease.  "  In  pseudo-hvj)ertrophic  paralysis  the  size  of  the  muscle 
is  nothing,  the  weakness  is  everything  "  (Marie). 

The  loss  of  movement  sliows  a  somewhat  special  course,  which  gives  rise 
to  characteristic  attitudes.  At  the  onset,  when  but  few  fibres  are  affected, 
simple  wealmess  is  present  ;  the  child  runs  about  less,  and  falls  easily. 
Later,  in  the  upright  position,  the  patient  assumes  a  special  attitude,  and 
waddles  like  a  duck.  He  appears  kipped,  separates  his  legs  and  curves  his 
back  in  a  posterior  direction,  in  order  to  restore  equilibrium — in  fact,  the 
extensor  muscles  of  the  trunk,  which,  though  enlarged  in  size,  are  weakened, 
can  no  longer  oppose  the  tendency  of  the  body  to  fall  forward,  and  the 
patient  therefore  pulls  his  shoulders  as  far  backwards  as  possible.  When 
the  muscles  of  the  lower  limbs  and  of  the  sacro-lumbar  mass  are  very 
much  weakened,  the  patient  experiences  the  greatest  difficulty  in  raising 
himself  from  the  prone  position.  He  is  compelled  to  execute  this  move- 
ment by  a  series  of  manceuvres  in  which  the  arms  are  used,  because 
he  can  no  longer  employ  the  muscles  of  the  legs  and  of  the  trunk  for  this 
purpose. 

In  order  to  get  up,  he  first  turns  on  his  stomach,  which  in  itself  is  difl&cult. 
He  then  raises  his  body  with  his  hands,  and  throws  the  trunk  backwards, 
in  order  to  assume  the  stooping  position.  He  now  proceeds  to  raise  himself. 
The  legs  are  extended,  while  the  arms  are  applied  to  the  groimd  to  support 
the  trunk.  The  hands  are  then  brought  close  to  the  feet,  pulled  upwards 
towards  the  knee,  and  take  higher  points  of  support,  the  patient,  as  it  were, 
climbing  up  himself. 

The  feet  often  show  deformities,  such  as  bilateral  equinus  and  forced 
extension  of  the  first  phalanges. 

In  some  cases  the  face  has  participated  in  the  muscular  weakness  (gaping 
mouth  and  incomplete  opening  of  the  eyelids). 

Course — Diagnosis. — Pseudo-hypertrophic  paralysis  commences  with- 
out fever  and  without  pain,  but  dullness  of  the  intellect  is  frequently  noted. 
The  symptoms  run  a  very  slow  course.  The  tendon  reflexes  are  preserved, 
the  muscles  are  not  affected  by  fibrillary  tremors,  the  muscular  swellings 
only  reach  their  maximum  after  one  or  two  years,  and  the  period  of  paralysis 
supervenes  in  a  progressive  manner.     A  period  of  arrest  in  the  disease,  or 


2042  TEXT-BOOK  OF  MEDICINE 

a  remission  which,  may  last  for  several  years,  is  sometimes  seen  when  the 
apparent  hypertrophy  is  confirmed.  The  progressive  course  of  the  disease 
is,  however,  practically  fatal.  The  destruction  of  the  muscle  and  the  loss 
of  power  become  general,  and  the  patient,  who  can  no  longer  leave  his  bed, 
lies  absolutely  paralyzed. 

AU  the  other  functions  are  well  carried  out,  and  yet  the  patient  finally 
becomes  marasmic,  or  dies  from  some  intercurrent  disease  (bronchitis, 
pneumonia). 

Pseudo-hypertrophic  muscular  paralysis  has  a  mean  duration  of  from 
ten  to  eighteen  years,     A  longer  duration  is  exceptional. 

Progressive  muscular  atrophy,  infantile  paralysis,  and  paraplegia  will 
not  be  confounded  with  pseudo-hypertrophic  muscular  paralysis,  as  the 
signs  of  the  latter  disease  are  characteristic.  Until  matters  change,  we  must 
separate  from  pseudo-hypertrophic  paralysis  cases  of  true  muscular  hyper- 
trophy which  supervene  in  adults,  and  which  show  only  very  remote 
resemblance  to  the  disease  just  described. 

Thomsen's  disease  is  accompanied,  it  is  true,  by  muscular  hypertrophy, 
but  never  by  atrophy.  The  stifEness  of  the  muscles  which  characterises  it 
appears  only  after  voluntary  movement.  It  soon  ceases,  and  the  patient 
can  then  use  his  limbs,  as  in  the  normal  condition.  We  never  find  club-foot 
or  deformities  of  the  limbs. 

Faradization  appears  to  be  the  most  efficient  treatment  in  pseudo- 
hypertrophic paralysis.  The  ingestion  of  thymus  or  of  extract  of  thymus 
is  indicated  (Pitres). 


,VIII.  PROGRESSIVE  ATROPHIC  MYOPATHY. 

After  his  remarkable  researches  on  progressive  muscular  atrophy  in 
adults,  Duchenne  turned  his  attention  to  a  similar  condition  in  infancy. 
He  clearly  saw  that  this  amyotrophy  of  infancy  presents  special  characters, 
that  it  almost  always  commences  in  the  face,  and  gives  the  Uttle  patient  a 
peculiar  appearance ;  but,  in  spite  of  these  distinctive  signs,  and,  indeed,  of 
many  others,  he  was  of  opinion  that  this  progressive  atrophy  in  infancy  was 
a  variety  of  the  progressive  type  of  muscular  atrophy,  which  has  in  both 
cases  primary  and  characteristic  lesions  in  the  anterior  cornua  of  the  grey 
substance  of  the  cord. 

After  important  researches,  however,  Landouzy  and  Dejerine  showed 
that  this  amyotrophy  in  infancy  is  not  a  variety  of  progressive  muscular 
atrophy,  as  was  formerly  thought.  They  grouped  the  symptoms  together, 
adding  new  signs,  studying  the  lesions  ;  they  showed  that  it  is  a  disease  of 
the  muscles,  and  not  of  the  spinal  cord ;  and,  finally,  they  made  of  it  a 
distinct  morbid  entity,  which  they  named  progressive  atrophic  myopathy. 


DISEASES  AFFECTING  THE  LOCOMOTOR  SYSTEM       204;{ 

Tho  condition  hero,  then,  until  jjroof  bo  furnished  to  tlie  ooatrary,  is  one  of 
myopnt  hy,  and  not  of  myelopathy. 

Description.  Progressive  atrophic  myopathy  may  appear  at  any  ago, 
but  is  most  frequent  in  early  childhood.  In  the  infant  it  is  always  ushered 
in  by  more  or  less  marked  atrophy  of  the  muscles  of  the  face.  The  atrophy 
of  the  orbicularis  palpebrarum  and  of  the  labial  muscles  gives  a  peculiar 
expression  to  the  face.  During  repose  the  child  has  a  gaping,  dull,  in- 
diiferent  air  ;  the  lips  project ;  the  forehead  is  smooth.  In  the  various 
movements  which  the  face  makes  we  find  that  the  occlusion  of  the  eyelids 
is  incomplete.  During  the  act  of  smiling  the  mouth  opens  very  widely, 
and  the  patient  grins  from  ear  to  ear. 

The  muscles  supplied  by  the  facial  nerve  are  the  only  muscles  of  the 
liead  affected  by  this  atrophy  (muscles  of  expression),  and  they  are  attacked 
almost  simultaneously.  The  movements  diminish  in  proportion  as  the 
atrophy  progresses,  but  it  is  a  question  of  atrophy,  and  not  of  paralysis. 

The  course  of  the  facial  atrophy  is  very  slow.  It  takes  years  to  develop, 
and  it  is  only  after  a  long  period  that  the  atrophy  affects  the  other  muscles 
of  the  body. 

After  the  face,  the  muscles  of  the  shoulder  and  of  the  arm  are  the  first 
to  atrophy,  and  here,  as  in  the  face,  the  onset  is  insidious,  the  course  very 
slow  and  symmetrical,  without  either  sensory  or  paralj'-tic  troubles.  The 
special  topography  of  the  atrophies  at  this  period  of  the  disease  realizes 
the  facio-scapulo-humeral  type.  The  muscles  of  the  forearm  and  of  the 
hand  atrophy  very  late  ;  wasting  of  the  muscles  of  the  lower  limbs  then 
follows. 

In  this  disease  the  muscles  never  show  hypertrophy  or  pseudo-hyper- 
trophy. The  retraction  of  the  mtisciilar  tissue  sometimes  produces  a  pro- 
minent cord  under  the  skin.  Fibrillary  contractions  of  the  muscles  are  not 
seen,  and  the  electrical  reactions,  which  are  normal  in  quality,  are  diminished 
in  quantity,  parallel  vrith  the  progress  of  the  atrophy.  The  tendon  reflexes 
persist  for  a  long  whUe  ;  trophic  troubles  are  not  seen. 

Such  is  the  usual  picture  of  the  disease  in  the  child.  When  the  disease 
commences  in  the  adult  (which  is  far  more  rare),  the  symptoms  are  the  same, 
but  the  localization  of  the  atrophy  presents  some  difference.  According  to 
the  muscles  invaded,  we  find  a  facio-scapulo-humeral,  a  scapulo-humeral, 
and  a  femoro -tibial  type. 

As  regards  the  anatomical  lesions,  the  nervous  system  presents  no 
change.  The  muscles  are  affected  with  simple  atrophy,  without  appreciable 
change  in  the  sarcolemma.  Sometimes,  however,  we  find  interfascicular 
cirrhosis,  but  the  condition  is  then  one  of  atrophic  cirrhosis.  In  the  same 
way  as  in  pseudo-hypertrophic  paralysis,  it  is  the  hypertrophic  cirrhosis 
which  predominates. 


2044  TEXT-BOOK  OF  MEDICINE 

The  tendons  sometimes  encroach  upon  the  body  of  the  muscle,  and  this 
fact  explains  the  cord  sometimes  felt  near  the  insertion  of  the  tendons. 

In  order  to  explain  the  mode  of  invasion  of  the  muscles,  Babinski  has 
put  forward  the  theory  that  the  muscles  which  are  first  developed  are  the 
first  to  be  attacked  by  the  disease. 

As  accessory  or  consecutive  lesions  to  the  atrophy  of  the  muscles,  Dejerine 
has  noted  antero-posterior  flattening  of  the  thorax,  Hallion  frequency  of 
spontaneous  fractures,  and  Marie  considerable  diminution  in  the  antero- 
posterior diameter  of  the  cranium,  which  contrasts  with  the  increase  in  the 
transverse  diameter. 

From  the  description  of  the  disease  we  see  that  it  cannot  be  confounded 
either  with  progressive  muscular  atrophy  (Duchenne's  type,  Vulpian's  type) 
or  with  infantile  paralysis.     The  face  is  spared  in  both  these  diseases. 

The  prognosis  is  grave,  but  the  course  is  extremely  slow.  Collateral 
or  direct  heredity  is  the  only  factor  in  pathogenesis  with  which  we  are 
acquainted. 


PART  XI 

VENEREAL  DISEASES 

I.  GONORRH(EA. 

Bacteriology. — The  gonococcus  appears  under  the  microscope  as  a  dlplo- 
coccus,  staining  readily  with  the  aniline  dyes,  and  decolorizing  with  Gram's 
method. 

The  two  portions  of  the  diplococcus  look  like  two  coffee-beans,  having 
their  plane  surfaces  opposite  to  one  another,  and  separated  by  a  clear  line. 

The  grouping  in  pairs  is  the  special  feature.  The  diplococci  may  form 
small  masses  of  four  or  of  eight  elements,  but  they  are  always  present  in 
even  numbers.  They  never  form  chains.  Live  gonococci  are  mobile, 
exclusive  of  Brownian  movements. 

The  discharge  in  the  stationary  stage  of  the  malady  shows  pus  cells 
crowded  with  gonococci.  Extracellular  masses  are  also  found.  At  the 
onset  we  see  especially  cast-ofi  epithelial  cells,  with  gonococci  against  their 
surface,  but  not  in  their  interior. 

The  cultivation  of  the  gonococcus  demands  the  emplo}Tnent  of  special 
media,  containing  albumin.  The  gonococcus  does  not  grow  on  the  usual 
media  (broth,  agar,  and  gelatine).  It  is  strictly  aerobic,  and  so  delicate 
that  the  culture-tubes  must  be  at  once  placed  in  an  oven  at  37°  C.  Bumm 
has  succeeded  in  cultivating  on  tubes  of  coagulated  human  serum.  This 
method  is  not  suitable  in  practice.  Wertheim  has  improved  the  technique 
by  adding  agar  to  the  serum,  and  the  medium  usually  employed  at  the 
present  time  is  known  as  Wertheim's  medium.  It  is  composed  of  a  mixture 
of  agar  with  ascitic  or  pleuritic  serous  fluid.  This  medium  is  solid.  De 
Christmas  has  recently  advised  rabbit's  serum,  coagulated  by  heat.  Be- 
zan(,'ou  and  Griffon  recognize  the  advantages  of  this  medium,  but  they 
prefer  blood- agar  as  the  best  medium  for  the  practical  culture  of  the  gono- 
coccus. The  early  appearance  of  the  colonies  on  the  surface  of  the  blood- 
agar,  and  the  morphological  clearness  of  the  gonococcus  developed  upon 
this  medium,  render  it  excellent  for  diagnostic  purposes.  As  the  cultures 
remain  alive  for  more  than  six  months,  the  medium  is  excellent  for  pre- 
serving the  gonococcus. 

2045 


2046  TEXT-BOOK  OF  MEDICINE 

The  gonococcus  is  only  inoculable  in  the  human  species.  Attempts 
made  to  inoculate  animals  have  always  failed.  Animals  have  been  inocu- 
lated with  pure  cultures.  Although  these  inoculations  have  been  made  into 
the  urethra,  the  joints,  and  the  conjunctivae  of  new-bom  rabbits,  the  only 
result  has  been  slight  and  transient  inflammation  due  to  the  trauma,  Halle, 
using  a  gonococcus  of  exceptional  virulence,  has  caused  death  in  the  mouse 
by  large  intraperitoneal  injections  of  a  pure  culture  of  the  gonococcus  from 
a  case  of  periarthritis  of  the  elbow- joint.  This  case  is  so  far  imique.  For 
practical  purposes,  we  may  consider  the  gonococcus  as  non-pathogenic  in 
animals. 

The  gonococcus  must  not  be  confounded  with  the  pseudo -gonococcus. 
Many  diplococci  show  certain  analogies  with  the  gonococcus—a  fact  of  great 
importance  in  legal  medicine.  When  we  find  in  the  interior  of  the  pus  cells 
masses  of  diplococci  like  coffee-beans,  and  decolorizing  rapidly  with  Gram, 
we  can  be  sure  that  they  are  gonococci.  Nevertheless,  in  a  legal  case,  if  we 
have  only  dried  pus  to  work  with,  we  must  reserve  our  judgment. 

Although  the  gonococcus  is  the  cause  of  gonorrhceal  urethritis,  every 
urethritis  is  by  no  means  gonorrhceal.  The  urethra  is  rich  in  organisms  ; 
we  find  in  it  free  cocci,  cocci  in  the  cells,  cocci  in  pairs  or  in  chains,  bacilli, 
sarcinae,  etc.  A  urethral  discharge  may  be  due  to  these  organisms,  to  gout, 
to  rheumatism,  and  to  the  use  of  certain  drugs,  such  as  iodine  and  cantharides, 
but  the  gonococcus  is  not  present.  Septic  urethritis  may  follow  the  use  of 
an  infected  catheter.  Urethritis  may  occur  in  syphilis,  and  as  the  result 
of  ascending  or  descending  tubercular  infection.  In  each  case,  however, 
the  gonococcus  is  absent. 

In  gonorrhceal  pus  we  also  find  other  organisms  which  are  normal  in- 
habitants of  the  urethra  or  of  the  vagina,  and  which  play  an  important 
part  in  the  sequelae  of  gonorrhoea,  especially  in  the  chronic  stage.  Eraud 
has  stated  that  the  gonococcus  may  be  present  in  the  urethra  of  a  healthy 
man,  just  as  the  pneumococcus  may  exist  in  normal  saliva.  It  is  said  to  be 
devoid  of  virulence.  Straus  has  reported  a  case  of  gonococcic  arthritis 
which  developed  apart  from  any  contagion.  The  prevalent  opinion  is, 
however,  that  the  true  gonococcus  is  non-saprophytic.  Every  case  of 
gonorrhoea  results  from  contagion. 

The  inoculation  of  the  gonococcus  usually  takes  place  during  sexual 
intercourse.  This  condition,  however,  is  not  absolutely  indispensable,  since 
Bumm  has  experimentally  produced  gonorrhoea  by  inoculation  of  a  man 
with  virulent  cultures  of  the  gonococcus. 

^Etiology. — The  chances  of  inoculation  vary  in  different  persons,  and 
in  each  person  according  to  the  state  of  receptivity.  In  this  respect  fatigue, 
drinking,  and  repeated  coitus  have  an  undoubted  influences.  Moreover,  a 
first  attack,  instead  of  conferring  immunity,  renders  a  second  attack  more 


VENEREAL  DISEASES  2047 

likoly.  In  those  casea  revivificjition  of  gerrns  existing  in  a  latont  state  in 
the  urethra  lias  been  suggested.  The  statement  may  be  true,  but  it  has 
been  exaggerated.  In  any  case,  it  is  not  applicable  to  attacks  occurring 
several  years  apart.  In  women  leueorrhcea  appears  to  facilitate  contagion, 
and  to  increase  the  virulence  of  the  gonococcus.  The  menstrual  period  has 
the  same  effect.  A  woman  who  in  the  intervals  of  her  periods  is  but  little 
apt  to  transmit  gonorrhoea  becomes  an  active  centre  of  contagion  during 
menstruation.  The  menstrual  period  is  also  favourable  to  gonorrhoea! 
rheumatism. 

Description. — Let  us  first  consider  gonorrhoea  in  men.  The  appearance 
of  symptoms  is  usually  preceded  by  an  incubation  period  of  three  to  five 
days.     During  this  time  the  genital  organs  do  not  present  any  abnormality. 

On  the  third  or  fourth  day  a  burning  sensation  is  felt  at  the  end  of  the 
penis.  The  meatus  is  slightly  red,  and  the  lips  are  swollen  and  moist.  The 
glans  gradually  swells,  and  the  urethral  discharge  appears.  This  discharge, 
which  is  clear  and  thready  at  first,  rapidly  becomes  yellowish  or  greenish. 
It  is  sometimes  tinged  with  blood.  On  the  linen  it  leaves  a  stain,  which  is 
green  at  the  centre  and  yellow  at  the  periphery.  On  pressure,  we  can 
always  squeeze  out  a  few  drops  of  pus,  even  though  none  is  apparent  at  the 
meatus.  After  a  few  days  the  inflammation  becomes  severe,  the  penis  is 
swollen,  the  discharge  is  thick  and  profuse,  and  the  constant  presence  of  the 
pus  between  the  glans  and  the  prepuce  may  provoke  balanoposthitis. 
The  urethra  can  be  felt  as  a  tender  cord  on  the  lower  surface  of  the  penis. 
The  chordee  is  sometimes  so  painful  during  erection  that  the  patient,  in 
order  to  gain  relief,  attempts  to  straighten  the  penis  by  breaking  the  cord. 
The  effort  succeeds,  but  the  infiltration  of  pus  and  urine  into  the  inflamed 
tissues  leads  to  serious  mischief. 

During  micturition  the  burning  sensation  along  the  urethra  reaches  its 
maximum  (chaude-'pisse).  In  acute  cases  the  pain  is  unbearable,  and  the 
patient,  when  passing  water,  goes  through  various  contortions  without 
succeeding  in  relieving  the  pain.  He  holds  his  water  as  long  as  possible — 
as  a  result,  retention  of  urine  is  often  seen.  Gonorrhoea,  however,  is  not 
always  so  painful.  The  patient  complains  of  a  strain.  The  discharge  may 
then  be  the  chief  symptom,  and  the  term  "  running  "  is  applied ;  but  the 
nature  of  the  disease  is  identical. 

Acute  gonorrhoea  may  be  accompanied  by  fever  and  gastric  disturbance. 
At  night  the  patient  suffers  tortures  from  the  incessant  and  painful  erections. 
When  the  inflammatory  process  is  of  moderate  severity  it  is  limited  to  the 
anterior  urethra  ;  when  it  is  more  acute  it  may  involve  the  posterior  urethra 
and  neck  of  the  bladder. 

As  examination  of  the  perineum  does  not  always  reveal  the  exact  extent 
of  the  mischief,  the  method  of  using  two  glasses  must  be  employed.     For 


2048  TEXT-BOOK  OF  MEDICINE 

this  purpose  the  urine  is  collected  in  two  portions.  The  portion  collected  in 
the  first  glass  contains  flocculi  of  muco-pus  from  the  urethra  ;  the  second 
glass  is  to  receive  the  urine  still  contained  in  the  bladder.  If  the  second 
portion  contains  shreds  of  muco-pus,  the  posterior  urethra  is  inflamed.  In 
the  latter  event,  between  the  acts  of  micturition  a  small  quantity  of  muco- 
pus  takes  a  backward  course,  passing  through  the  sphincter  into  the  bladder, 
where  it  mixes  with  the  urine.  Each  specimen  of  urine  examined  will, 
therefore,  contain  muco-pus.  This  distinction  between  anterior  and  pos- 
terior urethritis  is  considered  to  be  of  importance  as  regards  treatment. 

Fatigue,  walldng,  prolonged  standing,  and  alcohol  increase  the  pain  and 
the  discharge. 

Gronorrhoea,  when  untreated,  lasts  from  four  to  six  weeks.  The  dis- 
charge gradually  becomes  yellow,  greyish,  less  thick,  and  less  profuse.  The 
pain,  whether  spontaneous  or  provoked  by  micturition,  is  less  severe.  The 
night's  rest  is  no  longer  disturbed  by  erections,  but  every  morning  a  drop 
of  yellowish  discharge  can  be  squeezed  out  from  the  meatus.  In  some  cases 
the  morning  drop  indicates  the  passage  of  the  disease  into  the  chronic  stage 
of  gleet.  As  long  as  this  slight  discharge  persists,  the  patient  is  liable  to  a 
relapse  as  the  result  of  walldng,  alcoholic  excess,  or  of  sexual  intercourse. 
These  relapses  may  occur  more  than  once,  and  on  each  occasion  the  gono- 
coccus  is  found,  although  it  may  have  disappeared  in  the  intervals  between 
the  attacks.  In  the  latter  variety  the  gonorrhoea  is  localized  in  the  cul-de- 
sac  of  the  membranous  portion  of  the  urethra,  whence  it  is  very  hard  to 
dislodge. 

In  women  acute  gonorrhoea  is  characterized  by  vulvitis,  by  yellowish 
or  greenish  vaginal  discharge,  and  by  burning  and  smarting  in  the  vagina, 
which  renders  examination  very  difficult.  The  acute  stage  is  usually  of 
short  duration,  and  the  gonorrhoea  rapidly  becomes  painless,  which  in  part 
explains  why  contagion  is  spread.  In  acute  gonorrhoea  the  vaginal  pus 
contains  gonococci,  but  after  the  acute  stage  they  are  not  found  in  the 
vagina,  although  they  are  present  in  the  urethra.  Gonorrhoeal  urethritis 
in  women  provokes  violent  pain  on  micturition.  A  drop  of  pus  can  be 
squeezed  out  from  the  meatus  when  pressure  is  made  on  the  urethra  from 
behind  forwards.     Cystitis  of  the  neck  of  the  bladder  is  common. 

A.  Local  Complications. 
Complications  in  Man. — During  the  acute  stage  the  infection  may 
extend  either  deeply,  causing  periurethral  lesions  (folliculitis,  cavernitis, 
and  cowperitis),  or  along  the  surface,  attacking  the  mucous  membranes 
continuous  with  that  of  the  urethra  (balano-posthitis,  prostatitis,  epididy- 
mitis, cystitis,  and  pyelonephritis).  The  latter  troubles  are  the  result  of 
ascending  infection.     The  lacunae,   crypts,   and  glandular  canals,   which 


VENKRRAL  DISEASES  2019 

communicate  with  the  urethra,  are  often  infected.  The  result  is  abscesses 
or  reservoirs  containing  gonococci,  ready  to  reinfect  the  urethra  aitftr  ap- 
parent recovery  from  the  gonorrhoea.  The  prostatitis  may  be  acute  or 
chronic.  It  is  usually  a  direct  consequence  of  posterior  urethritis.  In  most 
cases  there  is  merely  congestion  of  the  organ  ;  in  some  suppuration  occurs. 

Orchitis,  or  rather  epididymitis,  appears  during  the  third  or  fourth  week. 
It  is  accompanied  by  vaginal  it  is,  and  is  iishered  in  by  acute  pain  in  the 
testicle  and  along  the  cord.  The  scrotum  is  red  and  swollen.  The  pain  is 
increased  by  walking  and  by  the  friction  against  the  thighs  (patients, 
accordingly,  walk  with  their  legs  apart).  It  radiates  into  the  loins.  Orchitis, 
though  usually  single,  may  be  double,  the  testicles  being  attacked  siniul- 
taneouslv  or  in  succession.  It  recovers  without  suppuration,  save  in  ex- 
ceptional cases.  The  gonococcus  has  been  found  in  pus  of  suppurating 
orchitis. 

The  usual  treatment  consists  in  rest  in  bed,  leeches  in  acut€  cases,  and 
in  the  application  of  belladonna  and  mercury  ointment,  with  the  use  of 
a  suspensory  bandage  in  less  severe  cases.  The  chief  danger  in  double 
orchitis  is  sterility,  due  to  azoospermia.  Resolution  is  slow  in  every  case. 
Induration  in  the  tail  of  the  epididymis  lasts  for  many  months. 

Peritonitis,  though  extremely  rare,  has  been  seen.  It  is  strictly  localized. 
The  pathogenesis  admits  of  various  explanations.  The  ascending  infection 
is  said  to  take  place  by  the  lymphatics  and  bloodvessels  of  the  spermatic 
cord ;  or  by  the  upper  extremity  of  the  vas,  which,  like  the  vesiculse  seminales, 
is  covered  with  peritoneum  ;  or,  lastly,  by  a  special  lymphatic  of  the  vas. 

The  name  gleet  is  given  to  the  slight  chronic  discharge  that  may  follow 
gonorrhoea.  Gleet  is  usually  painless,  except  for  the  drop  of  pus  wliich  can 
be  squeezed  from  the  meatus  on  rising.  The  patient  has  no  trouble.  The 
discharge  may  be  increased  as  the  result  of  fatigue,  of  excesses,  or  of  the 
abuse  of  beer.  Between  the  attacks  the  muco-pus  may  contain  the  micro- 
organisms usually  found  in  the  urethra,  or  the  microbes  of  suppuration. 
The  gonococcus  usually  reappears  only  during  the  attacks.  Stricture  of  the 
urethra,  with  its  many  complications,  is  a  remote  result  of  gonorrhoea. 

Complications  in  Women. — Ascending  gonorrhoea  is  far  more  serious 
in  women  than  in  men.  It  commences  in  the  cervix.  It  then  invades  the 
body  of  the  uterus,  setting  up  acute  metritis,  due  to  the  gonococcus,  which 
may  or  may  not  be  associated  with  other  organisms.  Chronic  metritis  may 
follow  the  acute  trouble,  or  may  occur  from  the  first  in  the  course  of  chronic 
gonorrhoea. 

Acute  bartholinitis  is  nearly  always  gonorrhoeal ;  the  chronic  is  always 
so.  Bacteriological  examination  reveals  either  the  gonococcus  alone  or  the 
association  of  the  gonococcus  with  anaerobic  organisms.  The  pui>  from  the 
dandular  abscess  in  the  latter  case  is  often  foetid. 


2050  TEXT-BOOK  OF  MEDICINE 

In  its  ascending  course  the  gonococcus,  which,  may  or  may  not  be 
associate  with  other  organisms,  may  lead  to  salpingitis,  ovaritis,  peri- 
metritis, and  peritonitis.  Bosc  has  collected  twenty  cases  in  which  the 
gonococcus  was  the  cause.  In  three  of  these  cases  the  gonococcus  was 
found  not  only  in  the  pus,  but  also  in  the  waUs  of  the  tubes.  Wertheim  has 
thus  shown  that  the  microbes  traverse  the  wall  of  the  tube  in  order  to  reach 
the  ovaries  and  the  peritoneum.  Hartmann  and  Morax  have  found  the 
gonococcus  thirteen  times  in  pus  from  the  tubes,  and  in  thirteen  other  cases 
the  pus  was  sterile.  It  contained  the  streptococcus  four  times,  the  Bacillus 
coli  once,  and  the  pneumococcus  once.  Raymond  has  shown  that  the 
infection  spreads  from  the  uterus  to  the  tube  by  ascending  along  the  mucous 
membrane. 

It  is,  therefore,  proved  that  the  gonococcus  is  most  often  in  evidence  in 
many  diseases  of  the  uterus,  adnexa,  and  pehdc  peritoneum.  The  lesions 
produced  by  the  gonococcus  predispose  to  the  development  of  streptococcal 
infection  after  delivery  or  miscarriage.  We  know  that  gonococcal  infection 
and  puerperal  infection,  either  alone  or  in  combination,  are  the  two  great 
causes  of  salpingitis,  ovaritis,  perimetritis,  periovaritis,  and  peritonitis. 

Clinically,  pelvic  gonorrhoea  in  women  difiers,  according  as  it  is  acute 
or  chronic.  The  acute  form  is  characterized  by  the  appearance  of  marked 
pelvic  reaction  a  few  days  after  contamination.  The  symptoms  of  pelvic 
uifection  are  liable  to  supervene  at  the  first  menstruation  after  the  con- 
tagion. The  menses  may  be  advanced  or  delayed.  In  any  case,  they  are 
nearly  always  afiected.  The  symptoms  are  acute  pain  in  the  lower  part  of 
the  abdomen,  extreme  sensitiveness  of  the  abdominal  wall,  vomiting,  and 
constipation.  Fever  may  or  may  not  be  present.  If  the  lesions  are  marked 
on  the  right  side,  they  may  simulate  appendicitis.  Vaginal  examination  is 
difficult.  We  sometimes  find  in  the  culs-de-sac  a  firm  mass  fixing  the 
uterus. 

The  acute  form  remains  stationary  during  the  menstrual  period,  and 
the  symptoms  then  improve  so  much  that  recovery  is  expected.  As  the 
next  period  becomes  due,  the  peritoneal  symptoms  reappear.  This  form  is 
called  remittent  by  Noggerath.  It  may  end,  when  untreated,  in  suppura- 
tion, although  at  first  it  may  be  a  question  of  serous  perimetro-salpingitis 
rather  than  one  of  true  pelvic  suppuration.  These  forms  anatomically 
resemble  gonorrhceal  orchitis  in  man. 

The  chronic  form  may  follow  acute  attacks,  or  may  be  chronic  from  the 
first.  It  is  characterized  by  mild  peritoneal  reaction  and  by  menstrual 
troubles,  with  amenorrhoea  preceding  the  periodic  metrorrhagia.  Gonor- 
rhoea must  be  thought  of,  if  a  young  woman,  after  the  first  few  indulgences 
in  intercourse,  complains  of  pain  and  of  menstrual  disturbances  which  cannot 
be  explained  by  her  general  condition.     The  peritoneal  syndrome  seen  in 


VENEREAL  DISEASES  2051 

the  acute  form  is  replaced  by  a  uterine  syndrome,  comprising  pain  in  the 
lower  part  of  the  abdomen,  especially  on  walking,  neuralgia  in  the  pelvis, 
and  leucorrhosa. 

These  forms  of  pelvic  infection  in  women  never  endanger  life,  but  they 
induce  sterility  and  nervous  troubles,  rendering  the  woman  an  invalid. 
They  demand,  therefore,  early  and  thorough  treatment. 

The  diagnosis  of  these  pelvic  troubles  is  a  gynaecological  question. 
When  we  find  inflammatory  masses  around  the  uterus  and  its  adnexa,  we 
must  always  think  of  gonorrhoea  as  the  cause.  In  order  to  make  sure,  a 
minute  examination  of  the  patient  is  necessary,  and  in  the  absence  of 
delivery,  miscarriage,  or  uterine  trauma,  we  must  at  once  suspect  the 
gonococcus.  Young  girls  may,  after  gonorrhceal  vulvitis,  suffer  from  the 
foregoing  peritoneal  troubles,  since  gonorrhoea  is  far  from  rare  in  children. 
In  them  it  may  assume  three  chief  forms — acute  general  peritonitis,  which 
is  sometimes  grave,  sometimes  benign ;  localized  peritonitis ;  and  subacute 
peritonitis. 

The  treatment  of  pelvic  gonorrhoea  in  women  comprises  two  distinct 
parts — prophylactic  treatment,  in  which  the  object  is  to  prevent  sup- 
puration in  the  lesions  present ;  and  curative  treatment,  in  which  the  object 
is  to  relieve  the  troubles  of  suppurative  pelvic  peritonitis,  the  ovaries,  the 
tubes,  and  the  pelvic  peritoneum  forming  an  inflammatory  area  around  the 
uterus. 

As  regards  prophylactic  treatment,  we  must  distinguish  cases  in  which 
the  gonorrhceal  infection  is  limited  to  the  uterus,  with  or  without  slight 
salpingitis,  and  cases  in  which  the  gonorrhceal  infection  has  become  general 
in  the  adnexa.  In  the  case  of  gonorrhcsal  metritis,  the  uterus  must  be 
dilated  and  copious  intra-uterine  douches  given  daily.  Bozemann's  cannula 
is  most  useful.  For  irrigations,  solutions  of  sublimate  or  of  permanganate 
of  potassium  may  be  employed.  If  the  irrigations  do  not  cure  the  metritis, 
or  if  they  do  not  prevent  the  extension  of  the  gonococcus  to  the  tubes  and 
peritoneum,  an  injection  of  tincture  of  iodine  is  given  with  Braun's  syringe 
twice  a  week.  The  injection  should  be  followed  by  a  douche  of  boiled 
water,  in  order  to  remove  the  excess  of  iodine.  Absolute  rest  in  bed  is 
essential  during  the  treatment.  It  is  necessary  to  commence  the  treatment, 
even  though  the  period  has  not  completely  stopped,  and  to  suspend  it  only 
during  the  active  stage  of  the  flow.  We  know  how  menstruation  favours 
the  growth  of  the  gonococcus  and  increases  its  virulence. 

If  the  patient  is  already  suffering  from  salpingo-ovaritis,  the  intra- 
uterine douches  are  given,  and,  in  addition,  copious  vaginal  douches  at  a 
temperature  of  115°  to  120^  F.  Hot  compresses  should  be  applied  to  the 
abdomen. 

In  more  advanced  cases,  where  the  tubes,  ovaries,  uterus,  and  pelvic 


2052  TEXT-BOOK  OF  MEDICINE 

peritoneum  are  matted  together,  surgical  intervention  becomes  necessary ; 
but  we  must  remember  that  gonococcal  suppuration  has  a  marked  tendency 
to  recover,  and  we  must  give  the  patient  the  full  benefit  of  this  fact.  The 
simplest  procedure,  such  as  incision  of  the  posterior  cul-de-sac,  is  at  times 
sufficient.  We  can  by  such  an  incision  evacuate  large  collections,  which 
are  often  aseptic,  because  we  find  in  pelvic  gonorrhoea  serous  perimetro- 
salpingitis, which  clinically  resembles  the  streptococcal  collections  of  pus 
in  the  organs  and  in  the  pelvic  peritoneum. 

Curettage  should  never  be  advised.  While  this  operation  gives  excel- 
lent results  when  the  uterus  contains  fragments  of  placenta  and  pieces  of 
membrane,  yet  in  gonorrhoeal  endometritis  we  must  not  perform  it.  In 
the  latter  case,  the  infection  is  deeply  seated  in  the  culs-de-sac  of  the  glands, 
so  that  the  curette  may  favour  the  penetration  of  the  gonococci. 

B.  Gonococcal  Infection  of  the  Blood. 

Any  individual,  man  or  woman,  suffering  from  an  apparently  simple 
blennorrhagia,  may  be  attacked,  at  a  given  moment,  with  gonococcal 
infection  of  the  blood.  The  gonococcus  enters  the  blood  through  the 
venous  system,  and  the  infection,  at  first  local,  becomes  general.  Eor  this 
result,  it  is  not  even  necessary  that  the  gonorrhcea  be  active.  A  person 
looks  upon  a  declining  gonorrhoea  as  a  negligible  quantity,  when  there 
suddenly  appears  an  infection  of  the  blood,  that  only  too  often  proves  fatal. 
These  eventualities  demand  recognition.  Gonorrhoea  is  not  merely  a  local 
infection,  capable  of  causing  such  neighbouring  lesions  as  epididymitis 
and  salpingitis  ;  the  gonococcus,  having  entered  the  blood,  may  cause  the 
most  varied  and  the  most  formidable  lesions ;  acute  and  chronic  arthritis, 
ulcerative  endocarditis,  pericarditis,  broncho-pneumonia,  infarcts  in  the  lung, 
pleurisy,  peritonitis,  meningitis,  phlebitis,  infection  simulating  typhoid 
fever,  etc.,  are  complications  imputable  to  the  gonococcus. 

Infection  Simulating  Typhoid  Fever. — The  following  case  is  taken 
from  my  clinical  lectures  :  * 

.  On  February  9,  1909,  a  young"  man  was  admitted,  complaining  of  headaclie,  high 
fever,  and  continuous  diarrhoea  ;  the  condition  had  lasted  for  a  week,  and  his  physician 
had  diagnosed  typhoid  fever.  The  patient  certainly  had  the  look  of  a  typhoid  case. 
Lenticular  rose  spots  were  present  on  the  abdomen,  the  spleen  was  enlarged,  and  the 
temperature  was  102'°o  F.     Sweating  was  most  profuse  and  constant. 

On  the  second  day  after  his  admission,  a  harsh  mitral  murmur  was  audible.  The 
man  had  never  had  rheumatism.  The  appearance  of  endocarditis  and  the  profuse 
sweating  gave  us  cause  to  think.  While  endocarditis  is  frequent  in  articular  rheumatism, 
and  also  in  certain  infections,  it  is  very  rare  in  the  course  of  typhoid  fever.  In  order 
to  decide  the  point  Widal's  test  was  made  (on  the  fifteenth  day  of  the  disease,  and 

*  Dieulafoy.  "  Deux  cas  d'infection  sanguine  gonococcic."  Clinique  Medicale  de 
VHotel-Dieu,  10^  et  11«  lemons,  1909. 


VKXKIJKAI.   DISKASKS  20r,3 

afrnin  on  the  grvcnticnlk  day),  willi  in'^^'iilivti  ro.suKs,  vvliirli.  ilmrofort!.  f'xclu<l(!(l 
typhoid  fi'vor. 

C'aii'fiil  (•xaniiiiiiiion  rovoah-d  a  slij^'lH  uioisluro  at  tlio  urinary  meatus,  and  llic 
im1ion<  tohl  us  that,  a  nioiitli  bororf.  lie  had  a  jrotiorrho-a.  in  wliicli  llii^  dischar^T"  coasod 
directly  tlio  i'(>vt>r  apijoarcd.     Thi'  ^'ouococcus  was  i'ouml  in  tlio  urrtliral  dischar^fo. 

Ac'fordinjrly,  wo  coiududod  that  tin^  patioiit  was  suiVi-riii^'"  t'roiii  a  ;rouoco<H;ic 
iniVctioii  of  the  hh)od,  rosom1)liiif,'"  tyjdioid  fovcr.  in  spito  of  tho  fact  that  articular 
mnnift'statioiis,  whicli  aro  tlie  common  liall-mark  of  ^'•ouoeoccic  infections,  wore  absent- 

Le  Phiy  made  an  examination  of  the  blood,  and  obtained  cultures  of  the  gonococcufi 
in  a  pure  state,  uo  other  micro-ovfiranisms  liein^r  present. 

Sero-diajsrnosis  was  again  i^mployed,  and  revealed  the  absence  of  Eberth's  bacillus, 
of  the  A  and  B  paratyphoid  bacilli,  of  Giirtner's  i)aratyi)hoid  l)acillus,  and  of  the 
colon  bacillus. 

Our  conclusit>u.  theref(U'e,  was  correct.  Tlie  urine  was  copious,  and  did  not 
contain  albumin,  but  the  situation  grew  worse.  The  eruption  no  longer  deserved 
the  name  of  rose  spots ;  some  of  tlie  elements  were  prominent  reddish  papules.  The 
pulse  rate  was  l-D.  the  temperatiire  105^  F.,  the  tougue  was  dry  and  red,  the 
sweating  was  abuudant,  the  diai'rhcea  was  profuse,  the  murmur  remained  harsh, 
and  broncho-pneumonia  of  the  left  lung  appeared.  The  gonococcus  associated  with 
the  pneumococcus  was  found  in  the  sputum.  Injections  of  Wright's  gonococcic 
vaccine  were  given,  and  the  results  furnished  by  the  opsonic  index  were  recorded. 
The  symptoms  steadily  improved,  and  recovery  at  length  resulted. 

The  following  cases  are  of  a  sianlar  character: 

Thayer's  Case. — A  young  man,  who  had  been  suffering  from  gonorrhoea  for 
three  months,  was  taken  ill  with  headache,  malaise,  and  fever  (104°  F.).  The 
tongue  was  I'ed  and  the  spleen  was  enlarged.  Some  atypical  rose  spots  appeared 
on  the  abdomen.  A  systolic  murmur  was  audil^le.  Under  these  circumstances,  the 
diagnosis  remained  in  doubt  :  typhoid  fever,  or  gonococcal  septicfemia.  with  endo- 
carditis. Widal's  reaction  proved  negative,  and  blood  cultiu-es  revealed  the  gono- 
coccus; the  case  was,  therefore,  gonococcal  infection  of  the  blood,  simulating  typhoid 
fever. 

In  Harris  and  Johnston's  ca.se  the  diagnosis  was  in  favour  of  typhoid  fever,  but 
the  finding  of  the  gonococcus  in  the  blood  cleared  up  the  matter. 

The  above  cases  show  that  gonococcal  infection  may  simulate  typhoid 
fever  very  closely,  and  that  diagnosis  may  be  impossible  unless  we  employ 
sero-diagnosis  and  cultures  of  the  blood.  ^ 

The  following  case  (Surgeon-Major  Scherrer)  is  very  suggestive : 

A  soldier,  who  had  just  taken  part  in  a  test  march,  was  admitted  to  hospital 
on  March  5,  1909.  Three  days  later  a  trifling  urethral  discharge  was  discovered  by 
chance;  gonococci  were  present  in  great  numbers.  The  discharge  had  lasted  two 
weeks,  and  the  patient  had  apparently  forgotten  it.  On  the  evening  of  March  4,  the 
man,  who  had  not  felt  well  for  three  days,  was  taken  ill  with  chills,  headache,  and 
marked  lassitude.  He  s^ient  a  sleepless  night,  sweating  profusely.  Next  morning  his 
t<^mperature  was  lOo"  F.  In  the  evening  it  rose  to  104'.3'^  F..  and  the  jmlse 
rate  was  100.  Slight  dyspnoea  and  copious  diarrliosa  were  present.  During  the  next 
few  days  the  jnilse  was  dicrotic,  the  prostration  was  complete,  and  the  temperature 
very  high. 

The  diagnosis  was  strongly  in  favour  of  typhoid  fever,  but  Widal's  reaction  was 
negative.  The  condition  became  worse.  Hiccough  set  in,  the  belly  was  distended  and 
very  tender  on  pressure,  a  soft  me.so-systolic  murmur  Avas  audible.  Peritonitis  was 
now   suspected.      On   March    12,   pleuritic  effusion  was  found,  and  an  exploratory 

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2054  TEXT-BOOK  OF  MEDICINE 

puncture  gave  exit  to  a  turbid  fluid,  rich  in  gonococci.  The  patient  became  worse, 
and  died  in  a  state  of  collapse. 

The  autopsy  showed  that  the  cause  of  death  was  a  generalized  gonococcia,  no  lesion 
of  typhoid  fever  being  present.  The  findings  were  :  peritonitis  with  matting  of  the 
intestinal  coils,  and  some  purulent  fluid  in  the  pelvis.  A  smear  from  the  false 
membranes  covering  the  kidney  showed  numerous  gonococci.  Lungs  collapsed. 
About  a  pint  of  fluid  in  each  pleural  cavity,  this  fluid  being  purulent  and  containing 
many  gonococci.  The  mitral  valves  had  lost  their  transparency,  and  their  free  edge 
was  oedematous;  a  smear  made  from  a  concretion  on  the  mitral  valve  showed 
gonococci.  •  Urethra  thickened,  mucus  membrane  covered  with  a  viscid  deposit  in 
which  the  gonococcus  was  present.     No  trace  of  any  of  the  lesions  of  typhoid  fever. 

In  this  case  death  was  due  to  superacute  gonococcic  infection  of  the  blood,  and 
occurred  but  eight  days  after  the  patient  took  to  his  bed.  He  had  sufEered  from 
an  attack  of  gonorrhoea,  so  mild  that  he  had  forgotten  it. 

In  my  patients  who  suffered  from  gonococcic  blood-infection,  the  gono- 
coccus was  still  found  in  the  blood,  weeks  after  recovery. 

Articular  Manifestations. — Gonorrhoeal  rheumatism  ;  may  appear 
during  the  acute  stage,  or  during  the  decline,  even  after  the  discharge  has 
Leased,  but  more  often  in  persons  with  a  gleet.  In  exceptional  cases, 
according  to  Griffon,  it  may  precede  the  symptoms  of  urethritis — that  is 
to  say,  between  the  moment  of  contagion  and  the  commencement  of  the 
discharge.  Leyden  has  reported  a  case  of  gonococcal  arthritis  without  any 
sign  of  gonorrhoea. 

The  rheumatism  generally  supervenes  in  the  course  of  gonorrhoeal 
urethritis,  but  it  has  also  been  seen  in  persons  with  gonorrhoeal  ophthalmia. 
It  appears  to  be  more  common  in  men  than  in  women.  It  is  sometimes  seen 
in  children,  following  purulent  ophthalmia  or  vulvo- vaginitis.  It  may  occur 
in  various  forms.  The  general  rheumatic  form,  which  is  very  rare,  at  first 
sight  simulates  an  attack  of  rheumatic  fever,  with  these  differences,  how- 
ever— that  the  profuse  sweats  are  usually  absent,  that  the  general  symptoms 
are  less  severe,  and  that  salicylate  of  soda  has  no  effect.  In  this  acute  poly- 
articular form  several  joints  are  affected  together  or  in  succession,  but  in  a 
few  days  the  trouble  becomes  limited  to  one  or  two  jomts,  showing  a  marked 
preference  for  the  knee,  the  elbow,  and  the  wrist.  In  another  form  the 
arthritis  is  mono -articular  from  the  first.  Its  seat  of  election  is  the  knee 
and  the  elbow.  It  may,  however,  develop  in  the  instep,  in  the  wrist,  in  the 
costo-sternal  joints,  or  in  the  stemo- clavicular  articulation. 

These  pseudo-rheumatic  manifestations,  which  are  at  times  very  painful, 
may  affect  the  periarticular  tissue  even  more  than  the  joint  itself.  They 
are  accompanied  by  swelling,  induration,  and  redness  of  the  tissues  to  the 
extent  of  simulating  cellulitis.  The  effusion  may  be  sero-fibrinous,  sero- 
purulent,  or  purulent.  In  exceptional  cases  the  pus  may  make  its  way 
through  the  capsule  of  the  joint,  and  spread  under  the  skin  and  between 
the  neighbouring  muscles.     The  acute  arthritis  may  be  present  only  in 


VENEREAL  DlSliiASES  2055 

oiitlirui  (art]inil«^M<i),  or  may  change  into  liydraHlirosis  of  long  fliiration. 
(Umorrlupal  rluuiniatism  may  also  assume  the  tyfKi  of  hydrarthrosis  from 
the  first. 

Gonorrluua  may  give  rise  to  spondijlose  rhizomelifpic  (Marie).  We  may 
find  ankylosis  of  the  vertebral  column,  and  sometimes  also  of  the  shoulders 
and  hips.  It  is  strange  that  the  other  joints  are  spared.  I  have  seen  the 
following  case  at  the  Hotel-Dieu  : 

Tho  patient,  on  admission,  walked  into  the  ward  with  his  back  arcliod  and  liis  head 
bont  forwards.  AV'hon  ho  was  spoken  to  he  raised  liis  head  a  Uttie,  but  his  ))ack  re- 
mained bont,  and  ho  could  not  straighten  it.  When  be  was  told  to  pick  up  anything, 
lie  flexed  tho  trunk  on  the  pelvis  ;  but  this  flexion  being  insufficient,  he  was  compelled 
to  bend  his  knees,  and  to  lower  himself  stiffly,  in  order  to  touch  the  floor.  When  ho  was 
in  bed,  he  placed  one  pillow  lujder  his  neck  and  another  under  his  knees.  In  this  way 
ho  avoided  the  pain  caused  by  straightening  his  spine.  Percussion  of  the  spine  was 
painful,  but  the  pain  was  not  fixed,  as  in  Pott's  disease.  No  deformity  of  the  vertebra 
was  present. 

The  disease  was  of  three  years'  duration.  It  had  commenced  with  pain  in  the 
vertebral  column.  The  whole  spine  was  the  seat  of  incomplete  and  painful  ankylosis. 
The  shoulders  and  the  hips  were  not  affected.  The  case  was  therefore  an  imperfect 
example  of  Marie's  syndrome.  This  case  is  interesting  as  regards  its  aetiology,  the 
gonorrhoea  having  been  surprised  flagrante  delicto.  Gonorrhoea  has  figured  in  the 
ajtiology  of  several  cases  (Leri,  Bouchard),  but  in  this  case  it  had  been  present  in  a 
chronic  state  for  four  years,  and  the  vertebral  pain  had  come  on  six  months  after  the 
appearance  of  the  discharge. 

Gronorrhceal  arthritis  often  runs  a  subacute  course.  It  has  a  tendency 
to  pass  into  the  chronic  state,  and  to  be  followed  by  adhesions  which  limit 
movement  or  which  favour  dislocations.  These  dislocations  impede  the 
free  play  of  the  articular  surfaces.  Widal  has  shown  the  previous  role  of 
hydrarthrosis  in  the  pathogenesis  of  spontaneous  dislocation  of  the  elbow 
due  to  gonorrhoeal  mischief.  True  ankylosis,  which  is  rare,  follows  the 
so-called  plastic  form.  Cornil  has  made  a  microscopic  examination  in  a 
case  of  gonorrhoeal  rheumatism  with  ankylosis  and  deformity.  The  lesions 
were  especially  characterized  by  invasion  of  the  cartilage  by  the  synovial 
membrane,  and  by  the  tendency  to  fibrous  and  bony  ankylosis. 

Another  feature  of  gonorrhoeal  arthritis  is  the  early  and  rapid  muscular 
atrophy,  which,  even  in  the  absence  of  ankylosis,  hampers  for  a  long  while 
the  functions  of  the  affected  limb.  Deformities  of  the  joints  are  often 
present,  especially  in  certain  chronic  forms.  Chronic  gonorrhoeal  rheu- 
matism may  assume  two  different  types — the  chronic  fibrous  type  and  the 
nodular  pseudo-gouty  type.  The  nodular  type  has  a  predilection  for  the 
small  joints.  The  X  rays  have  shown  the  nature  and  extent  of  the  bony 
lesions,  and  Achard  has  demonstrated  that  in  gonorrhoeal,  as  in  ordinary 
arthritis  deformans,  we  find  lesions  of  the  bones  and  of  the  periosteum  and 
osteophytes.  When  the  joints  of  the  fingers  are  affected,  the  fingers  may 
have  a  peculiar  fusiform  shape  {doigt  en  radis,  Fournier).     Lastly,  gonorrhoeal 

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2056  TEXT-BOOK  OF  MEDICINE 

rheumatism  may  cause   the    affected   joint  to    become   a    locus  minoris 
resistenticB.     The  tubercle  bacillus  may  then  invade  the  joint. 

The  tendon  sheaths,  especially  those  on  the  dorsal  aspect  of  the  wrist, 
and  the  bursse,  especially  the  subcalcaneal,  are  often  affected,  either  alone 
or  at  the  same  time  as  the  joints.  Talalgia  of  gonorrhoeal  origin  is  now  well 
recognized.  It  is  very  persistent,  often  lasting  for  months.  It  commences 
either  as  a  lesion  of  calcaneal  bursa,  or  in  an  ossification  of  the  insertion  of 
the  plantar  fascia  and  of  the  tendo  Achillis  into  the  os  calcis.  It  is  said  that 
suppuration  never  occurs  in  the  bursa  (Fournier,  Verneuil). 

I  have,  however,  seen  an  interesting  case  of  suppuration  in  the  bursa  between  the 
great  trochanter  and  tensor  vaginae  femoris.  The  bacteriological  examination  was  most 
carefully  made  in  my  laboratory.  The  gonococcus  was  found  in  a  pure  state  in  the 
contents  of  the  pocket.  A  woman  who  had  suffered  from  very  mild  s3Tnptoms  of 
gonorrhoea  showed  a  series  of  joint  troubles,  which  ran  the  clinical  course  of  gonorrhoeal 
rheumatism.  The  knees  and  the  maUeoU  had  been  in  turn  attacked,  when  the  patient 
felt  acute  pain  in  the  left  thigh.  The  upper  part  of  the  thigh  was  swoUen,  but  streaked 
with  dilated  veins,  and  painful  on  the  sUghtest  touch.  We  succeeded,  however,  in 
making  out  a  very  tense  mass  beneath  the  glutei  and  the  tensor  vaginae  femoris.  Next 
day  the  situation  of  the  lesion  was  more  evident :  the  hip-joint  was  free,  the  trouble 
was  in  the  bursa,  between  the  trochanter  and  the  tensor  vaginae  femoris.  Fluctuation 
was  evident.  A  puncture  was  made,  and  the  pus  was  at  once  examined.  Stained 
films  and  cultures  on  appropriate  media  showed  that  the  gonococcus  was  alone  present. 
This  case  was  the  first  in  which  blood-agar,  as  advised  by  Bezan9on  and  GriflEon,  was 
employed  in  order  to  demonstrate  the  gonococcus.  The  patient  recovered  after  three 
punctures.  No  other  troubles  were  observed  in  the  synovial  membranes  or  in  the  . 
tendons  heaths. 

The  various  theories  put  forward  at  the  celebrated  discussion  at  the 
Societe  Medicale  des  Hopitaux  in  1867  regarding  the  nature  of  gonorrhoeal 
rheumatism  may  be  summed  up  as  follows  :  (1)  Gonorrhoeal  rheumatism  is 
an  ordinary  rheumatism,  developed  on  account  of  gonorrhoea ;  (2)  gonor- 
rhoeal rheumatism  is  the  result  of  a  special  intoxication,  which  differs  from 
the  rheumatic  diathesis. 

The  latter  theory,  put  forward  by  Fereol,  at  a  time  when  the  theories  of 
micro-organisms  were  in  their  infancy,  has  daily  gained  ground.  In  an 
individual  with  gonorrhoea  the  gonococcus  may  enter  the  circulation,  and 
give  rise  to  a  series  of  complications,  including  gonorrhoeal  rheumatism. 
This  entrance  of  the  gonococcus  into  the  blood-stream  takes  place  by  a 
kind  of  "  microbic  discharge."  Thayer  and  Blumer  have  caught  the 
process  in  the  act  by  obtaining  cultures  of  the  gonococcus  on  media  inocu- 
lated with  blood  withdrawn  during  life  from  the  brachial  vein  in  a  case  of 
gonorrhoeal  endocarditis.  There  is,  however,  no  septicaemia.  The  gono- 
coccus does  not  flourish  in  the  blood  of  the  general  circulation.  It  speedily 
confines  itself  to  the  serous  tissues,  and  especially  to  the  synovial  membranes 
of  the  joints  and  tendons.  Why  this  affinity  for  the  serous  tissues  ? 
Bezangon  and  Griffon  think  that,  while  the  parenchymata  can  destroy 


VENEREAL  DISEASF.S  20r.7 

in  slfn  organisms  brought  })y  the  blood,  tlie  scnms  niombranes  (organs  of 
feoble  vitality  and  of  cells  not  liiglily  dilTerentiated)  defend  themselvea 
feebly  against  this  invasion,  and  that  the  struggle,  which  is  in  favour  of  the 
organism  in  all  the  other  regions,  is  in  favour  of  the  microbes  in  the  serous 
membranes. 

However  this  may  be,  tliero  is  a  long  list  of  cases — twenty-nine — regarding  tho 
presence  of  tho  gonococcus  in  gonorrhtual  arthritis.  I  may  mention  the  observations 
of  Doutschraann  (1890),  Lindemann  (1892),  Stem  (1892),  Rendu,  Hock  (1893), 
Neisser  (1894),  Bordoni-Uffreduzzi  (1894),  and  that  of  Finger  ( 1894),  concerning  arthritis 
of  tho  left  knee,  following  gonorrho?al  ophthalmia  in  a  new-born  infant.  Haushalter 
mentions  an  example  of  gonorrhoeal  rheumatism  which  supervened  during  the  course 
of  gonorrhoeal  ophthalmia  in  a  child  twenty-five  days  old.  Griffon  has  published  a  very 
interesting  case  of  a  similar  nature:  A  new-bom  infant  suffered  from  purulentophthalmia 
and  multiple  arthritis,  in  which  the  gonococcus  existed  alone  or  in  association  with  other 
organisms.  I  may  also  quote  Seiffert's  case  of  a  girl,  four  years  of  age,  with  gonor- 
rhu'al  vulvitis  and  multiple  arthritis.  One  wrist  became  swollen,  and  the  gonococcus 
was  found  in  the  Huid  removed  by  puncture.  Cultures  of  this  organism  were  also 
obtained  by  sowing  the  pus  in  the  Huid  from  an  ovarian  cyst.  Finally,  Morcier  and 
Metenier  have  seen  a  case  of  arthritis  of  the  knee  due  to  the  gonococcus,  in  the  course 
of  an  attack  of  gonorrhoea.  The  identity  of  the  gonococcus  was  established  by  micro- 
scopical examination  and  by  cultures. 

The  cases  of  tenosynovitis  in  which  the  gonococcus  has  been  found  are  quite  as 
conclusive,  although  they  are  not  so  numerous.  I  may  quote  that  of  Tollemer  and 
Macaigne  (1893),  that  of  Jacobi  and  Goldmann  (1894),  and  lastly  one  of  my  own, 
already  mentioned. 

The  question  is,  therefore,  decided.  The  articular  manifestations  of 
gonorrhoeal  rheumatism  are  of  an  infective  nature,  and  are  due  to  the 
presence  of  the  gonococcus  in  the  joints,  synovial  membranes,  buisse,  and 
tendon  sheaths.  If  the  search  for  the  gonococcus  has  often  been  negative 
in  the  past,  it  is  because  we  did  not  know  how  to  cultivate  this  microbe, 
which  requires  special  media,  and  which  is  so  delicate  that  it  must  be  sown 
and  placed  in  the  oven  as  soon  as  it  is  withdrawn  from  the  synovial  fluid. 
On  the  other  hand,  it  seems  to  disappear  rapidly  from  exudates  ;  whence 
the  precept  of  making  the  analysis  as  soon  as  possible  after  the  onset  of  the 
lesion.  The  case  of  peritrochanteric  synovitis  already  mentioned  is  most 
instructive  from  this  point  of  view.  Three  punctures  were  made,  some  days 
apart.  In  the  first  (made  on  the  day  after  the  symptoms  appeared) 
numerous  gonococci  were  found ;  in  the  second  the  result  was  positive, 
but  the  colonies  were  fewer  in  number ;  in  the  third  the  result  was 
negative. 

Burci  and  Bespighi  have  published  a  very  suggestive  case.  The  fluid 
removed  from  the  knee  was  sterile.  A  buttonhole  incision  was  therefore 
made  in  the  sxmovial  membrane,  and  the  vegetations  covering  it  were 
curetted.     In  the  debris  thus  removed  the  gonococcus  was  found. 

Positive  results  in  gonorrhoeal  arthritis  will  become  more  numerous  in 


2058  TEXT-BOOK  OF  MEDICINE 

the  future.  In  order  to  explain  the  so-called  sterile  effusions,  it  is  unneces- 
sary to  invoke  the  influence  of  the  nervous  system  or  the  action  of  a  toxine 
of  which  we  have  but  an  imperfect  knowledge. 

The  treatment  of  gonorrhcBal  rheumatism  is  chiefly  local.  In  the  acute 
stage  the  joint  must  be  fixed  in  good  position  after  an  ointment  of  methyl 
salicylate  or  Trousseau's  plaster  has  been  applied.  Later,  blisters,  counter- 
irritants,  and  massage  will  hasten  resolution  and  prevent  stiffness.  In  the 
suppurative  form  surgical  intervention  is  indicated. 

Gonorrhoeal  periostitis  is  not  uncommon.  It  is  found  in  the  neighbour- 
hood of  the  epiphyses,  either  alone  or  in  conjunction  with  periarthritis. 
Finger  has  found  the  gonococcus. 

Gonorrhoeal  pleurisy  has  been  demonstrated  by  bacteriological  examina- 
tion, Mazza,  Bordoni-Affreduzzi,  and  Cardile  having  found  the  gonococcus 
in  the  pleuritic  fluid.  In  one  of  my  reported  cases  (Clinique  de  VSotel- 
Dieu)  the  gonococcus  was  found  in  the  sputum,  it  was  a  case  of  gonococcal 
pneumonia. 

Cardio- Vascular  System. — Gonorrhoeal  endopericarditis  may  be  inde- 
pendent of  the  rheumatic  attack,  since  the  articular  manifestation  and  the 
cardio- vascular  manifestation  are  both  dependent  on  the  gonococcal  infec- 
tion. As  a  matter  of  fact,  gonorrhoeal  endopericarditis  has  occurred  in 
some  instances  apart  from  any  joint  trouble.  Several  of  these  cases  are 
mentioned  in  Cart's  paper. 

Prevost.  Endocarditis  appearing  on  the  fifth  day  of  an  attack  of  gonorrhoea,  and 
unaccompanied  by  arthritis.  In  a  fatal  case  of  ulcerative  endocarditis,  consecutive  to 
gonorrhoea.  His  found  diplococci  resembUng  the  gonococcus  and  decolorizing,  with 
Gram.  Councilman,  in  1893,  saw  a  case  of  gonorrhoea,  with  arthritis,  pericarditis,  and 
abscesses  in  the  cardiac  muscle.  The  gonococcus  was  found  in  the  urethra,  joints, 
pericardium,  and  abscesses.  Winterberg,  in  1894,  found  the  gonococcus  in  the 
mitral  valve  in  a  case  of  ulcerative  endocarditis,  consecutive  to  gonorrhoea  with  arthritis. 
Leyden,  in  1893,  proved  the  presence  of  the  gonococcus  in  the  valvular  thrombus  of  the 
left  ventricle  in  a  case  of  endocarditis  following  on  gonorrhoea,  with  arthritis  and 
epididymitis. 

Thayer  has  reported  the  case  of  a  woman  who  died  from  general  gonococcal  infection, 
with  ulcerative  endocarditis.  The  bacteriological  examination  revealed  the  presence 
of  the  gonococcus  in  the  vegetations  on  the  mitral  valve.  In  one  of  Rendu  and  Halle's 
cases  the  symptoms  of  the  gonococcal  infection  were  obscure.  It  began  with  metritis, 
and  involved  the  elbow  and  the  endocardium.  The  autopsy  revealed  the  gonococcus 
in  the  pericardium  and  in  the  vegetations  of  the  endocardium  ;  cultures  showed  that  the 
gonococcus  was  not  associated  with  other  microbes. 

Widal  and  Faure  BeauMeu  have  found  the  gonococcus  in  the  blood  during  Kfe, 
while  the  autopsy  showed  endocarditis,  with  gonococci  in  the  mitral  vegetations. 

It  is,  therefore,  proved  that  the  gonococcal  infection  may  become  general, 
and  determine  pericarditis,  endocarditis,  and  abscesses  in  the  breast,  with 
or  without  concomitant  gonorrhoeal  arthritis.  The  endocarditis  may  be 
simple,  relatively  benign,  and  analogous  in  every  respect  to   rheumatic 


VENEREAL  DISEASES  2059 

endocarditis,  or  it  may  be  niiilij};nant  and  of  tho  aoptica^inic  or  typhoid 
variety. 

In  addition  to  tho  cardiac  complications,  let  mo  note  gonorrhoBal  phlebitis, 
of  which  undoubted  cases  have  been  reported. 

Other  Complications. 

Nervous  System. — Tlie  nervous  system  may  be  attacked  by  the  gonor- 
rhoea! infection.  Peripheral  neuritis  is  the  most  important  lesion,  and  is 
usually  found  in  the  lower  limbs.  Many  years  ago  Fournier  noted  the  fre- 
quency of  sciatica.  It  is  usually  benign,  of  short  duration,  and  is  not 
followed  by  atrophy.  Cros  has  collected  cases  of  crural  and  lumbo- abdominal 
neuralgia.  I  have  seen  two  cases  of  intercostal  neuralgia.  Gonorrhoea! 
myelitis  has  been  described  by  several  writers.  It  usually  assumes  the 
diffuse  dorso-lumbar  type.  In  the  only  case  in  which  a  bacteriological 
examination  has  been  made  staphylococci  were  found  in  the  effusion  around 
the  pia  mater.     The  gonococcus  was  absent  (Barrie). 

The  cranial  meninges  and  the  brain  itself  may  be  attacked  by  gonorrhoea. 
Cerebral  complications  are,  however,  very  rare.  They  may  be  of  four 
distinct  types — delirious,  maniacal,  meningitic,  and  apoplectic.  In  the  two 
latter  the  prognosis  is  very  grave. 

Kidney. — Albuminuria  is  frequent.  We  may  justly  admit  a  gonorrhoeal 
nephritis,  dependent  on  the  ascending  migration  of  the  gonococcus  or  on 
secondary  infections.  It  is  more  often  consecutive  to  changes  in  the  epi- 
thelium produced  by  elimination  of  the  toxines. 

Sense  Organs. — The  gonococcus  may  develop  on  the  conjunctiva,  and 
give  rise  to  most  serious  purulent  ophthalmia.  Two  cases  may  be  met  with  : 
(1)  An  individual  suffering  from  gonorrhoea  has,  in  addition,  gonorrhoeal 
conjunctivitis  due  to  auto-contagioni ;  (2)  conjunctivitis  in  a  person  who 
is  free  from  urethral  or  vaginal  gonorrhoea.  In  this  event  the  conjunctivitis 
is  due  to  hetero-contagion.  This  form  is  seen  in  the  new-born  from  infec- 
tion during  delivery.  The  existence  of  a  benign  so-called  spontaneous  con- 
junctivitis has  been  admitted.     It  is  due  to  infection  by  the  blood-stream. 

Auditory  troubles  of  labyrinthine  origin  have  been  noted. 

The  [lonorrhaal  erythemata  may  be  simple,  nodular,  urticarial,  poly- 
morphous, or  purpuric.  They  may  occur  apart  from  any  absorption  of 
balsams.     Cutaneous  horns  have  at  times  been  met  with. 

Ano-Rectal  Gonorrhoea. — This  localization  of  gonorrhoea  is  extremely 
rare.  It  is  more  common  in  women  than  in  men.  The  close  relation 
between  the  vulvar  and  anal  orifices  make  inoculations  of  the  anus  more 
easy  in  women.     Ano-rectal  gonorrhoea  may  be  acute  or  chronic. 

In  the  acute  form,  the  margin  of  the  anus  is  erythematous  or  shows 
geographical  ulcers.     The  rectal  mucous  membrane  is  red,  swollen,  thickened, 


2060  TEXT-BOOK  OF  MEDICINE 

and  ulcerated.  It  bleeds  readily,  and  in  some  cases  vegetations  are  seen. 
There  is  a  constant  discharge  of  muco-pus.  The  symptoms  are  those  of  more 
or  less  severe  proctitis — itching,  burning,  pain  radiating  along  the  sacrum  to 
the  bladder,  uterus,  loins,  and  thighs.  The  pain  on  defeecation  is  sometimes 
most  acute,  on  account  of  the  spasm  of  the  sphincter  and  of  the  fistulae 
which  are  usually  present.  With  the  tenesmus  and  incessant  desire  to 
stool  we  often  find  a  more  or  less  extensive  prolapse  of  the  mucous  mem- 
brane of  the  rectum.  Dysuria  is  the  rule.  The  anal  discharge  is  slight  at 
fijst,  but  soon  becomes  abundant,  purulent,  and  yellow,  as  in  gonorrhoeal 
vaginitis.  It  causes  excoriation  of  the  skin  at  the  margin  of  the  anus. 
The  local  condition,  which  is  exceedingly  painful,  may  cause  fever  and 
anorexia.  Gonorrhoeal  proctitis  is  similar  in  its  course  and  duration  to 
gonorrhoeal  urethritis.  It  only  becomes  chronic  in  the  absence  of  treatment. 
The  chronic  form  is  exceptional,  and  when  it  is  present  it  persists  indefinitely. 
Gonorrhoeal  proctitis  is  not  exempt  from  complications.  Some  are  early — 
condylomata,  ano-rectal  abscess,  and  fistula ;  others  are  late — stricture  of 
the  rectum. 

The  diagnosis  is  important.  Simple  rectitis  from  pederastia,  ano-rectal 
chancre,  fistula,  piles,  and  polypi  must  be  distinguished  from  ano-rectal 
gonorrhoea. 

The  treatment  consists  in  lavage  with  solutions  of  corrosive  sublimate 
(1  in  2,000)  or  of  permanganate  (1  in  3,000).  Tuttle's  cannula  may  be 
employed  for  rectal  irrigation.  Sitz-baths  are  to  be  recommended.  In  the 
intervals  of  lavage  the  diseased  parts  should  be  dusted  with  iodoform,  oxide 
of  zinc,  or  aristol. 

Diagnosis. — In  man  gonorrhoeal  urethritis  is  usually  easy  to  recognize. 
Urethritis,  due  to  the  passage  of  septic  instruments  or  consecutive  to  coitus 
with  a  woman  suffering  from  leucorrhoea,  is  distinguished  by  its  short  dura- 
tion and  by  the  benign  nature  of  the  local  troubles.  Chancre  of  the  anterior 
urethra  is  sometimes  accompanied  by  purulent  discharge,  but  palpation 
reveals  the  presence  of  a  hard  nodule.  As  regards  acute  gouty  urethritis, 
it  is  far  from  being  accepted.  In  all  these  cases,  moreover,  bacteriology 
will  decide  the  point.  Microscopical  examination  of  the  pus  after  staining 
with  methylene  blue  will  give  prompt  information,  and  it  will  be  unnecessary 
to  make  cultures  with  the  pus.  The  morphological  features  of  the  gono- 
coccus  are  :  diplococcus,  grouped  en  masse,  intracellular,  and  decolorized 
after  Gram's  reaction.  The  aspect  of  the  pus  cells,  crammed  with  diplo- 
cocci,  leaves  no  room  for  doubt. 

It  is  a  different  matter  when  the  discharge  is  scanty  and  matutinal,  or 
when  it  is  reduced  to  a  few  shreds  suspended  in  the  urine  passed.  We  must 
then  collect  the  morning  drop  or  squeeze  the  shreds  between  two  slides, 
repeat  the  examinations  as  long  as  they  are  negative,  and  especially  have 


VENEREAL  DISEASES  20r,l 

recourse  to  rulluros  on  ;4)}Ji(>priiite  media.  TIk;  culture  is  diliicult  to  make, 
but  the  information  given,  if  it  is  positive,  is  so  important  that  it  must  be 
made  whenever  possible.  The  drop  or  the  shred  is  at  once  placed  on  the 
culture  medium  (blood-agar) — in  other  words,  the  drop  should  not  be  kept 
for  some  hours  in  a  i)ij)ette,  as  is  often  done  in  the  case  of  pus  or  of  exudates. 
The  gonococcus  rapidly  loses  its  vitality.  It  is  better  to  bring  the  patient 
to  the  laboratory,  and  as  soon  as  the  pus  has  been  sown  the  culture-tube 
must  be  placed  in  the  oven. 

In  chronic  gonorrhoea,  as  the  urethral  discharge  is  often  scanty,  we  may 
confound  it  with  the  discharge  which  accompanies  tuberculosis  of  the 
testicle  and  of  the  prostate.  All  doubt  will  be  removed,  however,  by 
examination  of  the  testicle  and  prostate  apart  from  bacteriological  examina- 
tion. In  women  gonorrhoea  is  far  more  difficult  to  diagnose.  The  dis- 
covery of  the  gonococcus  is  of  great  importance';  the  existence  of  urethritis 
is  a  diagnostic  point  of  value.  In  the  opposite  event  it  is  at  times  necessary 
to  examine  and  even  to  cultivate  the  contents  of  the  cervix  uteri. 

In  a  number  of  cases  of  cystitis,  orchitis,  and  especially  of  arthritis,  we 
are  called  upon  to  examine  for  gonorrhoea.  Without  mentioning  the 
principal  differences  between  true  and  gonorrhoeal  rheumatism,  it  is  well 
known  that  rest  in  bed  may  cause  so  great  a  diminution  in  the  urethral 
discharge  that  we  must  squeeze  the  penis  in  order  to  obtain  a  few  drops 
of  pus.  In  women  the  diagnosis  may  be  even  more  embarrassing,  but  the 
evolution  of  gonorrhoeal  arthritis  permits  us  to  make  a  diagnosis  even  in 
cases  where  gonorrhoea  cannot  be  suspected. 

When  the  gonorrhoeal  infection  simulates  a  typhoid  condition,  cultures 
made  from  the  blood  will  reveal  the  gouococcus. 

Treatment. — Gonorrhoea,  when  untreated,  shows  a  natural  tendency  to 
recover  in  a  few  weeks.  There  are,  however,  certain  hygienic  rules  which 
the  patient  should  follow  if  he  does  not  wish  the  discharge  to  increase,  and 
desires  to  escape  the  complications  already  described  :  rest,  abstention  from 
exercise — cycling,  dancing,  riding,  and  long  walks — suppression  of  all  alcohol, 
and  especially  of  beer,  of  acid  or  spiced  foods.  Alkaline  drinks  and  hot  baths 
are  all-important. 

In  men  the  bromides  should  be  given  for  the  nocturnal  erections.  When 
the  acute  stage  is  subsiding,  we  may  employ  astringent  injections  of  sulphate 
of  zinc,  tannin,  quinine,  nitrate  of  silver,  or  resorcin.  We  may  also  give 
cubebs,  copaiba,  or  sandal-wood  oil.  Considerable  improvement  may 
result  from  irrigation  of  the  urethra  with  a  solution  of  permanganate  of 
potash  (1  in  4,000).  In  anterior  urethritis  the  irrigation  is  made  with  the 
canal  open.  Two  litres  of  the  warmed  solution  are  allowed  to  flow  over  the 
surface  of  the  mucosa.  In  posterior  urethritis  the  pressure  of  the  fluid  must 
be  increased,  and  the  injection  made  to  enter  the  bladder.     The  urethra  is 


2062  TEXT-BOOK  OF  MEDICINE 

thus  washed  out  from  behind  forwards.  Microscopic  examination  is  required 
in  order  to  determine  the  therapeutic  indications.  If  the  gonococcus  is 
absent,  permanganate  of  potash  should  not  be  used.  If  another  organism 
is  present,  we  should  employ  injections  of  corrosive  sublimate  or  of  silver 
nitrate.  We  may  content  ourselves  with  ordering  balsams  if  we  do  not 
find  organisms  in  the  exudate.  The  chronic  nature  of  the  urethritis  may 
demand  instillation  of  nitrate  of  silver  by  G-uyon's  method. 

In  women  the  urethral  injections  should  be  supplemented  by  vaginal 
injections  of  a  very  hot  solution  of  permanganate  of  potash  twice  daily. 

Treatment  of  Gonorrhosal  Arthritis. — In  the  acute  stage,  the  joint  is 
fixed  in  good  position,  while  an  ointment  of  methyl-salicylate  is  applied ; 
we  may  also  employ  hot  compresses  or  apply  leeches,  giving  aspirin  or 
injections  of  morphine. 

At  the  Hotel-Dieu  we  have  obtained  excellent  results  with  douches  of 
superheated  air  (full  details  are  given  in  tlie  Appendix). 

Wright's  Gonococcic  ¥accine. — Details  are  given  in  the  Appendix.  I 
will  here  give  a  summary  of  lectures  published  in  the  Clinique  de  r Hotel- 
Dieu,  regarding  treatment  with  gonococcic  vaccine,  under  the  following 
headings  :  1,  urethritis  and  vulvo- vaginitis ;  2,  epididymitis  ;  3,  arthritis ; 
4,  general  gonococcic  infection. 

Urethritis. — According  to  Wright,  the  vaccine  lessens  the  discharge 
and  the  pain.  Mante  has  treated  three  cases  of  acute  urethritis ;  in  one 
case,  the  discharge  and  the  gonococci  disappeared  in  five  days ;  in  the  other 
two  cases  the  result  was  negative.  Brack,  writing  in  1909,  states  that  he 
had  no  success  in  acute  or  chronic  gonorrhoea  with  injections  of  gonococcic 
vaccine.     In  my  own  cases  the  results  have  not  been  very  conclusive. 

YulYO-Yaginitis. — Churchill  and  Soper's  results  are  as  follows :  Out  of 
eighteen  young  girls,  regularly  treated  with  the  vaccine,  nine  were  watched 
after  leaving  the  hospital.  Of  these  nine  cases  four  went  home  to  their 
parents  ;  three  showed  gonococci  several  months  later,  and  one  was  cured. 
As  regards  three  children  who  remained  in  hospital,  their  cure  was  per- 
manent. The  total  was  four  cures  in  seven  cases.  Two  others  left  the 
hospital,  and  had  shown  no  gonococci  for  a  week.  The  number  of  gono- 
cocci injected  varied  from  15  to  80  millions.  The  injections  did  not 
have  a  constant  effect  upon  the  vaginal  secretion,  which  diminished  or 
increased  without  furnishing  any  definite  rule  whereby  to  direct  the  treat- 
ment. 

Hamilton  and  Cooke  report  sixty  cases  of  vulvo-vaginitis  in  young 
girls,  dividing  them  into  two  groups  of  thirty  cases.  In  one  group  all  the 
patients  were  treated  with  the  vaccine;  of  the  other  group  none  were 
treated  with  the  vaccine.  In  the  first  group,  eighteen  left  the  hospital, 
free  from  discharge  and  from  gonococci ;  in  the  second  group  only  eight 


VENEREAL  DISEASES  20C3 

were  cured  in  tlie  same  time.  The  writers  conclude  that  the  vaccine  ^ivo3 
excellent  results  and  shortens  the  duration  of  the  disease.  They  think  it 
advisable,  though  not  absolutely  necessary,  to  take  the  opsonic  index  during 
the  treatment.  There  is  uo  relation  between  the  viilvo-vaginal  secretion 
and  tlie  oj)Souic  index. 

Ihitler  and  Long,  using  the  opsonic  index  as  a  guide,  have  employed 
the  vaccine  in  twenty-five  cases  of  gonococcal  vulvo-vaginitis  in  little 
girls  between  the  ages  of  one  and  twelve  years.  They  find  that  it  is  more 
efficacious  than  local  treatment ;  recovery  is  also  more  rapid.  The  effective 
doses  vary  greatly:  from  5  to  10  millions.  Large  doses  do  not  appear 
to  be  more  effective  than  small  ones. 

Epididymitis.— Bruck  has  used  Wright's  vaccine  in  thirteen  cases  of 
unilateral  gonococcic  epididymitis.  The  oldest  case  has  lasted  two  weeks, 
the  most  recent  two  days.  In  eight  of  the  patients,  recovery  was  complete 
after  twelve  to  fifteen  days.  A  young  man  under  my  care  was  given  six 
injections  (5  to  10  million  gonococci).     The  result  was  fairly  good. 

Arthritis. — The  joint  trouble  is  the  result  of  blood  infection,  and  we 
have,  in  several  cases  of  arthritis,  found  the  gouococcus  in  the  blood.  To 
quote  cases : 

1.  A  man.  aged  tliirty-one  years,  suffering  from  gonorrhoea,  felt  pains  in  the 
knees,  in  the  feet,  and  in  the  sterno-clavicnlar  and  tempero-maxillary  joints.  The  tem- 
perature was  100°  F.  Several  injections  of  5  million  gonococci  in  each  injection  were 
given.  The  condition  remained  stationary.  Further  injections  were  given.  Pains 
appeared  in  the  shoulder  and  in  the  left  wrist.  The  rheumatism  ran  a  subacut-e  course 
without  becoming  localized  in  one  joint  more  than  another. 

Subsequently,  we  injected  10  million,  and  then  50  million  of  gonococci.  The 
patient  was  discharged  convalescent. 

2.  A  man  was  admitted  for  arthritis  of  the  right  foot.  The  joints  of  the  toes  were 
very  painful.  Movement  caused  great  distress,  and  walking  was  practically  impossible. 
No  fever  ;  general  condition  excellent. 

An  injection  of  5  miUion  gonococci  was  given  every  other  day.  Improvement 
soon  showed  itself.  Walking  became  possible,  the  swelling  of  the  foot  diminished 
and  the  ui-ethral  discharge  disappeared.  The  patient  asked  for  more  injections,  which 
were  given  ;  massage  was  also  ordered.  A  month  later  the  foot  was  almost  well,  but 
the  stiffness  of  the  toes  persisted,  and  the  dorsal  surface  of  the  foot  became  swollen 
after  too  much  walking. 

3.  A  young  woman  was  suffering  from  vaginitis  and  from  artlu-itis  of  the  I'ight 
wrist,  which,  with  the  back  of  the  hand,  was  enormously  swollen.  The  pains  were 
so  severe  that  the  patient  got  no  rest.  Flexion  and  extension  of  the  joint  were 
impossible.  The  temperature  was  101°  F.  The  affected  region  was  covered  with  wet 
dressings,  and  injections  of  5  million  gonococci  were  given.  No  improvement  followed. 
Injections  of  10  million  gonococci  were  then  given.  The  result  was  not  favourable ; 
leeches  were  apjdied  to  the  back  of  the  hand,  dressings  of  methyl-salicylate  ointment 
were  put  on,  and  the  wi-i.st  was  treated  with  a  douche  of  superheated  air.  The  pains 
were,  perhaps,  a  little  relieved.  Two  more  injections  gave  no  result.  The  joint 
remained  painful  and  showed  a  tendency  to  become  ankylosed ;  for  this  condition 
massage  was  tried. 


2064  TEXT-BOOK  OF  MEDICINE 

Mante  has  treated  four  cases  of  g-onorrhceal  arthritis  with  injections  of  5  to  15 
million  gonococci.  In  the  first  case  (tibio-tarsal  joint),  the  pain  became  less  after  the 
first  injection,  but  reappeared  at  the  end  of  forty-eight  hoiu-s. 

In  two  other  cases  (arthritis  of  the  knee-joint)  the  jy&in  diminished  very  much 
after  the  first  injection.  Disappearance  of  the  effusion  and  fall  of  temperature  followed 
after  an  interval  varying*  from  three  days  to  two  weeks.  The  fourth  patient  was  still 
under  treatment. 

Mainini  has  published  four  cases  of  gonorrhoeal  arthritis  treated  with  vaccine. 
The  doses  used  were  enormous,  200  to  300  million  gonococci.  The  results  were 
poor;  the  injections  lessened  the  pain,  but  the  improvement  was  transient,  "and 
after  the  analgesic  effect  of  the  injection  had  disappeared  the  pains  became  just  as  bad 
as  ever."  He  could  give  no  definite  results  as  to  the  efficacy  of  the  vaccine  as  regards 
the  duration  of  the  arthritis,  and  the  patients  required  surgical  treatment  to  obtain 
movement  in  the  affected  joints.  He  found  that  the  opsonic  curve  was  capricious  and 
did  not  furnish  j)ractical  information  as  to  the  course  of  local  infection. 

Rufus  Cole  and  Meakins  have  published  several  cases  with  the  opsonic  curves. 
Their  conclusions  are :  '•  It  is  diificult  to  deny  the  efficacy  of  gonococcic  vaccine  in 
gonorrhoeal  arthritis,  but  we  must  remember  that  many  cases  recover  with  other 
methods  of  treatment.  Our  impression  is  that  the  vaccine  treatment  gives  g-ood 
results,  but  many  cases  are  requii-ed  in  order  to  form  a  definite  judgment.  We  are 
less  positive  regarding  the  value  of  the  opsonic  index  as  a  g'uide  to  the  administration 
of  the  vaccine.  We  do  not  tliink  that  the  accumulation  of  the  negative  phases  is  a 
daug'er.  In  no  case  have  we  found  the  vaccine  to  be  harmful,  and  this  fact  is  a  suffi- 
cient justification  for  the  treatment  of  gonorrhoeal  arthritis  with  the  vaccine  in  doses  of 
500  to  1000  million  gonococci,  repeated  every  seven  to  ten  days.  Further  statistics 
will  either  confirm  or  condemn  this  method." 

In  my  own  cases  of  gonococcic  infection  simulating  typhoid  fever,  injections  of 
vaccine  appeared  to  have  had  a  fairly  favourable  result.  At  the  present  time,  exact 
dosage  is  wanting  in  the  application  of  Wright's  vaccine.  The  question  of  the  opsonic 
index  is  discussed  in  the  Appendix. 

The  injection  causes  no  local  reaction.  The  millions  of  attenuated  gonococci, 
injected  subcutaneously,  are  harmless  locally.  In  two  or  three  cases  slight  and  passing 
erythema  has  been  seen.  The  therapeutic  effects,  obtained  in  urethritis  and  vulvo- 
vaginitis, are  somewhat  contradictory.  In  some  cases  they  have  been  good,  in  others 
moderate  or  neg'ative,  no  matter  what  dose  of  vaccine  was  injected.  Tliis  statement 
also  holds  good  in  the  ease  of  gonococcic  arthritis. 


II.  SOFT  CHANCRE. 

The  word  "  chancre,"  formerly  synonymous  with  rodent  ulcer,  is  now  used 
exclusively  to  designate  two  varieties  of  contagious  ulcerations,  which  are 
in  most  cases  of  venereal  origin.  These  two  varieties,  clearly  separated  in 
1850  by  Hunter,  E,icord,  and  Bassereau,  are  the  soft  chancre  and  the  hard 
or  syphilitic  chancre.  Both  chancres  result  from  infection,  but  in  the 
former  case  the  infection  remains  local,  in  the  latter  it  becomes  general. 

.etiology. — The  simple  chancre  is  rare  when  strict  cleanliness  is  observed. 
It  is,  therefore,  more  common  in  hospital  patients.  The  contagion  is  effected 
by  inoculation.  The  pus  of  the  chancre,  even  in  a  dilute  condition,  repro- 
duces the  lesion.    A  scratch,  an  erosion,  or  a  vesicle  of  herpes,  serves  as  the 


V  KX  K I M-:  A  1.   1 » I S  I«:  A  S  IvS  2065 

point  of  entrance,  Imt  in  most  casus  the  cnLiiince-;,'ate  is  not  found.  In 
00  cases  ont  of  100  the  soft  chancre  is  of  venereal  origin.  Contamination 
is  })088iblo  during  the  entire  duration  of  the  disease,  not  only  from  one 
subject  to  another,  hut  also  indefinitely  in  the  same  subject  by  auto- 
inocuhition. 

The  soft  chancre  is  in(>culabKi  in  the  monkey.  In  1882  Fournicr  and 
Krishaber  made  142  inoculations,  with  success  in  60  per  cent.,  in  the  macaque, 
baboon,  and  other  small  apes.  Toniasczewski  has  made  subcutaneous  in- 
oculations of  cultures  on  blood-agar  of  the  bacillus  of  soft  chancre  in  two 
different  species  of  monkeys.  The  ulcerations  which  developed  some  days 
later  contained  a  bacillus  which  gave  on  culture  the  characters  of  Ducrey's 
bacillus.     Inoculation  in  man  produced  the  soft  chancre. 

The  micro-organism  of  the  soft  chancre  is  a  bacillus  described  by  Ducrey. 
It  is  found  in  abundance  in  the  pus  oozing  from  the  chancre.  It  has  the 
following  characters  :  Rape-seed  bacillus,  with  rounded  ends,  taking  the 
stain  only  at  its  extremities,  while  its  central  part  remains  colourless.  It 
does  not  remain  stained  by  Gram's  method.  In  sections  at  the  edges  of  the 
chancre  it  occurs  in  the  form  of  small  chains  of  strepto-bacilli. 

Ducrey's  bacilli  cannot  be  cultivated  on  the  ordinary  media.  Bezan9on 
and  Griffon,  while  making  researches  on  pus  taken  from  patients  under  my 
care,  have  succeeded  in  cultivating  the  bacillus  on  blood-agar.  We  have, 
therefore,  a  definite  culture  medium  which  is  of  practical  use.  In  order  to 
obtain  cultures  of  Ducrey's  bacillus  for  purposes  of  diagnosis,  it  is  sufficient 
to  sow  on  a  tube  of  blood-agar  the  pus  which  has  been  allowed  to  collect  on 
the  surface  of  the  ulceration  after  previous  disinfection.  The  colonies  are 
rounded,  greyish,  and  separated  from  one  another.  The  microbe  shows 
certain  peculiarities  when  it  develops  in  the  fluid  portion  of  the  culture 
medium.  If  we  examine  a  drop  of  the  liquid  which  bathes  the  sloping 
portion  of  the  blood-agar  tube,  we  find  very  thin  chains,  which  are  exces- 
sively long,  and  composed  of  bacilli  individually  smaller  than  those  found 
in  the  colonies  on  the  solid  portion  of  the  medium.  One  of  these  colonies, 
when  inoculated  in  man,  produces  a  typical  soft  chancre. 

Symptoms. — The  soft  chancre  is  nearly  always  genital  or  perigenital. 
In  men  it  appears  on  the  prepuce,  in  the  preputial  fold,  on  the  glans,  within 
the  meatus,  or  on  the  scrotum,  where  it  is  nearly  always  secondary.  In 
women  it  is  usually  found  on  the  fourchette,  in  the  fossa  navicularis,  on  the 
labia  majora  and  minora,  in  the  lower  part  of  the  vagina,  and  upon  the 
cervix  uteri.  It  develops  secondarily  on  the  neighbouring  parts,  especially 
on  oozing  or  excoriated  surfaces,  such  as  haemorrhoids.  The  extragenital 
soft  chancre  may  be  found  in  any  part  of  the  body,  principally  upon  the 
fingers,  and  exceptionally  on  the  face. 

As  the  soft  chancre  is  inoculable  and  auto-inoculable,  we  can  readily 


2066  TEXT-BOOK  OF  MEDICINE 

follow  its  evolution  by  covering  the  inoculated  area  with  a  watch-glass. 
This  method  is  an  excellent  diagnostic  measure,  but  it  is  not  superior  to 
the  discovery  of  the  baciUus  in  the  pus.  After  inoculation  with  pus  fxom 
the  surface  of  the  chancre  or  from  the  suspected  ulcer,  the  inoculation 
chancre  appears  in  about  twelve  hours  as  a  red  areola.  This  areola  gradually 
increases  in  si2;e,  and  a  small  phlyctenule,  filled  with  muco-pus,  appears  on 
the  second  or  third  day.  Below  the  phlyctenule  we  find  a  superficial 
ulcer. 

The  soft  chancre  is  an  ulcer  with  rounded  or  oval  reddish  edges,  which 
are  clean-cut,  often  undermined,  and  rolled  on  themselves.  The  floor  of 
the  ulcer,  which  may  be  more  or  less  deep,  is  dirty,  greyish,  pulpy,  and 
irregular.  It  is  important  to  note  that  the  underlying  tissues  are  supple 
and  soft.  The  pain  is  usually  trifling,  and  the  patient  continues  to  attend 
to  his  business. 

After  one  or  more  weeks  the  floor  of  the  chancre  cleans  up,  granulations 
appear,  the  ulcer  fills  up,  and  healing  follows.  In  some  cases  the  soft  chancre, 
even  though  carefully  treated,  is  very  persistent  and  rebeUious.  In  other 
cases  healing  takes  place  on  one  side,  while  the  ulceration  extends  on  the 
opposite  side.  The  chancre  is  then  said  to  be  serpiginous.  The  healing 
process  leaves  traces,  though  they  may  be  much  less  pronounced  than  the 
extent  and  the  depth  of  the  ulceration  would  lead  us  to  suppose.  A  white 
cicatrix  results.  It  feels  like  a  traumatic  scar,  and  does  not  rest  upon  an 
indurated  base. 

In  addition  to  the  typical  chancre,  several  other  varieties  have  been 
described.  The  simple  chancre  may  be  phagedsenic,  acneiform,  pimply> 
ecthymatous,  or  fissured. 

The  number  of  soft  chancres  may  be  considerable,  on  account  of  the 
liability  to  reinoculation.  They  often  cause  complications,  which  are  mostly 
dependent  on  secondary  infections.  The  soft  chancre,  like  every  ulceration, 
serves  as  a  breeding-ground  for  micro-organisms,  which  cause  either  in  situ 
or  at  a  distance  (by  lymphatic  infection)  various  troubles.  Among  them 
we  may  note  phimosis,  paraphimosis,  and  buboes  in  the  glands  receiving  the 
lymphatics  from  the  infected  areas.  Glandular  enlargement  is  the  rule  in 
soft  chancre.  In  some  cases  much  pain  and  swelling  are  present,  and 
suppuration  follows.  The  ulceration  thus  produced  has  in  most  cases  the 
clinical  characters  of  a  large  soft  chancre.  Nevertheless,  it  appears  from 
the  researches  of  Straus  that  it  is  then  a  question  of  a  reinoculation  with 
Ducrey's  bacOlus  or  an  ulceration  at  first  due  to  the  ordinary  micro-organisms 
of  suppuration.  And,  indeed,  if  the  ulcerated  bubo  is  kept  well  covered 
with  antiseptic  dressings,  the  chancre-like  character  is  absent,  and  healing 
takes  place  as  in  an  ordinary  wound. 

Phagedsena  is  not  special  to  the  soft  chancre  ;  it  is  also  found  on  the 


VENERKAL  DISEASES  206? 

surface  of  many  forms  of  ulceration.  Molecular  ^'angrene,  which  has  been 
compared  to  hospital  or  to  woimd  ganprcnc,  is  clmrnctfrized  by  continuous 
extension  of  the  primary  ulconition,  vvhi(-h  gains  Ixith  in  depth  and  in  (jxtent, 
and  exposes  the  patient  to  the  risk  of  local  and  general  complications  in  the 
absence  of  speedy  and  effective  treatment.  The  proof  that  the  phagcdaenic 
chancre  is  due  to  secondary  infection  is  that  antiseptic  dressings  carefully 
applied  from  the  onset  of  the  trouble  limit  the  number  and  the  gravity  of 
these  complications. 

Treatment. — The  first  indication  is  the  necessity  of  rigorous  antisepsis. 
Frequent  washing  with  antiseptic  lotions  should  be  prescribed.  Carbolic 
acid  solution,  sublimate  lotion  (1  in  2,000)  locally,  baths,  and  dressing  with 
iodoform,  iodol,  salol,  etc.,  are  indicated. 

If  these  measures  do  not  hasten  the  healing  of  the  chancre,  weak  caustics 
should  be  employed — nitrate  of  silver  in  a  3  per  cent,  solution,  carbolic  acid 
(1  in  10),  chloride  of  zinc  paste.  If  these  measures  fail,  we  must  use  Vienna 
paste  or  the  thermo-cautery. 

The  diagnosis  of  soft  chancre  from  the  syphilitic  chancre  and  from  herpes 
is  given  in  the  next  section. 

III.  HARD  OR  SYPHILITIC  CHANCRE  {TREPONEMA  PALLIDUM), 

etiology. — Syphilis,  except  in  the  hereditary  and  conceptional*  forms, 
begins  with  a  chancre,  and  the  virus  may  be  furnished  either  by  the  chancre 
or, by  the  mucous  patches.  The  chancre  always  develops  at  the  point  of 
contamination.  Two  kinds  of  chancre  occur — genital  and  extragenital. 
The  former  are  nearly  always  of  venereal  origin,  the  latter  much  less  often 
so. 

The  contagion  in  the  case  of  extragenital  chancres  may  take  place  in 
various  ways.  Let  me  mention  suckling,  whether  the  infant  suffering  from 
mucous  patches  in  the  mouth  transmits  the  disease  to  the  wet-nurse  or  the 
nurse  suffering  from  mucous  patches  on  the  nipple  infects  the  nursling. 
Articles  used  by  a  syphilitic  person — feeding-bottles,  pipes,  spoons,  or 
drinking-glasses — may  be  the  origin  of  the  chancre.  Let  me  note  buccal 
chancres  in  glass-blowers  and  in  musicians  playing  wind  instruments,  and 
chancres  contracted  by  physicians,  midwives,  and  laundresses.  These  pro- 
fessional chancres  almost  always  occur  on  the  fingers.  Infected  instruments 
may  give  rise  to  a  chancre  (catheterization  of  the  Eustachian  tube,  dental 
operations).  Vaccination,  when  the  vaccinator  is  suffering  from  recent 
syphilis,  may  transmit  the  disease,  and  the  subject  thus  infected  may  in 
turn  transmit  s}'philis  ;  hence  arise  the  epidemics  of  vaccinal  syphilis. 

The  hard  chancre  may  develop  on  any  region,  and  on  the  most  accessible 

*  Conceptional  syphilis  is  syphilis  transmitted  to  the  mother  by  a  foetus  bom  of  a 
syphilitic  father. 


2068  TEXT-BOOK  OF  MEDICINE 

mucous  membranes.  In  men  it  usually  occurs  on  the  inner  surface  of  the 
prepuce,  on  the  frenum,  on  the  glans,  upon  the  cutaneous  surface  of  the 
penis,  within  the  urethra,  upon  the  scrotum,  and  at  the  root  of  the  thighs. 
In  women  the  hard  chancre  often  passes  unnoticed.  The  mucous  membrane 
of  the  vagina,  the  cervix  uteri,  the  vulva,  the  meatus  urinarius,  and  the 
fourchette  are  the  usual  situations  for  it.  Among  the  venereal  chancres  we 
must  include  those  of  the  anal  and  buccal  mucous  membranes  from  abnormal 
coitus.  Nevertheless,  many  buccal  chancres  are  not  of  venereal  origin. 
They  are  found  especially  on  the  lips,  tongue,  and  tonsils.  In  591  cases  of 
extragenital  chancres  under  Fournier,  Nivet  found  338  bucco-pharyngeal 
chancres,  and  75  chancres  of  the  head.  The  body  was  attacked  107  times, 
the  limbs  54  times,  and  the  neck  7  times. 

Roux  and  Metchnikoff  have  inoculated  a  female  chimpanzee  with 
syphilis.  The  chancre  appeared  twenty-six  days  after  inoculation.  It  then 
became  indurated,  and  a  typical  mass  of  enlarged  glands  appeared,  one 
large  gland  being  surrounded  by  small  glands.  In  1882  Martineau  and 
Hamonic  produced  syphilis  in  a  large  macaque  monkey,  "  which  presented 
a  typical  hard  chancre,  followed  by  secondary  troubles." 

Description. — The  incubation  period  is  from  three  to  four  weeks. 
Every  chancre  is  composed  of  a  mass  of  embryonic  cells,  forming  a  tumour 
at  the  expense  of  the  derma  and  hypo  derma.  The  appearance  of  the  chancre 
differs  on  the  skin  and  on  the  mucous  membranes.  On  the  skin  it  is  covered 
with  a  crust,  due  in  part  to  the  presence  of  the  stratum  corneum.  As  this 
stratum  does  not  exist  in  the  mucous  membranes,  the  changes  in  the  mucous 
epithelium  soaked  in  purulent  fluid  end  in  the  formation  of  a  flabby,  greyish, 
and  diphtheroid  membrane. 

Let  us  first  consider  the  chancre  of  the  mucous  membranes,  taking  a 
chancre  on  the  corona  of  the  glans.  At  first  we  find  a  papule,  which  des- 
quamates. This  papule,  which  is  not  painful,  and  does  not  itch,  has  a  dark 
colour  like  that  of  muscle.  After  a  few  days  a  very  superficial  ulcer  appears. 
The  ulcer  is,  however,  more  apparent  than  real,  since  it  is  formed  at  the 
expense  of  tissue  which  is  often  prominent.  The  ulcerated  chancre  may  be 
very  small ;  it  is  usually  about  as  large  as  a  lentil.  Its  edges  are  adherent, 
thick,  and  regular.  They  never  present  the  segments  which  make  up  the 
polycyclical  border  of  herpes.  The  edges  are  not  clean-cut,  and  there  is 
not  ulceration  in  the  true  sense  of  the  word.  The  floor  of  the  chancre  is 
smooth,  varnished,  and  at  times  greyish  and  diphtheroid.  When  the  thin 
covering  membrane  is  removed,  the  floor  of  the  chancre  has  a  reddish  appear- 
ance, with  papillse.  The  secretion  from  the  chancre  is  scanty  and  serous. 
The  chancre  rests  upon  an  indurated  base.  Cicatrization  takes  place  in 
four  or  five  weeks,  and  the  chancre  is  replaced  by  a  reddish  induration, 
which  may  last  for  several  months. 


VKNKi;i:.\L  1)Isi;asi-;s  2or,n 

Tlif  cutarn'oiis  chiiiicio  (uipiile,  face,  scrotum,  llii|^li.s)  lias  a  somewhat 
(lilTcnMit.  i*vi»liili(m.  At  lirst  it  is  a  reddish  croHivc,  pirnpln.  It  then  m- 
l.iij^t'S,  Ix'comiti^f  ])r(imiiu'rit,  and  is  covorod  witli  a  cruKt.  It  is  always 
painless.  '  'liiis  t'litriistcd  diaiKTc  resembleK  ordinarv  ecthyma,  Imt.  on 
ivnioval  of  tlu^  ])n'viously  softened  (^ust  tlu;  chancre  shows  its  special 
characteristics — Hat  or  sliii;htly  convtix  surface,  which  is  erosive,  hut  not 
much  ulcerated,  smooth,  reddishlike  muscle,  often  bleeding,  and  studded 
with  papilhv.  A  little  jms-like  secretion  is  sonu'times  found.  The  edges  of 
the  chancre  are  flat,  and  iu)t  clean-cut.  Strictly,  there  is  no  edge,  because 
there  is  no  ulceration.  The  base  of  the  chancre  is  indurated  and  parch- 
ment-like. On  the  nose,  on  the  thigh,  and  on  certain  other  regions,  the 
chancre  may  be  of  large  size. 

Every  hard  chancre  is  accompanied  by  adenitis  involving  several  glands. 
This  adenitis  does  not  appear  before  the  seventh  day,  and  its  localization 
depends  upon  the  situation  of  the  chancre  (groin,  axilla,  and  neck).  One 
gland  is  usually  larger  than  the  others,  because  it  is  in  more  direct  com 
munication  with  the  lymphatics  from  the  infected  area.  The  glands  are 
small,  hard,  and  usually  painless.  They  roll  under  the  linger,  and  do  not 
cause  periadenitis.  They  show  no  tendency  to  suppurate,  and  as  they 
persist  for  months  and  years  after  the  chancre,  they  are  of  considerable 
value  in  making  a  retrospective  diagnosis. 

After  a  short  time  enlarged  glands  are  also  found  in  other  regions,  espe- 
cially in  the  neck.     Enlargement  of  the  spleen  has  been  noted  in  some  cases. 

The  appearance  of  the  chancre  is  usually  accompanied  by  general  troubles 
— lassitude,  fever,  headache,  osteoscopic  pains,  insomnia,  arthralgia,  etc. 
The  secondary  troubles  may  appear  before  the  cicatrization  of  the  chancre 
or  some  weeks  after  it.  The  chancre  itseK  may  be  the  starting-point  of  a 
mucous  patch. 

The  hard  chancre  is  generally  single  ;  nevertheless,  v/e  may  find  two  or 
three,  but  they  are  nearly  always  contemporaneous — or,  at  least,  when 
there  is  reinoculation,  it  occurs  soon  after  the  appearance  of  the  first  chancre, 
and  not  at  a  later  date,  as  happens  in  the  case  of  the  simple  chancre. 

Under  the  microscope  the  chancre  shows  an  infiltration  of  the  dermis  by 
leucocytes.  Endarteritis  is  practically  constant.  These  vascular  lesions 
bear  witness  to  the  special  predilection  of  syphilis  for  the  arteries  in  the  early 
as  weU  as  in  the  later  stages. 

Diagnosis. — The  discovery  of  the  Treponema  'pallidum  has  rendered  the 
diagnosis  of  syphilis  easy  in  doubtf  id  cases  ;  but  for  the  present  let  us  confine 
ourselves  to  the  resources  of  clinical  medicine,  taking  a  chancre  of  the  genital 
organs  or  of  some  other  region  in  a  man  or  a  woman,  and  considering  the 
distinction  from  soft  chancre  and  from  herpes. 

The  distinctive  signs  of  the  ordinary  svphilitic  chancre  are  : 

ir.  '  131 


2070  TEXT-BOOK  OF  MEDICINE 

1.  The  hard  chancre  has  an  incubation  period  of  three  or  four  "weeks ; 
the  soft  chancre  appears  one  or  two  days  after  contagion ;  herpes  appears 
spontaneously,  and  relapses  at  more  or  less  lengthy  intervals. 

2.  The  hard  chancre  is  a  projection  of  the  dermis,  erosive  rather  than 
ulcerative.  It  is  excavated  like  a  cup,  "with  a  crown-like  contour,  some- 
times thickened  and  raised,  so  that  the  depth  of  the  ulceration  is  apparently 
increased.  It  has  not  clean-cut  edges.  In  the  soft  chancre  no  projection 
of  the  dermis,  no  hypertrophic  tendency.  On  the  contrary,  a  true  ulcera- 
tion, with  clean-cut  edges,  and  more  or  less  deep,  from  the  rapid  and  com- 
plete destruction  of  the  epidermis  and  of  the  suppurative  melting  of  the 
papillary  and  dermic  layers.  In  herpes  erosion  of  small  extent,  and  more 
superficial  than  that  of  chancre. 

3.  In  the  syphilitic  chancre  regular  outlines,  never  presenting  the  fes- 
tooned segment  which  the  poly  cyclical  outlines  of  the  herpetic  ulcers  often 
form. 

4.  The  syphilitic  chancre  is  nearly  always  single,  never  confluent,  and 
not  reinoculable  ;  the  soft  chancre  is  often  multiple,  sometimes  confluent, 
and  reinoculable  to  infinity. 

5.  The  floor  of  the  hard  chancre  is  at  times  diphtheroidal  and  greyish, 
as  long  as  it  is  covered  by  a  membrane  formed  of  the  soaked  and  altered 
epithehum ;  but  after  the  removal  of  this  membrane  the  floor  is  seen  to  be 
red,  smooth,  shiny,  studded  with  papillae,  and  covered  "with  scanty  serous 
secretion.  The  floor  of  the  soft  chancre  is  uneven,  worm-eaten,  anfrac- 
tuous, and  covered  "with  abundant  purulent  secretion. 

6.  When  we  press  the  hard  chancre  between  the  fingers,  we  have  great 
difiiculty  in  squeezing  out  a  little  liquid ;  when  we  knead  the  base  of  the 
chancreform  herpes  (in  this  form  the  herpes  is  soHtary  and  simulates  the 
dwarf  chancre),  we  can  squeeze  out  a  deep  amber-coloured  serum,  and  after 
wiping  the  surface  we  can  repeat  the  operation,  obtaining  the  same  serous 
oozing. 

7.  The  base  of  the  hard  chancre  is  indurated.  This  parchment-like 
induration  is  one  of  the  most  striking  features,  and  is  not  found  in  the  soft 
chancre. 

8.  In  the  case  of  the  syphilitic  chancre  the  glands  are  hard,  practically 
painless,  and  distinct  from  one  another.  They  show  no  tendency  to  sup- 
purate. In  the  case  of  the  soft  chancre  the  glands  are  enlarged,  painful, 
and  accompanied  by  periadenitis.  They  sometimes  form  masses,  and  have 
a  marked  tendency  to  suppurate. 

Such  are  the  distinctive  signs  between  the  hard  chancre,  the  soft  chancre, 
and  herpes.  Nevertheless,  we  may  meet  "with  very  difficult  cases.  I  aUude 
to  the  mixed  chancre.  This  variety  at  first  presents  the  characters  of  the 
soft  chancre.     In  its  subsequent  course  the  distinctive  characters  are  not 


YKNEHKAL  DISEASKS  2071 

woU  clofincd,  tlio  buboos  may  suppurate,  and  later  the  secondary  symptoms 
appear. 

Wc  must  also  make  a  diagnosis  in  the  case  of  encrusted  chancres  of  the 
skin,  which  are  often  large  and  hypertrophic,  but  in  which  (the  crust  having 
been  removed)  we  find  the  characteristics  mentioned  under  Chancre  of  the 
Mucous  Membranes. 

The  chancre  of  scabies  has  nothing  in  common  with  the  syphilitic  chancre, 
except  its  situation  on  the  penis.  It  is  often  multiple,  papular,  covered  by 
a  crust,  and  accompanied  by  the  characteristic  burrow  of  the  acarus. 

The  pustules  of  ecthyma  are  readily  recognized  by  their  mode  of  develop- 
ment, their  colour,  and  the  absence  of  induration.  As  regards  the  ulcerated 
syphilides  of  the  secondary  and  terti9,ry  periods,  the  nature  of  the  lesion, 
the  course  of  events,  and  the  absence  of  glandular  enlargement  will  prevent 
confusion  with  the  chancre. 

Multiple  Forms  of  the  Syphilitic  Chancre. — I  have  so  far  described  the 
usual  form  of  the  syphilitic  chancre.  The  chancre  may,  however,  be  giant, 
ulcerous,  phagedaenic,  and  hypertrophic. 

The  giant  chancre  may  be  as  large  as  a  crown-piece.  In  my  lectures  at 
the  Hotel-Dieu  I  showed  a  giant  chancre  of  the  thigh  larger  than  a  florin. 
In  Gastou's  case  a  giant  chancre  of  the  abdomen  measured  over  2  inches  in 
diameter.  In  Fournier's  case  a  giant  chancre  of  the  elbow  was  as  large  as 
a  crown-piece.  The  giant  chancre  is  very  rare  on  the  genital  organs.  It  is 
usually  found  on  the  limbs,  trunk,  or  face,  and  runs  the  same  course  as  the 
ordinar}^  chancre. 

The  ulcerous  chancre  is  generally  of  large  size.  I  said  above  that  one 
of  the  characteristics  of  the  ordinary  chancre  is  that  it  is  exulcerated  without 
ending  in  true  ulceration.  This  is  true,  but  yet  some  chancres  show  deep 
and  extensive  ulceration.  These  chancres  are  usually  extragenital.  When 
the  thickened  and  stratified  crusts  are  removed,  we  jBmd  a  somewhat  ex- 
cavated iJceration,  with  prominent  edges.  Sometimes,  indeed,  on  the  lips 
excavations  occur,  and  at  first  sight  we  are  tempted  to  think  that  the  lesion 
will  be  followed  by  deep  and  deformed  scars.  And  yet  "  things  nearly 
always  turn  out  well,  and  after  recovery  the  lips  become  practically  normal  " 
(Fournier).  This  paradox  arises  from  the  fact  that  the  ulcerative  action 
limits  itself  to  the  specific  neoplasm,  and  does  not  encroach  upon  the  neigh- 
bouring tissues.  The  chancre  is  autophagous,  and  produces  the  ulceration 
at  its  own  expense,  thus  differing  from  the  phagedaenic  chancre. 

The  diagnosis  of  this  chancre  is  generally  easy ;  nevertheless,  in  two 
cases  which  appeared  to  be  ulcerous  chancres  the  histological  examination 
by  Darier  revealed  a  lymphosarcoma  of  a  special  species,  which  is  not  un- 
common in  the  skin  and  in  the  glands.  At  the  present  day  we  can  examine 
for  the  treponema. 

131—2 


2072  TEXT-BOOK  OF  MEDICINE 

The  pliagedsenic  chancre  is  fortunately  very  rare.  The  phagedsena  may 
extend  in  area  and  in  depth,  destroying  the  tissues,  and  leaving  behind  it 
deformities  and  deep  scars.  In  one  of  Fournier's  cases  the  chancre  ran  a 
rapid  but  painless  course,  and  destroyed  the  entire  lower  lip.  In  another 
case  a  phagedsenic  chancre  destroyed  the  ear.  In  a  case  of  Mencault  a 
phagedgenic  chancre  destroyed  the  inguina,l  region. 

The  syphilitic  chancre  may  hypertrophy,  reaching  the  size  of  a  cherry 
or  even  of  an  apricot.  These  hypertrophic  chancres  form  bleeding,  ulcerated, 
and  more  or  less  encrusted  tumours.  We  must  be  carefid  not  to  confound 
them  with  epitheliomata — an  error  that  has  led  to  an  operation  when  the 
chancre  would  have  been  cured  in  a  few  weeks.  Hypertrophic  chancres  are 
very  rarely  found  on  the  genital  organs.  They  have  a  marked  predilection 
for  the  face.  In  one  of  Trelat's  cases  two  ulcerative  chancres  as  large  as 
nuts  were  present  on  the  chin.  In  a  case  of  Mauriac  the  hypertrophic 
chancre  on  the  lower  lip  formed  a  tumour  as  large  as  a  lady-apple.  I  have 
seen  a  hjTpertrophic  chancre  of  the  size  and  shape  of  a  large  almond. 

All  the  above  forms  of  chancre  are  simply  morphological  varieties  of  the 
ordinary  syphilitic  chancre.  The  form,  the  dimensions,  and  the  appearances 
of  the  syphilitic  chancre  may  vary,  but  the  fundamental  characters  of  the 
chancre  do  not  vary.  Diagnosis  is,  therefore,  possible.  The  induration  of 
the  bed  of  the  chancre,  the  characters  of  the  adenopathy,  the  evolution  of 
the  chancre  (including  the  period  of  incubation),  and  the  appearance  of  the 
secondary  troubles,  will  reveal  the  nature  of  the  chancre,  even  in  the  most 
abnormal  forms.  In  cases  of  dispute  the  discovery  of  the  treponema  will 
confirm  the  diagnosis. 

Bacteriology— Treponema  Pallidum.— In  May,  1905,  Schaudinn  dis- 
covered the  pathogenic  agent  of  syphUis.  He  called  it  first  Spirochwta 
pallida,  and  later  Treponema  pallidum.  We  shall  keep  the  term  Treponema 
pallidum,  which  appears  to  be  more  correct. 

If  the  discovery  of  the  treponema  has  been  long  delayed,  it  is  because 
its  detection  is  exceedingly  delicate,  in  that  the  organism  does  not  stain 
readily  .with  the  usual  methods  (whence  the  name  " iKilliclum").  The 
technique  is  as  follows  : 

In  the  serous  fluid,  obtaining  by  curettage  of  cutaneous  lesions 
(chancres,  mucous  patches,  etc.),  it  can  be  stained  by  Giemsa's  method. 

The  surface  of  the  lesion  is  cleaned  with  pledgets  of  wool  soaked  in 
normal  saline  solution,  and  the  edges  are  scratched  with  the  back  of  a 
bistoury  until  clear  serous  fluid  appears ;  the  third  or  fourth  drop  is 
collected  (serum  of  a  light  rose  colour  is  the  easiest  to  examine).  The 
drop  is  spread  out  on  a  slide  so  as  to  form  a  very  thin  layer,  and  is  then 
thoroughly  dried. 

It  is  unnecessary  to  fix  old  and  well   dried  films.     In  fresh   films, 


VKNKIIFAL  DISEASES  2073 

fixation  is  enV'ctetl  hy  lieat,  ur  by  ahsolutii  alcohol  (fifLeon  to  twenty 
minutes). 

To  stain  the  parasite,  10  drops  of  Giemsa's  solution  are  mixed  with 
10  CO.  of  distilled  water,  which  must  not  be  acid.  The  smear  is  covered 
witb  the  stain  and  is  then  held  over  a  small  ilune  until  the  steam  first 
begins  to  come  off.  The  heating  is  then  stc»pped,  and  the  stain  poured  off 
after  fifteen  seconds.  This  operation  is  performed  four  times,  but  on  thelast 
occasion  the  stain  is  not  poured  ofl'  for  a  full  minute.-  The  film  is  washed 
in  water  anil  dried. 

Examination. — The  search  is  chiefly  to  those  parts  of  the  film  where 
red  corpuscles  are  found,  avoiding  such  parts  as  are  too  thick  and  con- 
sequently too  dark.  The  Trcjwiiema  is  stained  a  deep  red.  Its  detection  is 
sometimes  most  tedious. 

If  an  ultra-microscope  is  used,  a  drop  of  serum  is  placed  between  a 
slide  and  a  cover-glass  and  examined.  The  Treponema  is  then  very  easily 
seen  ;  it  appears  brightly  illuminated  and  very  mobile  against  the  dark 
background.     This  method  is  the  most  practical. 

In  the  ease  of  the  viscera  or  other  organs,  the  preceding  methods  may 
be  employed,  but  it  is  better  to  impregnate  a  fragment  of  tissue  with 
nitrate  of  silver  and  then  to  cut  thin  sections.  The  Treponema  is  stained  a 
deep  black  by  the  reduced  silver.* 

Lifferential  Characters. — The  Treponema  ixdlidum  is  recognized  by  the 
following  characters  :  It  is  a  small  filiform  element  from  6//  to  14//  in  length 
by  0'25/i  in  breadth,  twisted  into  a  spiral  with  from  six  to  twenty-six 

*  An  excellent  method  of  impregnation  with  silver  nitrate  is  as  follows  (Levaditi)  : 
Fragments  of  tissue,  2  to  3  mm.  thick  are  fixed  in  10  per  cent,  formalin 
for  twenty-four  hours,  and  are  next  hardened  in  alcohol  (96  per  cent.)  for 
twenty-faur  hours.  Thev  are  washed  in  distilled  water,  until  they  fall  to  the  bottom 
of  the  receptacle  (five  to  fifteen  minutes).  They  are  then  placed  in  absolutely  clean 
flasks,  with  ground  glass  stoppers,  and  contauiing  the  silver  solution : 

Nitrate  of  silver  ..  ..  ..  ..  loO  gr.  to  3  gr. 

Distilled  water  ..  ..  ..  .,         1(X)  c.c. 

Tlie  flasks  containing  the  specimens  are  kept  for  tlu-ee  days  in  the  oven  at  38°  C,  and 
in  the  dark.  (They  may  be  left  for  four  or  five  days.)  The  specimens  are  then  quickly 
washed  in  distilled  water  and  placed  in  Ramon  y  Cajal's  reducing  solution  at  the 
laboratory  temperature. 

Pyrogallic  acid  ..  ..  ..  ..  ..         4  grama. 

Formalin  ..  ..  ..  ..  ..  ,.  .5  c.c. 

Distilled  water  ..  ..  ..  ..  ..        95  c.c. 

They  remain  twenty-four  hours  in  this  solution,  and  are  next  washed  in  water  for  some 
hours.  They  are  dehydrated  and  embedded  in  paraffiu.  The  sections  should  not  be 
thicker  than  om- 

No  counter  stain  is  employed  for  the  groundwork  of  the  .section. 


2074  TEXT-BOOK  OF  MEDICINE 

extremely  close  and  fine  turns.  Its  length  is  equal  to  that  of  a  red  corpuscle 
or  of  a  lymphocyte.  The  body  is  said  to  be  cylindrical,  and  a  flagellum  has 
been  described  at  each  extremity.  A  membrana  undulans  is  not  found. 
We  may  meet  with  treponemata  that  are  straight  in  a  part  of  their  length, 
while  others  .are  very  short,  and  show  only  three  or  four  undulations.  It 
is  rare  to  find  an  operculum  in  the  length  or  at  one  extremity  of  the  para- 
site. The  Tre;poneriia  performs  movements  of  flexion  and  torsion,  affecting 
the  entire  organism.  The  disposition  of  the  turns  of  the  spiral  is  not 
modified  during  the  different  manifestations  of  activity,  but  is  the  same 
as  it  is  during  rest. 

Some  authorities  have  described  atypical  and  degenerative  forms 
(granular,  straight,  retracted,  and  thickened  treponemata,  as  well  as  Y- 
shaped  forms,  said  by  certain  writers  to  be  treponemata  in  process  of  repro- 
.duction). 

We  must  not  confuse  the  Treponema  ^pallidum  with  certain  sapro- 
phyHc  or  pathogeni-c  spirilla  found  on  the  mucous  membranes  or  on  cutaneous 
ulcers.  Thus  the  Spirocliceta  refringens,  which  is  not  pathogenic,  is,  as  its 
name  indicates,  strongly  refracting,  and  very  readily  stainable.  Further, 
the  turns  of  the  spiral  are  less  numerous,  and  the  thickness  is  greater.  Its 
colour  with  Giemsa's  stain  is  blue,  and  not  pale  rose.  The  spirochsete  of 
the  mouth  and  teeth — the  Spirochceta,  pyogenes — the  Spirochceta  pallidula 
of  CasteUani,  the  spirochEete  of  Vincent  (angina),  Obermeier's  spirocheete 
(recun^ent  fever),  and  the  spirochsete  of  ulcerated  carcinomata  resemble  the 
SpirocJiceta  refringens  in  that  they  stain  readily,  and  are  thicker  and  less 
undulated  than  the  Treponema  of  syphilis. 

There  also  exists  a  spirillum  which  has  the  attributes  of  the  Treponema 
and  which  can  be  distinguished  from  it,  according  to  BertareUi,  only  by 
its  more  rapid  staining  with  methylene  blue :  tliis  pseudo-treponema  was 
found  by  Le  Play  and  Sezary  in  a  chancreform  angina  from  which  a 
patient  in  my  wards  was  suffering. 

Localization  of  the  Parasite. — The  Treponema  is  frequently  found  in  the 
chancre  and  in  the  satellite  gland.  It  has  been  discovered  in  the  spots 
of  the  roseola,  and  it  has  been  found  in  90  per  cent,  of  the  mucous  patches 
and  secondary  papules.  The  results  of  the  blood  examination  are  not 
constant. 

In  hereditary  syphilis  the  Treponema  is  very  abundant  in  the  viscera, 
especially  in  the  liver  and  in  the  suprarenal  glands.  It  has  been  found  in 
the  pancreas  and  in  the  parotid  gland.  It  is  far  less  often  found  in  the 
visceral  lesions  of  acquired  syphilis.  At  the  present,  it  has  been  found 
in  the  suprarenal  capsules,  in  a  gumma  of  the  liver,  in  aortitis,  in  cerebral 
arteritis,  and  in  the  cerebro-spinal  fluid.  It  appears  to  be  absent  in  certain 
syphilitic  lesions  of  the  viscera ;  for  example,  icterus  gravis,  which  seems 


VENEREAL  DISEASES  2075 

to  he  toxic  in  origin.  The  Tre/iuncma  is  absent  in  parasyphilitic 
aflections  of  tiio  nervous  system  (tabes,  general  paralysis).  During  preg- 
nancy, it  may  bo  found  passing  through  the  placenta  from  the  mother  to 
tho  fo'tus. 

Inoculation  in  Aniniah. — Attempts  at  making  cultures  of  tiio  Treiwncma 
have  so  far  been  fruitless,  but  certain  facts  demonstrate  its  pathogenic 
action.  In  fact,  inoculation  of  secondary  syphilitic  products  lias  not  only 
produced  in  the  chimpanzee,  the  macaque,  the  gibbon,  and  the  orang-outang 
sucii  specilic  lesions  as  chancre,  mucous  patches,  and  secondary  eruptions, 
but  the  parasite  found  in  man  has  also  been  discovered  in  the  different 
exudates  and  in  the  blood  of  these  animals  (Hoffman,  Metchnikoff).  The 
parasite  appears  to  possess  but  slight  resistance.  At  48'  C.  it  loses  its 
virulence,  and  is  no  longer  inoculable.  It  preserves  its  virulence  when 
mixed  with  glycerin.  These  findings  deserve  mention  by  reason  of  their 
bacteriological  importance,  and  also  because  they  may  lead  to  rational 
methods  of  treatment  and  of  diagnosis. 

Prognosis. — Is  it  possible,  given  a  chancre,  to  say  whether  the  resulting 
troubles  will  be  benign  or  grave  ?  It  is  certain  that  extragenital  chancres 
are  usually  more  ser-ious  than  venereal  chancres,  and  that  certain  cases  of 
syphilis  derived  from  the  same  source  are  malignant,  while  others  are  trifling. 
Other  facts  are,  however,  quite  opposed  to  this  point  of  view.  Much 
depends  upon  the  question  of  the  soil,  although  it  may  not  be  possible  to 
state  exactly  the  conditions  modifying  the  virulence  of  the  infective  agent. 
Treatment. — At  all  times  the  idea  of  excising  the  chancre  has  been 
present  in  the  mind  of  physicians,  but  though  we  may  thus  get  rid  of  the 
ulceration,  we  do  not  suppress  the  period  of  incubation.  Accordingly,  this 
method  has  been  practically  abandoned. 

Leloir  has  reported  the  case  of  a  student  who,  after  a  suspected  coitus,  watched  most 
carefully  for  the  possible  appearance  of  a  chancre.  It  appeared,  and  although  excision 
was  at  once  performed,  the  disease  ran  its  course,  the  economy  being  already  infected. 
Augagneur  performed  circumcision  immediately  after  coitus  with  a  syphihtic  woman — 
tliat  is  to  say,  before  the  period  of  incubation  ;  nevertheless  the  chancre  developed  in  the 
scar  on  the  prepuce. 

In  most  cases  of  indurated  chancre  we  are  content  to  prescribe  cleanli- 
ness and  antiseptics,  such  as  iodoform,  salol,  or  aristol. 

In  a  series  of  experimental  studies  on  inoculated  syphilis  in  the  anthro- 
poid apes,  Metchnikoff,  after  having  discovered  the  attenuation  of  the 
syphilitic  virus  by  passing  it  through  certain  lower  species  of  monkeys,  has 
employed  antisyphilitic  vaccination.  This  method  has  not  yet  been  put 
into  practice  in  man.  The  use  of  a  serum  will  not  be  possible  until  a 
method  of  cultivating  the  Treponema  has  been  discovered. 

As  soon  as  the  chancre  is  recognized,  we  must  employ  mercurial  treat- 


2076  TEXT-BOOK  OF  MEDICINE 

ment  (inunctions,  pills  of  protoiodide,  or,  better,  daily  injections  of  ^  grain 
of  biniodide  of  mercury).  The  injections  are  given  for  ten  days  in  the 
month,  and  must  be  repeated  every  month  for  a  year.  It  is  essential  to 
treat  syphilis  from  its  onset  and  never  to  lose  sight  of  mercurial  treatment. 
The  most  serious  trouhles  (cerebral  arteritis,  nephritis,  etc.),  may  appear  during 
the  first  year  after  infection. 

Certain  new  methods  of  treatment  have  recently  been  put  in  practice ; 
two  of  these  may  be  mentioned  briefly :  hectine  and  Ehrlich's  606.  They 
are  both  preparations  of  arsenic,  and  are  both  given  by  injection. 

Hectine  is  given  in  doses  of  10  to  20  centigrams  in  a  gram  of  distilled 
water. .  Hallopeau  claims  that  syphilis  can  be  aborted  in  the  earliest  stage 
by  daily  injections  extending  over  a  period  of  thirty  days ;  the  chancre, 
however,  should  not  be  more  than  twenty  days  old.  The  injections  are 
made  in  the  neighbourhood  of  the  chancre.  Augagneur,  Moutot  and 
others  have  not  confirmed  Hallopeau's  results. 

Ehrlich's  606  is  employed  in  doses  of  40  to  60  centigrams ;  it  may  be 
given  by  intravenous  or  intramuscular  injection.  For  intravenous  injection 
Ehrlich  and  McDonagh  advise  0*5  gram  for  a  man  and  0*4  gram  for  a 
woman.  They  repeat  the  injection  in  five  days  in  most  cases,  and  give  a 
third  injection  in  six  weeks,  if  the  Wassermann  reaction  is  positive. 


IV.  FULMINANT  GANGRENE  OF  THE  PENIS.* 

Clinical  Cases. — A  young  man  was  admitted  under  my  care  for  gangrene  of  the 
penis.  The  odour  was  very  offensive.  The  cedematous  penis  looked  hke  a  black- 
pudding  ;  the  anterior  two-thirds  were  as  black  as  coal,  and  the  rest  was  of  a  violet 
colour.  On  the  dorsal  surface  there  were  vesicles,  from  which  foetid  Uquid  escaped ; 
the  prepuce  resembled  a  bell-clapper.  The  glans  was,  so  to  say,  set  in  the  gangrenous 
prepuce.  Crepitation  was  not  present ;  gaseous  gangrene  was  therefore  absent— an 
important  point.  No  hsemorrhage,  no  purulent  discharge.  The  urine  flowed  freely, 
but  infiltrated  the  dead  tissues.  The  scrotum  was  red  and  cedematous,  but  not  gan- 
grenous. The  inguinal  glands  were  enlarged  and  movable  ;  they  were  not  painful. 
The  patient  was  prostrated  ;  the  temperature  was  101°  P. 

In  addition  to  the  gangrene  of  the  penis,  rounded  ulcers  were  present  in  the  perianal 
region.  A  painless  ulcer  was  present  on  the  dorsum  of  the  tongue.  On  the  middle 
finger  of  the  right  hand  we  found  a  peri-ungual  ulceration,  which  had  given  rise  to 
lymphangitis  of  the  forearm.  The  patient  complained  of  dysphagia,  and  examination 
of  the  throat  showed  a  greyish  ulcer  on  the  right  pillar  of  the  fauces.  How  had  the 
gangrene  of  the  penis  commenced  ?  The  lesion  appeared  to  have  occurred  in  two  stages. 
The  onset  had  been  characterized  by  painless  swelHng  of  the  penis,  and  rapid  gangrene 
had  followed. 

What  was  the  cause  of  this  rapid  gangrene  ?  In  order  to  answer  this  question,  it 
was  necessary  to  review  the  causes  of  gangene  of  the  genital  organs. 

Diabetes  is  one  of  the  causes.     Fournier  and  Vaquez  have  quoted  cases. 


*  Dieulafoy,  CUnique  Medicate  deVHotel-Dieu,  1906,  vol.  v.,  p.  40. 


VKN  K I ;  i:  A I  -  I » I  s  i«;  .\  s  ms  2077 

Gangreno  may  b©  caused  by  parapliimnsis,  pliiiiidsiH,  and  Imlano-pofitliitiH,  consocu 
tivo  to  vogotalions,  hikI  liard  und  .suft  cliaiuins  nf  tlio  yroftvi;  and  <>i  tlu<  j^lurm. 
Balanopost  liitis  is  infcitioii  of  tlin  j^lan.s  and  pn^jtucn.  S(<V(iral  ()athii^'cni(;  rnicroboH 
liav»»  lHH>n  iiu  riiniiiatod — an  iiiocnlabli"  and  vory  nKjbilc  spirillum  (JJordal  and  Bataillo); 
ttiuuMiibic-  mirrobes  (Hist);  a  small,  t  bin  anaorobin  bacillii.s,  givinf<  off  a  frrtid  odour 
from  its  oulturos  (N'inoont).  'I'lifso  patliogonic  agents  multiply  tho  better  in  that 
thoy  are  {)rotoeted  from  tho  oxygon  of  tho  air  by  tho  anatomical  conformation  of  tho 
prepuce.  Tho  vogotationa  developed  in  tho  gi-oove  and  around  tho  glans,  as  well  as 
tho  balano-posthitia  and  phimosis,  produce  conditions  favourable  to  gangrene  of  the 
pre])uco  and  glans. 

Simple  cliancres,  says  Foamier,  by  reason  of  their  special  virulence,  are  liable  to 
produce  gangrenous  balano-posthitis.  Those  chan(;res  are  often  hidden  under  the 
prepuce,  which  become  aulematous  ;  jjhimosis  follows,  foul-smelling  fluid  exudes  from 
t  he  preputial  orilice,  and  in  a  few  days  gangn^ne  is  evident.  The  sloughing  jtrepuce  some- 
time perforates  laterally,  and.  as  Diday  says,  tho  glans  shows  its  nose  at  the  window. 
At  ot  her  times  the  gangrene  destroys  a  part  of  the  prepuce,  and  may  (Microach  upon  the 
glans.  ]icsidcs  these  partial  forms,  there  are  some,  says  Balzer,  in  wliich  tho  gangrene 
invades  the  skin  of  the  penis,  tlie  scrotum,  and  even  tho  corpora  cavernosa. 

In  my  patient  there  was  no  reason  to  suppose  gangrene  consecutive  to  these  different 
causes  ;  but  might  there  not  be  a  hard  chancre,  complicated  by  gangrene  ?  Griffon 
has  published  a  case  in  wlxich  a  hard  chancre  of  the  prepuce  gave  rise  to  gangrene,  which 
destroyed  the  penis  and  the  suprapubic  region.  In  this  case,  says  Foumier,  it  was  a 
question  of  early  tertiarism.  Nothing  similar  was  present  in  my  qase.  In  the  absence 
of  any  other  cause,  I  finally  diagnosed  spontaneous  fulminant  gangrene  of  the  penis — 
spontaneous  in  tliat  we  know  not  the  cause  ;  fulminant  in  that  the  sloughing  strikes  the 
tissue  "  like  a  stage- trick." 

The  prognosis  was  most  grave,  because  of  the  general  infection,  as  sho\\ii  by  tho 
ulceration  of  the  nails,  tongue,  and  throat.  In  such  a  case  of  septicaemia,  treatment 
had  little  chance  of  success.  Le  Dentu  made  vigorous  use  of  the  thermo-cautery, 
and  apphed  dressings  of  formalin  to  the  scarifications.  The  sjonptoms  grew  worse,  and 
the  patient  died  in  coma. 

I  saw  a  similar  case  in  the  Saint-Antoine  Hospital.  A  patient  came  imder  my  care 
with  fulminant  gangrene  of  the  penis  and  secondary  pueumonia.  He  died  rapidly, 
the  whole  penis  having  been  destroyed  before  death.  The  histological  examination  hy 
Giraudeau  revealed  neither  arteritis  nor  phlebitis.  The  process  was  one  of  fulminant 
gangi'ene. 

Fournier's  case  :  A  healthy  young  man  felt  sUght  pain  in  the  penis.  He  vomited, 
fever  appeared,  the  penis  swelled  up  and  became  red,  and  the  pain  increased.  Next 
day  patches  of  gangrene  were  visible.  In  three  days  the  sloughing  involved  the  prepuce 
and  the  scrotum,  wliile  a  tract  of  lymphangitis  started  from  the  gangrenous  region,  and 
ended  in  the  groin,  where  it  gave  ri.se  to  an  abscess.  An  eruption  of  purpura  appeared 
at  several  spots.  Nevertheless,  the  symptoms  improved,  and  recovery  finally  followed. 
Troisfontaine's  case  :  A  youth  felt  pain  behind  the  glans.  Next  day  the  prepuce 
was  oedematous.  During  the  follo^ving  days  the  penis  swelled  up ;  the  i^ain  was  severe  ; 
foul,  bloodstained  hquid  flowed  out  from  the  preputial  orifice ;  the  inguinal  glands 
enlarged  ;  the  temperature  was  104°  F.  ;  the  general  condition  was  bad  ;  and  the  raphe 
became  gangrenous.  A  wide  incision  showed  that  the  slough  had  invaded  the  sub- 
cutaneous tissue  and  fascia,  and  had  hoUowcd  a  funnel-shaped  hole  in  the  corpus 
cavemosum.     The  sloughs  were  cut  away  with  scissors.     Recovery  followed. 

Brocq's  case  :  On  June  1  a  soldier  was  taken  ill  with  fever,  and  found  that  liis  prepuce 
was  swollen.  Next  day  his  general  condition  was  bad,  and  delirium  set  in  on  June  3. 
The  penis  was  swollen  right  up  to  the  pubes,  the  skin  was  blackish,  and  gangrene  was 
obvious.      Free  incision.     Although  some  relief  followed,  vomiting  came  on,  and  the 


2078  TEXT-BOOK  OF  MEDIOmE 

temperature  rose  to  104°  F.  At  night  two  more  incisions  were  made.  The  glans  was 
foimd  to  be  intact.  On  June  4  the  stench  was  fearful.  On  June  5  penis  was  black  and 
sloughing,  scrotum  involved,  temperature  over  104°  F.  On  June  7  improvement 
set  in,  and  the  fever  diminished.  The  sloughs  commenced  to  separate,  repair  took  place 
slowly,  and  about  the  middle  of  July  the  patient  left  the  hospital. 

Description. — This  variety  of  gangrene  is  not  uncommon.  In  1883 
Fournier,  who  first  described  it,  had  seen  five  cases.  In  1896  Emery,  in  his 
thesis,  published  twenty-three  cases.  Next  come  the  cases  of  Fournier, 
Danlos,  Druelle  and  Nicolau,  Darses,  Grisel,  and  my  two  cases — a  total  of 
thirty-one  cases. 

The  disease  is  practically  confined  to  the  male  sex.  One  case  m  a 
woman  has  been  quoted  by  Brissaud  and  Sicard  : 

A  vesicle  appeared  on  the  right  labium  majus  of  a  healthy  woman.  On  the  third 
day  of  the  disease  pains  radiating  to  the  vulva,  no  glands  in  the  groin,  bloody  discharge 
from  the  vulva.  On  the  fourth  day  blackish  slough  on  each  side,  fulminant  gangrene, 
temperature  102°  F.  On  the  fifth  day  gangrene  spreading,  odour  offensive.  The 
patient  died  on  the  seventh  day,  her  temperature  being  106°  F.  The  urine  did  not 
contain  sugar  or  albumin.  The  blood  taken  on  the  sixth  day  gave  pure  cultures  of 
streptococci.     Anaerobes  were  not  looked  for. 

This  variety  of  gangrene  has  been  called  "  spontaneous,"  for  the  reason 
that  we  do  not  know  its  cause.  It  is  evidently  an  infective  process,  but  it 
is  hard  to  say  whence  the  infectious  agent  comes,  and  why  it  has  such 
virulence.  In  some  cases  it  has  appeared  in  persons  who  had  an  abrasion 
or  an  excoriation,  caused  by  scratching  in  the  case  of  eczema  ;  but  this 
entrance  gateway  is  rarely  present,  and,  again,  these  small  lesions  are  seen  in 
many  people  who  never  show  any  sign  of  gangrene. 

The  disease  is  nearly  always  seen  in  young  subjects.  In  thirty-one  cases 
I  find  an  old  man  and  three  infants.  My  patient  at  the  Hotel-Dieu  was 
twenty-five  years  of  age.  By  some  writers  this  genital  gangrene  is  said  to 
form  part  of  the  specific  venereal  infections — gonorrhoea  and  soft  and  hard 
chancres — or  it  is  said  to  result  from  excessive  coitus.  Fournier  has  rightly 
refuted  these  opinions.  The  disease  commences  in  a  healthy  person,  with 
itching  or  pain  in  the  prepuce  or  in  the  penis.  The  prepuce  takes  on  a 
reddish  tinge  and  swells  up.  The  patient  and  the  physician  are  not  alarmed. 
The  swelling  of  the  prepuce  determines  phimosis,  and  it  is  not  rare  to  find 
slight  discharge  due  to  balano-posthitis.  The  appearance  of  these  symp- 
toms leads  to  a  question  of  gonorrhoea  or  of  soft  chancres  in  the  groove 
around  the  glans.  The  patient  feels  some  alarm,  but  does  not  suspect  the 
storm  that  is  brewing.  "  The  contrast  is,  indeed,  remarkable  between  the 
apparently  benign  onset  and  tlie  malignant  character  of  the  resulting  lesion. 
In  a  few  hours  the  scene  changes.  The  penis,  which  has  become  painful, 
swells  as  a  whole,  and  becomes  oedematous,  being  converted  into  a  pudding 
— at  first  rosy,  then  red,  and  finally  livid.     Bullae  often  appear.     Matters 


VENEREAL  DISEASES  2079 

remain  in  this  state  for  some  twenty-four  to  thirty  hours,  and  then  a  new 
symptom  iiulioative  of  gangrene  reveals  itself  "  (Kournier). 

Greyish  or  yi'll(»\vish  insensitive  patches  a])})ear  on  the  prepuce,  penis, 
and  scrotum.  They  are  patches  of  gangrene.  At  this  moment  we  cannot 
say  whether  the  slough  will  stop  or  spread.  Sometimes  the  mortification 
is  limited  ;  at  other  tin-.^s  it  spreads  to  the  penis,  scrotum,  glans,  and  corpora 
cavernosa  with  astonishing  rapidity.  In  the  thirty-one  cases  which  I  have 
collected  the  regions  invaded  by  gangrene  were  as  follows  : 

In  eight  cases  the  sloughing  was  limited  to  the  prepuce,  which  was  partially  or 
totally  destroyed.  These  are  the  most  benign  cases.  In  twelve  cases  the  slough  in- 
vaded the  prepuce  and  the  raphe,  Avith  or  without  participation  of  the  scrotum.  Such 
was  the  case  in  my  patient  at  the  Hotel-Dieu.  In  three  cases  the  gangrene  was  limited 
to  the  glans.  In  five  cases  the  corpora  cavernosa  and  the  glans  participated  in  the 
gangrenous  infection,  and  the  distribution  of  the  sloughing  was  as  follows :  Gangrene 
of  the  prepuce  and  glans  (CJeUier) ;  gangrene  of  the  raphe  and  of  the  corpus  cavomosum 
(Trois-fontaines) ;  gangrene  of  the  raphe,  glans,  and  corpus  cavemosum,  the  glans  being 
represented  only  by  a  small  bud  (Foumier) ;  gangrene  of  raphe,  scrotum,  and  glans, 
the  latter  being  quite  destroyed  (Foumier) ;  gangrene  of  the  raphe,  part  of  the  glans, 
and  part  of  the  corpora  cavernosa  (Darses) ;  gangrene  of  the  entire  penis  (my  case  at 
the  Saint- An toine  Hospital). 

To  resume  the  description  of  the  disease.  The  dead  tissues  give  off  a 
most  offensive  odour,  and  become  as  black  as  coal.  Greenish  streaks  and 
islets  of  healthy  skin  sometimes  stand  out  against  the  black  tint  of  the 
eschar.  The  presence  of  gas  has  not  been  noted,  and  writers  upon  this 
disease  make  no  mention  of  it.  This  fact  is  noteworthy,  considering  the 
importance  of  fulminant  gangrene  in  which  gas  is  present.  The  general 
symptoms  increase  in  severity,  the  temperature  rises  to  104°  F.,  and  the 
patient  is  plunged  in  a  state  of  prostration  bordering  upon  adynamia.  The 
prognosis  appears  to  be  very  grave — the  patient  seems  certain  to  die,  and 
if  life  is  saved  there  is  great  likelihood  that  he  will  lose  a  part  of  the  genital 
organs.  The  latter  supposition  is  usually  erroneous,  since  in  reality  this 
fulminant  gangrene  is  rarely  fatal,  and,  on  the  other  hand,  the  repair  of  the 
dead  tissues  is  so  good  that  deformity  is  quite  an  unusual  result. 

The  gravity  of  the  prognosis  depends  upon  the  complications  of  lym- 
phangitis, erysipelas,  and  cellulitis  rather  than  upon  the  gangrene.  As  a 
rule,  in  the  midst  of  the  gangrenous  stage,  often  about  the  eighth  day,  im- 
provement suddenly  sets  in.  At  the  same  time  the  local  condition  changes. 
The  eschar  is  detached,  leaving  in  its  place  a  healthy  granulating  wound, 
and  healing  takes  place.  In  the  case  of  the  glans  and  corpora  cavernosa 
the  lesions  may  not  recover  sujQ&ciently  to  prevent  serious  deformity. 

The  condition  of  the  inguinal  glands  in  hard  and  soft  chancres  is  well 
known  :  in  the  former  a  pleiad  of  glands  ;  in  the  latter  a  suppurating  bubo. 
Nothing  of  the  kind  is  seen  in  fulminant  gangrene.     The  glands  react  so 


2080  TEXT-BOOK  OF  MEDICINE 

little  that  in  most  cases  the  adenopathy  is  trifling.  Haemorrhages  have  been 
noted  in  five  cases.  Purpura  has  been  seen  three  times.  Lymphangitis 
has  been  present  in  several  cases.  The  presence  of  lymphangitis,  erythema, 
abscesses,  and  erysipelas  in  which  streptococci  have  been  found,  had  led 
writers  to  place  fulminant  gangrene  of  the  penis  among  the  streptococcal 
infections. 

Diagnosis. — The  diagnosis  of  declared  gangrene  is  easy.  The  black 
colour  of  the  integument,  the  oedematous  swelling  of  the  tissues,  and  the 
stench  from  the  gangrenous  region  are  the  indications.  It  is,  however, 
necessary  to  know  the  variety  of  gangrene  present.  Is  it  fulminant  gan- 
grene, .or  is  it  gangrene  secondary  to  trauma,  or  to  balano-posthitis,  soft 
chancres,  warts,  phimosis,  etc.  ?  In  order  to  differentiate  these  secondary 
gangrenes,  careful  inquiry  must  be  made  as  to  the  cause.  Analysis  of  the 
urine  will  settle  the  question  of  diabetic  gangrene.  There  is  a  variety  of 
urinary  gangrene  which  at  first  sight  simulates  spontaneous  gangrene.  It 
may  appear  as  the  result  of  infiltration  of  urine  due  to  a  stricture  of  the 
anterior  urethra.  In  such  a  case  the  gangrene  appears  first  in  the  penis, 
and  closely  resembles  spontaneous  gangrene.  The  passage  of  a  catheter  is 
the  best  way  to  decide  the  point. 

In  another  variety  of  urinary  gangrene  the  stricture  of  the  urethra  may 
not  be  complete.  The  flow  of  urine  is  fairly  free,  and  though  no  stricture 
is  present,  gangrene  closely  resembling  spontaneous  fulminant  gangrene 
supervenes.  It  commences  in  the  prepuce,  spreads  rapidly  to  the  raphe 
and  scrotum,  and  ends  in  death. 

How  can  we  arrive  at  the  diagnosis  when  the  disease  is  in  its  early 
stage  ?  The  prepuce  is  red  or  oedematous,  the  raphe  often  participates  in 
the  oedema,  and  the  patient  experiences  a  sensation  of  pain  or  of  burning. 
We  think  of  balano-posthitis,  of  lymphangitis  following  an  excoriation,  or 
of  soft  chancres  accompanied  by  phimosis,  but  a  scrupulous  examination 
leads  us  to  abandon  these  views.     Bullee  form,  and  gangrene  appears. 

Treatment. — The  patient  should  be  given  baths  if  he  can  bear  them  ; 
moist  dressings  should  be  applied  to  the  gangrenous  parts.  The  strength 
is  kept  up  with  stimulants,  and  surgical  intervention  is  employed  as  soon  as 
possible.  Free  incisions  as  well  as  scarification  with  the  thermo-cautery 
give  good  results.  In  one  of  Fournier's  patients  the  penis  was  gangrenous, 
and  the  scrotum  appeared  likely  to  share  the  same  fate.  Le  Dentu  at  once 
made  free  incisions  into  the  scrotum,  and  immediate  improvement  set  in. 

Pathogenesis  and  Pathological  Anatomy. — According  to  some  writers,  fulminant 
gangrene  of  the  penis  is  simply  a  gangrenous  lymphangitis  or  erysipelas.  They  base 
their  opinion  upon  the  coexistence  of  lymphangitis,  erysipelas,  and  gangrene,  and  on 
the  presence  of  streptococci.  I  would  refer  the  reader  to  my  clinical  lectures  on  this 
subject. 

In  several  cases  it  appears  that  the  streptococcus  is  at  fault.     In  many  other  cases, 


VKNKI.'KAL   DISKASKS 


2081 


howevor,  the  streptoroccus  is  absont,  uiul  in  ray  patimt  we  shall  see  tho  remilt  of  tho 
bacttifiologioal  exaininatiim. 

I  give  first  tho  losiims  found  at  thu  autopsy.  Kxcopt  for  a  pat<|j  of  mfinin^tis, 
the  examination  of  tho  viscera  was  noxativo.  Tho  l)larkiHh  gangrenous  colour  ex- 
tended to  the  root  of  tho  penis  with(nit  any  eioar  lino  of  dimarcation.  The  prepuce  was 
intiltratod  and  gangrenous.  Tlio  groove  between  tho  glans  and  tho  prepuco  was  of  a 
deep  red,  and  streaked  with  ha-morrhagie  hnes.  We  could  not  find  ulcers,  chancres, 
cicatrices,  or  pus  at  tho  bottom  of  tho  furrow.  There  was  no  balano-posthitis.  Soctionh 
of  tho  penis  showed  that  the  uret  lu^a  and  the  corpora  cavernosa  wore  normal.  They  were 
Borroundod  by  hard  connective  tissue.  The  histological  examination  gave  the  following 
results:  In  tho  prepuce  tho  necrosed  tissue  stained  a  uniform  rod  colour  with  eosin. 
The  nuclei  did  not  stain  with  h.-rmatoxylin,  and  very  high  magnification  was  required 
to  show  a  slight  embryonic  infiltration.  The  epidermis  and  the  internal  covering  of 
the  mucous  membrane  had  completely  disappeared.  Tho  dermis  was  ragged.  The 
connective  tissues  wore  dissociated  by  patches  of  fX'dema  and  fibrin.  Similar  lesions 
were  found  in  tho  balano-preputial  groove.  On  the  dorsum  of  the  penis  similar  lesions 
were  present.  They  did  not  penetrate  the  corpora  cavernosa.  At  tho  root  of  the 
penis  we  found  some  arteritis  and  phlebitis,  but  in  no  part  was  complete  or  partial 


Fi(..  Mo. — Pkn'is  :  Bacillus 
Septicus   and  Entekococcus. 


Fig.  01. — Blood  :  Bacillus 
Septicus   and  Enterococccs. 


thrombosis  present.  The  vascular  lesions  appeared  to  be  secondary,  and  not  primary. 
No  line  of  demarcation  with  leucocytic  infiltration  was  present.  The  transition  between 
the  healthy  and  the  diseased  tissue  was  insensible.  The  gangrenous  focus  in  the  tongue 
being  limited,  the  histological  picture  was  even  more  clear. 

Bacteriological  Examination. — I  shall  give  a  resume  of  the  bacteriological  examina- 
tion (smears,  cultures,  and  inoculations)  as  regards  the  penis,  the  meninges,  the  anal 
region,  and  the  blood.  Everywhere,  except  in  the  perianal  ulcerations,  we  found 
two  associated  microbes,  which  swarmed  from  the  penis  into  the  blood  and  the  brain. 

These  two  microbes  showed  the  following  characters  : 

1.  A  thick  aerobic  bacUlus,  having  rounded  ends,  and  staining  with  Gram.  Its 
centre  was  often  but  Uttle  stained  ;  its  length  varied  with  the  age  of  the  cultures  ;  it 
was  often  isolated  ;  it  occurred  at  times  in  the  form  of  a  diplobacUlus  or  of  small  masses  ; 
it  grew  readily  on  both,  and  gave  off  a  foetid  odour  ;  it  was  pathogenic  for  guinea-pigs, 
in  which  it  produced  gangrene.  These  characters  identified  it  as  the  BacUlus  septicus 
of  Legros  and  Lecene.     Legros  confirmed  my  view. 

2.  A  facultative  aerobic  and  anaerobic  diplococcus.     It  stained  with  Gram  and  was 


2082 


TEXT-BOOK  OF  MEDICINE 


characterized  by  an  astonishing  polymorphism  (small  cocci,  large  cocci,  short  chains  of 
diplococci  on  agar,  short  baciUi  in  old  cultures).  It  grew  readily  on  broth  and  agar, 
it  did  not  liquefy  gelatine,  and  it  was  very  long-lived.  These  characters  identified  it 
as  the  enterococcus  of  Thiercelin,  and,  as  a  matter  of  fact,  Thiercehn  identified  it. 

In  this  case  of  fulminant  gangrene  the  Bacillus  septicus  was  the  pathogenic  micro- 
organism. The  other  organism  appeared  to  play  quite  a  second  part.  There  was  no 
sign  of  the  streptococcus. 

What  is  the  BaciUus  septicus  ?  The  answer  is  given  by  the  following 
case,  taken  from  Legros's  thesis  : 

A  man  was  admitted  under  Pegrot  for  a  fracture  of  the  right  leg,  the  tibio-tarsal 
joint  being  widely  opened.  The  fracture  was  set,  and  an  injection  of  antitetanic  serum 
was  given.  Next  morning  the  temperature  was  104°  F.  On  removing  the  dressings, 
the  wound  was  blackish,  and  gave  off  an  offensive  odour.  Reddish  fluid  mixed  with 
bubbles  of  gas  flowed  out.  Amputation  through  the  middle  third  of  the  thigh  was 
performed.  In  the  lower  part  of  the  amputated  hmb  the  skin  had  a  bronzed  colour, 
and  gas  crepitation  was  noticeable.  Two  days  after  the  operation  the  flaps  were  slough- 
ing, the  upper  part  of  the  thigh  was  crepitant,  the  gangrene  was  extending,  the  stench 
was  unbearable,  and  death  supervened  six  days  after  the  accident. 


Fig.  95. —  Meninges  :  Bacillus 
SEPTictrs  AND  Enterococcus. 


Fig.  96.— Perianal  Ulceration; 
Enterococcus. 


Some  foul-smeUing  serous  fluid  had  been  taken  from  the  dead  muscles  two  days  after 
the  operation.  Three  species  of  microbes  were  isolated :  they  were  aerobic  by  prefer- 
ence. They  comprised  a  bacillus  with  the  characters  of  the  Bacillus  coli,  a  diplostaphylo- 
coccus  liquefying  gelatine,  and  a  special  bacfllus,  corresponding  in  its  morphological 
characteristics  to  the  species  predominating  in  direct  preparations  of  the  foul-smelling 
serous  fluid.  Of  these  three  species  the  last  one  alone,  when  injected  into  a  guinea-pig, 
gave  rise  to  rapid  gaseous  gangrene.  The  animal  died  in  forty-eight  hours,  the  affection 
being  characterized  by  its  invading  nature  and  by  the  enormous  lesions  in  the  muscles. 

This  bacUlus  has  been  described  by  Legros  and  Lecene  under  the  name 
of  the  BaciUus  septicus  aerohicus.  I  shall  not  describe  the  characters  of  this 
bacillus,  since  they  are  comparable  to  those  of  the  bacillus  found  in  my  case 
of  genital  gangrene,  with  this  exception — that  in  one  case  gas  was  present, 
whUe  in  the  other  it  was  absent. 


VKNEKKAF.  DISEASES  2083 

TIio  liarillus  se'})ticus,  says  Logros,  has  essential  charactora,  which  on  tho 
one  hand  sliow  its  rehition  to,  and  on  the  other  hand  its  difference  from,  the 
Vibrio  sejyticus  of  Pasteur.  Legros  has  reported  another  case  of  gaseous 
gangrene  duo  to  the  Bacillus  sej)ticus.  Jacobolli  of  Naples  has  also  pub- 
lished a  case  of  acute  gaseous  gangrene,  in  which  the  bacillus  isolated  had 
all  the  characteristics  of  the  Bacillus  septicns  of  Legros. 

These  cases  prove  that  the  Bcuyillxis  septictis  causes  fulminant 
gangrene,  with  production  of  gas.  In  my  patient,  however,  no  gas  was 
present.  The  same  bacillus,  therefore,  may  cause  gangrene  with  the 
presence  of  gas  and  gangrene  in  which  gas  is  not  present.  What  is  the 
explanation  ? 

It  is  opportune  at  this  point  to  discuss  the  question  of  specific  microbes. 
Do  they  exist  ?  The  answer  is  afiirmative.  They  cause  specific  diseases, 
and  it  was  a  stroke  of  genius  on  the  part  of  Trousseau  to  have  stated  that 
some  day  we  should  discover  specific  germs  in  the  case  of  certain  maladies  * 
Trousseau's  prediction  has  been  verified,  and  in  the  case  of  diphtheria  and 
typhoid  fever  the  specificity  clinically  created  by  Bretonneau  and  Trousseau 
has  been  confirmed  by  the  microbic  specificity.  These  views  on  this  subject, 
which  have  shed  much  light  on  the  pathogenic  chaos,  have  sometimes  over- 
shot the  mark ;  and  since  we  are  now  speaking  of  fulminant  gaseous  gan- 
grene, it  is  certain  that  we  were  too  accustomed  to  the  idea  that  these  cases 
depended  on  a  specific  infection  due  to  the  Vibrio  sefticus  of  Pasteur. 
The  pathogenic  action  of  the  ^^b^io  is  true  in  many  cases,  but  it  is  not 
the  specific  organism  in  every  case  of  fulminant  gaseous  gangrene. 
Other  organisms  may  produce  the  same  clinical  picture,  with  identical 
lesions. 

The  writings  of  Legros  will  convince  us  as  regards  this  point.  We  find 
a  series  of  organisms  capable  of  causing  fulminant  gaseous  gangrene.  Such 
are  the  Bacillus  emphysematis  maligni,  the  B.  fhlegmonis  emphysematoscB, 
the  B.  perfringens,  and  the  B.  septicns  aerobicus. 

It  is  evident,  says  Legros,  that,  in  addition  to  the  cases  of  acute  gaseous 
gangrene  described  by  surgeons,  we  may  also  find  more  benign  infections. 
They  are  due  to  the  same  pathogenic  agents,  and  are  characterized  by 
gaseous  oedema,  with  localized  putrid  decomposition.  Roger  ("  Les  Maladies 
Lifectieuses  "),  forsaking  the  idea  of  specificity  in  the  question  now  under 
discussion,  has  headed  his  chapter  "  Divers  Agents  des  Gangrenes  Gazeuses," 
and  side  by  side  with  the  Vibrio  septicus  he  places  "  a  series  of  microbes 
which  more  or  less  resemble  it  by  reason  of  their  biological  or  pathogenic 
properties." 

These  statements  are  true,  and  we  see  that  the  Bacillus  septicus  is  capable, 
like  the  organisms  just  mentioned,  of  producing  fulminant  gaseous  gan- 

♦  Vide,  Lecon  d'Ouverture  de  la  Clinique  de  V Hold-Dieu,  1898,  t.  i.,  1*"  le9on. 


2084  TEXT-BOOK  OF  MEDICINE 

grenes.  Nevertheless,  the  gangrene  in  my  patient  was  not  gaseous.  This 
fact  proves  that  the  Bacillus  septicus  under  certain  ill-defined  conditions 
may  engender  gaseous  or  non-gaseous  gangrene.  Furthermore,  the  produc- 
tion of  gas  was  not  noted  in  any  of  the  thirty- one  cases  of  fulminant 
gangrene  of  the  genitalia  mentioned  in  this  section. 

There  is  another  organ  in  which  the  gangrene  is  never  gaseous — the 
appendix.  I  have  pointed  this  fact  out  in  one  of  my  clinical  lectures.* 
As  the  question  is  of  importance,  I  am  desirous  of  briefly  discussing  it. 
Appendicular  pleurisy  is  often  putrid  and  gaseous.  It  would,  therefore, 
appear  logical  that  the  microbe  which  can  cause  putrefaction  in  the  pleura 
should  also  cause  putrefaction  in  the  appendix.  Such  is  not  the  case.  I 
have  seen  200  operations  for  appendicitis,  but  I  have  never  seen  gaseous 
gangrene  of  the  appendicular  focus  or  gaseous  phlegmon  in  its  waUs.  We 
do  see  fulminant  gangrene  in  the  appendix,  but  we  do  not  find  gas.  And 
yet  the  anaerobic  and  aerobic  flora  of  appendicitis  is  very  rich.  The  Bacillus 
septicus  aerobicus  has  even  been  found.  These  apparent  contradictions 
prove  that  we  have  much  to  learn. 

This  discussion  proves  that  fulminant  gangrene  of  the  penis  cannot  be 
included  under  gaseous  gangrene.  It  is  not  a  specific  disease  with  a  specific 
microbe.  We  must,  therefore,  exclude  the  formula  which  gives  the  strepto- 
coccus as  the  specific  agent.  It  is  inexact  to  say  that  this  gangrene  is  merely 
a  streptococcal  infection.  In  certain  cases,  especially  when  the  gangrene  is 
associated  with  erysipelas,  the  pathogenic  agent  appears  to  be  a  strepto- 
coccus, but  in  many  cases  the  streptococcus  is  absent,  and  we  find  other 
microbes.  In  my  patient  the  Bacillus  septicus  aerobicus  produced  first 
gangrene  and  then  fatal  septicaemia. 

This  study  in  bacteriology,  interesting  though  it  be,  only  serves  to  put 
off  the  pathogenic  problem,  without  solving  it.  While  admitting  that  the 
streptococcus,  the  Bacillus  septicus,  or  other  organisms,  may  produce  ful- 
minant gangrene  of  the  genitalia,  whence  come  these  organisms,  and  what 
is  the  cause  of  their  virulence  ?  Why,  on  the  one  hand,  fulminant  destruc- 
tion of  the  tissues,  and  on  the  other  hand  the  relatively  benign  nature  of  the 
disease  ?  We  do  not  know.  It  will  be  said  that  we  must  consider  the 
receptivity  of  the  soil.  What,  however,  does  this  statement  mean  ?  We 
do  not  know.  Most  of  the  patients  were  healthy  and  free  from  any  previous 
taint,  and  yet  fulminant  gangrene  set  in,  without  appreciable  cause  and 
without  proved  contagion. 

This  form  of  gangrene  has  weU-defined  characters.  The  presence  of 
gas  has  never  been  noted.  The  Bacillus  septicus,  which  in  surgical  trau- 
matisms produces  gaseous  gangrene,  caused  non-gaseous  gangrene  in  my 
patient.  Fulminant  gangrene  of  the  genitals  has,  then,  a  place  beside  the 
*  Dieulafoy,  Clinique  Medicah  deVHotd-Dieu,  t.  iv.,  p.  111. 


VKXKRKAI.    DISEASES  L'UH.. 

various  forms  of  gaseous  gangrene.  It  is,  moreover,  far  less  foriiudable. 
I  would  add  that  it  never  extends  beyond  the  genital  organs.  It  is  not 
invading,  like  the  gaseous  forms  of  gangrene. 

It  has  nothing  in  common  with  gangrene  due  to  vascular  lesions,  my 
case  being  an  irrefutable  proof  thereof.  In  this  case  there  was  no  phlebitis, 
no  arteritis  obliterans'.  The  toxic  agent  appeared  to  have  a  directly 
necrosing  action  on  the  tissues.  The  pathogenesis  of  this  variety  of  gan- 
grene is  not  yet  cleared  up.  For  the  present  the  term  "  spontaneous  " 
must  be  preserved. 


^  132 


PART  XII 

THE  INTOXICATIONS 

The  study  of  poisoning  belongs  specially  to  toxicology  and  forensic  medicine. 
Nevertheless,  certain  intoxications  are  intimately  connected  with  patho- 
logical studies  properly  speaking.  In  this  respect  I  may  mention  alcoholism, 
lead-poisoning,  and  hydrargyrism. 

I.  ALCOHOLISM. 

Alcoholic  drinks,  in  the  form  of  wine,  liqueurs,  absinthe,  beer,  etc.,  are 
the  more  formidable  in  proportion  as  they  are  of  inferior  quality. 

The  essences  (balm,  mint,  angelica,  peppermint,  etc.)  which  often  enter 
the  composition  of  liqueurs  increase  their  toxic  power,  although  it  is  not 
always  possible  to  state  the  exact  part  these  essences  take  in  the  morbid 
results.  Alcoholic  drinks  are  more  harmful  when  taken  in  the  morning  on 
an  empty  stomach  than  they  are  at  meal-times. 

Acute  Alcoholism. — Acute  alcoholism  is  known  as  drunkenness. 
Drunkenness  declares  itself  after  more  or  less  copious  libations  of  alcoholic 
beverages.  It  commences  with  a  period  of  excitation.  The  drunkard  has 
a  bright  eye  and  a  congested  face.  He  becomes  loquacious  and  noisy ;  he 
is  no  longer  master  of  his  feelings,  joy,  anger,  and  sadness  being  pushed  to 
their  extreme  limits.  Vertigo  soon  appears ;  the  gait  becomes  unsteady ; 
the  gastric  malaise  is  considerable  ;  the  face  is  pale  ;  the  sweating  is  profuse  ; 
and  some  of  the  fluid  taken  is  vomited.  After  vomiting  the  malaise  dis- 
appears, and  sleep  terminates  this  period  of  drunkenness,  which  leaves 
behind  it  only  slight  gastric  distress.  Vomiting,  however,  does  not  always 
occur,  and  the  fluids  ingested  are  not  always  rejected.  The  period  of 
excitation  then  gives  place  to  a  phase  of  depression  ;  the  drunken  man  falls 
down  unconscious  ;  the  respiration  is  embarrassed  and  stertorous,  as  in  coma  ; 
and  the  anaesthesia  and  the  muscular  relaxation  are  complete. 

If  the  drunkenness  results  from  the  ingestion  of  liqueurs  containing 
extracts  of  aromatic  plants,  such  as  absinthe,  bitters,  or  vermuth,  and 
especially  if  the  patient  is  addicted  to  their  use,  we  may  witness  epileptiform 
convulsions   (Farcy's   convulsive   drunkenness).     This  condition  lasts   for 

2086 


THE  INTOXICATIONS  2087 

some  hours,  and  the  patient  gradually  regains  his  faculties.  In  some  cases, 
however,  if  the  patient  has  al).sorbed  a  large  quantity  of  alcohol,  and  has 
been  exposed  to  cold  for  a  long  while,  the  central  teni]j('rature  falls  pro- 
gressively, and  death  may  residt. 

Chronic  Alcoholism. — Chronic  alcoholism  is  slowly  established,  and  the 
troubles  whicii  it  causes  concern  chieily  the  digestive  tract  and  the  nervous 
system. 

Their  predominance  in  one  or  other  of  these  two  systems  depends  upon 
hereditary  predisposition.  An  individual  bom  of  neurotic  parents,  or 
neurotic  himself,  may  from  the  first  show  severe  i^ervous  symptoms,  while 
in  another  alcoholic  such  troubles  will  be  indefinitely  delayed. 

Digestive  Troubles. — The  alcoholic  person  loses  his  appetite,  experiences 
a  burning  sensation  along  the  oesophagus  (pyrosis),  and  in  the  morning 
vomits  whitish  shreddy  matter  (mucus).  The  chronic  gastritis  of  drunkards 
is  at  times  complicated  by  ulceration.  Heematemesis  may  occur.  Some 
authors  admit  that  the  gastric  ulceration  of  alcoholic  origin  may  assume  the 
character  of  the  roimd  ulcer. 

As  the  portal  vein  carries  a  portion  of  the  ingested  alcohol  direct  to 
the  liver,  congestion,  steatosis,  and  fatty  cirrhosis  and  especially  atrophic 
cirrhosis,  are  frequent  in  alcoholics.  The  acute  icterus  of  drunkards  (Leudet) 
is  of  exceptional  gravity. 

Nervous  Troubles. — The  alcoholic  tremor  is  an  early  symptom.  It  is 
especially  marked  in  the  upper  limbs  and  hands,  and  is  most  severe  in  the 
early  morning,  when  the  stomach  is  empty.  It  improves  during  the  day 
under  the  influence  of  fresh  libations. 

Sensory  troubles  are  frequent.  Alcoholics  complain  of  headache,  giddi- 
ness, formication,  cramps  in  the  calves,  or  anaesthesia,  which  sometimes 
invades  half  the  body  (Magnan).  Hearing  and  sight  are  perverted,  and 
some  patients  experience  hallucinations,  epUeptiEorm  convulsions,  and 
attacks  of  acute  mania  or  of  lypemania  ;  others  suffer  from  cerebral  troubles 
which  resemble  those  of  general  paralysis,  and  have  been  described  under 
the  name  of  Alcoholic  Greneral  Pseudo-Paralysis.  At  the  present  day  the 
tendency  is  to  split  these  cases  into  two  classes — in  the  one  alcoholism  (in 
predisposed  individuals)  leads  to  general  paralysis ;  in  the  other  it  ends  in 
dementia. 

The  sleep  is  disturbed  by  nightmares  and  dreams.  The  patient  thinks 
that  he  sees  animals,  such  as  rats,  running  over  his  bed. 

Delirium  Tremens  is  an  acute  episode  of  chronic  alcoholism.  Sometimes 
it  is  provoked  by  excess  of  alcoholic  drinks,  and  at  other  times  it  complicates 
an  intercurrent  disease  (pneumonia,  rheumatism,  injury).  The  patient  is 
seized  with  violent,  noisy,  or  furious  deliriimi,  requiring  the  employment  of 
the  strait-jacket.     The    insomnia    is    complete,  and    the    movements    are 

132-2 


2088  TEXT-BOOK  OF  MEDICINE 

disordered.  The  attack  lasts  on  an  average  from  three  to  five  days,  and 
ends  in  deep  sleep.  Recovery  usually  occurs  when  the  patient's  tempera- 
ture remains  low.  If  deliriimi  tremens  appears  apart  from  any  febrile 
disease,  and  is  accompanied  by  a  temperature  rising  to  102°  F.,  the  situation 
becomes  very  grave,  and  the  patient  frequently  dies  (Magnan). 

We  may  see  in  alcoholics,  and  especially  in  women,  paralyses  which  com- 
mence in  the  lower  limbs.  They  are  localized  chiefly  to  the  antero- external 
group  of  the  muscles  of  the  legs,  whence  they  spread  to  the  other  muscles. 
In  severe  cases  the  upper  limbs  are  affected,  and  here,  too,  the  paralysis 
commences  in  the  extensors.  The  muscles  of  the  face,  of  the  neck,  and  of 
the  eyes  are  more  rarely  afiected.  The  paralysis  is  painful,  and  rapidly 
becomes  complete.  It  is  always  flaccid,  and  is  accompanied  by  pains  in 
the  muscles,  by  early  muscular  atrophy,  by  abolition  of  the  reflexes,  and 
by  loss  of  the  electrical  contractility.  It  is  curable  as  a  rule,  but  recovery 
is.  always  slow.  In  other  cases,  whether  paralysis  is  present  or  absent,  we 
find  troubles  of  locomotion  similar  to  those  of  locomotor  ataxia  (alcoholic 
pseudo-tabes). 

Whether  the  case  be  one  of  paralysis  or  of  pseudo-tabes,  if  the  atrophy 
is  very  marked  it  leaves  in  its  train  muscular  retractions  which  cause  de- 
formities of  the  limbs,  and  particularly  of  the  feet.  When  the  paralysis 
becomes  general  it  may  invade  the  muscles  of  respiration,  attack  the  heart 
itself  (Dejerine),  and  provoke  syncope  and  death.  It  has  an  acute  or  a 
subacute  course,  and  the  muscular  lesions  are  very  slowly  repaired.  Re- 
lapses are  frequent. 

The  peripheral  nerves  (peripheral  neuritis)  are  the  starting-point  of  these 
motor  troubles,  the  nerves  of  the  limbs  being  first  afiected  (Lancereaux, 
Oettinger,  Buzzard,  etc.).  No  form  of  toxic  neuritis  is  better  established 
than  the  alcoholic  form.  It  may  also  attack  the  cranial  nerves,  vagus, 
optic,  etc. 

Many  authors,  however,  admit  that  these  nervous  changes  are  them- 
selves consecutive  to  dynamic  lesions  of  the  cord  (Erb). 

Ocular  troubles  consecutive  to  chronic  intoxication  by  alcohol  are  very 
frequent.  They  consist  in  amblyopia  (toxic  amblyopia),  which  may  develop 
somewhat  rapidly,  and  afiect  both  eyes.  This  amblyopia  is  characterized 
by  a  more  or  less  marked  diminution  of  the  central  visual  acuity  (central 
scotoma),  while  the  periphery  of  the  visual  field  remains  unaffected.  The 
scotoma,  before  being  absolute,  exists  only  for  colours — that  is  to  say,  the 
examination  of  the  visual  field  with  a  white  object  causes  no  interruption, 
while  the  colour  cannot  be  seen  over  the  whole  extent  of  the  scotoma  if  a 
green  or  a  red  index  be  used  for  the  examination.  Patients  see  better  at 
sundown  (nyctalopia),  because  the  sensation  of  dazzling  disappears. 

The  ophthalmoscope  reveals,  as  a  rule,  no  lesion  in  the  fundus  oculi. 


THE  TXTOXTCATrDyS  2080 

In  some  cases  Uhthoff  found  decoloration  of  the  external  half  of  the  optif^ 
papilla.  If  the  amblyopia  is  treated  from  thr  onset,  it  disappears  without 
leaving  any  traces.  In  older  cases  coin}>lott!  re-establishment  of  vision  is 
almost  always  impossible. 

Alcoholic  poisoning  may  cause  paralysis  of  tlu'  motor  musch-s  of  the  eye. 
Acute  polio-oiu'epluilitis,  as  I  have  said  in  a  previous  chaptf-r,  may  some- 
times be  related  to  alcoholic  poisoning. 

Chronic  alcoholism  exercises  its  action  on  other  systems.  The  voice  is 
often  hoarse  and  rough  from  chronic  congestion  of  the  pharyngeal  mucous 
membrane  (graniUar  angina),  of  the  epiglottis,  of  the  arytenoids,  and  of  the 
laryngeal  mucosa.  Genital  weakness  and  impotence  are  not  uncommon. 
The  circulatory  troubles  depend  upon  the  atheromatous  condition  of  the 
vessels. 

Diagnosis — Prognosis. — The  characteristic  odour  of  the  patient's  breath 
serves  to  distinguish  the  coma  of  drunkenness  from  coma  or  apoplexy  asso- 
ciated with  other  morbid  conditions. 

The  various  troubles  which  depend  upon  chronic  alcoholism  will  be 
recognized  by  the  symptoms  previously  enumerated,  and  by  the  informa- 
tion furnished  by  the  patient.  And  yet,  in  the  face  of  such  troubles  as 
morning  vomiting,  tremor,  tendency  to  delirium,  and  lypemania,  the  in- 
formation given  by  alcoholic  patients  should  be  mistrusted,  as  some  stoutly 
deny  their  alcoholic  habits. 

The  alcoholic  paralyses  are  distinguished  from  myelitis  by  their  dis- 
semination, by  the  spontaneous,  and  especially  by  the  provoked,  pain,  by 
the  rapid  abolition  of  the  reflexes,  and  by  the  early  muscular  atrophy.  In 
pseudo-tabes  the  leg  is  never  thrown  to  the  left  or  to  the  right,  as  in  ataxia, 
and  the  patient  has  the  steppage  gait  (Charcot).  The  course  of  the  disease 
is  rapid,  and  not  slowly  progressive.  Recovery  is  frequent,  but  relapses 
are  to  be  feared. 

The  prognosis  of  acute  alcoholism  is  rarely  grave.  Chronic  alcoholism 
is  serious,  because  it  progressively  and  surely  induces  obstinate  gastritis, 
cirrhosis  of  the  liver,  arterial  atheroma,  delirium  tremens,  mania,  dementia, 
and  suicide.  The  influences  of  chronic  alcoholism  extend  to  the  descendants, 
for  the  children  of  alcoholic  parentage  are  sometimes  degenerates  (idiocy, 
scrofula,  epilepsy,  etc.). 

Pathological  Anatomy. — Congestion  of  the  lungs,  of  the  meninges,  and 
of  the  brain,  with  or  without  haemorrhage,  is  found  in  those  who  have  died 
from  acute  alcoholism  (Tardieu).  The  blood,  the  liver,  and  the  brain — in 
fact,  all  the  organs — are  impregnated  with  alcohol. 

Chronic  alcoholism  produces  two  classes  of  lesions — chronic  interstitial 
inflammations  of  the  cirrhotic  type  and  fatty  degenerations  of  the  paren- 
chyma.    The  stomach  is  sometimes  contracted,  sometimes  dilated.     The 


2090  TEXT-BOOK  OF  MEDICIITE 

mucous  membrane  is  tliickened,  injected,  and  ulcerated.  The  liver  shows 
cirrhosis  or  steatosis,  either  separately  or  in  combination.  The  heart  is 
fatty  and  the  vessels  are  affected  by  endarteritis  and  atheroma.  The  kidneys 
present  the  changes  of  sclerosis  and  of  fatty  degeneration.  The  laryngeal 
mucous  membrane  is  hypersemic  and  thickened.  The  meninges  are  con- 
gested and  inflamed.  They  sometimes  present  the  lesions  of  pachymenin- 
gitis. The  braia  is  affected,  and  its  surface  shows  numerous  foci  of  softening, 
which  explain  the  mental  troubles. 

Treatment. — In  a  drunken  man  it  is  necessary  to  provoke  the  rejection 
of  the  ingested  drink  by  vomitiug.  Acetate  of  ammonia  (20  drops  iu  a 
little  water)  and  coffee  are  useful  aids  for  stimulating  the  organism.  In 
some  alcoholic  patients  delirium  tremens  appears  to  be  favoured  by  too 
sudden  or  too  complete  a  suppression  of  alcohol.  In  this  case  beverages 
containing  wine  may  be  prescribed,  while  extract  of  opium,  chloral,  and 
bromide  of  potassium  should  also  be  administered.  It  is  evident  that  we 
must  employ  aU  possible  means  to  suppress  or  progressively  to  diminish 
the  quantity  of  alcohol,  as  this  is  the  cause  of  the  disease.  From  recent 
experiments,  the  serum  of  a  horse  accustomed  to  alcohol  is  said  to  contain 
an  anti-ethylin,  which  lessens  the  desire  for  alcoholic  drinks  after  injection 
into  man  (Broca,  Sapelier,  and  Thiebault). 

II.  MEKCUEIAL  POISONING— HYDEARGYRISM. 

Hydrargyrism  comprises  the  pathological  manifestations  caused  by  the 
accumulation  of  mercury  in  the  economy.  This  intoxication  may  be  of 
therapeutic  or  of  professional  origiu. 

iEtiology. — The  therapeutic  form  is  sometimes  consecutive  to  cutaneous 
absorption  from  mercurial  inunction  or  cauterization  with  acid  of  nitrate  of 
mercury ;  at  other  times  consecutive  to  intestinal  absorption  of  calomel,  or 
proto -iodide  of  mercury.     More  rarely  it  follows  baths  of  mercurial  vapour. 

The  administration  of  the  drug  must,  as  a  rule,  be  prolonged  for  a  certain 
time  in  order  to  cause  poisoning.  In  some  patients,  however,  a  single 
cauterization  has  given  rise  to  toxic  phenomena.  There  exists,  therefore, 
in  the  case  of  mercury,  as  of  many  medicinal  substances,  a  susceptibility 
which  varies  with  different  individuals,  and  which  cannot  be  foreseen.  This 
mode  of  mercurial  poisoning  is  much  less  frequent  than  it  was  formerly, 
because  saturation  of  the  economy  with  mercury  is  no  longer  considered 
indispensable  to  the  proper  action  of  the  drug. 

Professional  hydrargyrism  is  seen  in  miners  (Almaden,  Istria)  and  m 
workmen  who  handle  mercury  in  its  natural  state  (gilders,  makers  of 
looking-glasses  and  barometers),  or  the  salts  of  mercury  (hatters,  etc.).  The 
absorption  usually  takes  place  by  the  skin  and  the  respiratory  tract,  but  in 


THE  INTOXICATIONS  2091 

miners  the  drug  may  also  enter  by  the  digestive  tract,  as  the  metal  has  been 
found  in  the  stools.  Idiosyncrasy  plays  an  important  part  in  tliese  cases, 
just  as  in  the  preceding  form.  One  minor  will  suffer  from  poisoning  at  the 
end  of  seven  or  eight  hours  of  work,  while  another  will  resist  for  several 
weeks.     Tlic  same  holds  good  ainonj^  workinon  in  cities. 

Symptoms — Acute  Hydrargyrism. — The  therapeutic  form  usually  com- 
mences with  slight  stomatitis,  which  tends  to  increase  if  the  drug  is  con- 
tinued {vide  Mercurial  Stomatitis).  Such  accidents  are,  as  a  rule,  no 
longer  seen,  since  the  administration  of  mercury  is  usually  stopped  as  soon 
as  it  produces  symptoms,  except  in  very  urgent  cases. 

In  professional  hydrargyrism  the  first  symptoms  are  palpitation,  breath- 
lessness,  loss  of  appetite,  insomnia,  and  pallor — in  a  word,  a  collection  of 
troubles  affecting  the  general  health,  and  known  by  the  name  of  mercurial 
erethism  (Kussmaul).     Stomatitis  then  appears,  and  runs  its  usual  course. 

In  severe  cases  fever  occurs,  but  the  temperature  does  not  exceed  100'^  F. 
(Hallopeau).  The  appetite  completely  disappears,  and  diarrhoea  comes  on. 
The  urine  is  scanty,  dark  in  colour,  with  a  slight  trace  of  albumin.  The 
prostration  is  very  pronounced.  The  number  of  red  corpuscles  is  diminished 
(Gubler)  in  exceptionally  grave  cases,  and  haemorrhages  may  occur  from 
the  various  tracts.     Hsematuria  is  the  most  common  (Kussmaul). 

In  this  form  eruptions  may  appear,  constituting  the  so-caUed  hydrargyria. 
Bazin  has  described  three  forms.  The  slight  form  is  characterized  by  a 
simple  erythema,  localized  to  the  inner  surface  of  the  thighs,  to  the  scrotum, 
groins,  and  abdomen,  with  very  small  vesicles.  The  whole  surface  of  the 
sldn  covered  by  the  eruption  smarts  and  itches  most  severely.  The  febrile 
form  commences  like  the  preceding  one,  and  then  extends  to  the  whole  body, 
reaching  the  face  last  of  all.  The  eruption,  which  is  of  a  vivid  red,  sometimes 
morbilliform,  sometimes  scarlatiniform,  is  often  accompanied  by  sore  throat. 
About  the  fourth  day  vesicles  appear.  They  are  larger  than  in  the  pre- 
ceding form.  They  become  filled  with  fluid,  and  then  break,  leaving  moist 
and  yellowish  crusts.  For  about  a  week  the  temperature  stands  at  102°  F. 
The  severe  form  is  only  seen  when  mercurial  preparations  are  used  after 
the  appearance  of  the  first  patches.  The  skin  is  tense  and  painful,  the  face 
is  swollen,  and  the  fever  is  severe.  Grave  symptoms,  such  as  insomnia, 
delirium,  or  semi-coma  appear,  and  in  some  cases  death  has  supervened 
during  the  coma.  Recovery  is  common,  even  in  this  form  ;  but  during 
convalescence — that  is  to  say,  about  the  middle  of  the  second  week — 
abscesses,  adenitis,  phlegmons,  and  patches  of  gangrene  often  appear. 

In  the  more  severe  cases  of  acute  mercurialism  the  stomatitis  is  accom- 
panied by  swelling  of  the  neck  and  suppuration  of  the  parotid  and  cervical 
glands  (Gubler),  or  by  parenchymatous  glossitis,  and  sometimes  by  gan- 
grenous ulcers,  which  leave  unsightly  scars. 


2092  TEXT-BOOK  OF  MEDICINE 

We  shall  study  later  the  nervous  troubles  and  the  peripheral  neuritis 
which  result  from  chronic  hydrargyrism.  In  both  cases  they  may  be  due 
to  acute  hydrargjTism,  and  acute  polyneuritis  is  sometimes  seen  during  the 
course  of  active  mercurial  treatment,  but  difiers  from  the  chronic  forms  in 
that  it  is  more  generalized.  The  muscular  atrophy  is  very  pronounced,  and 
the  tendon  reflexes  are  diroinished.  ■ 

Chronic  Hydrargyrism. — This  form  is  scarcely  ever  seen  to-day,  except 
in  professional  hydrargyrism.  Mercurial  erethism  is  here  found  in  a  com- 
plete manner,  and  is  more  marked  than  in  the  acute  form.  The  face  is  pale, 
the  breath  is  foetid,  the  teeth  are  loose,  and  have  a  greenish- brown  colour, 
being  rough  and  rugose,  with  transverse  striae,  which,  as  it  were,  fit  into  one 
another  (Letulle's  mercurial  teeth).  Diminution  of  the  blood-corpuscles  is 
constant. 

At  this  period  a  tremor  commences  in  the  upper  extremities,  and  then 
reaches  the  lower  limbs,  the  head,  and  the  tongue.  It  is  sometimes  more 
pronounced  on  one  side  than  on  the  other,  usually  ceases  during  rest,  appears 
on  the  occasion  of  movement,  and  is  increased  by  fatigue,  emotion,  or  by 
the  abuse  of  alcohol.  At  first  it  is  only  slight,  but  it  finally  renders  all  work 
impossible.  It  lasts  for  weeks  or  for  months,  even  after  the  patient  ceases 
from  work.  In  some  cases  it  lasts  for  years  after  every  cause  of  intoxication 
has  been  removed. 

We  sometimes  see  in  the  miners  of  Almaden  and  Istria  contractures 
which  are  limited  to  the  extremities,  although  they  may  become  general. 
They  are  usually  intermittent,  and  appear  in  the  form  of  attacks.  In  Spain 
they  are  called  by  the  name  of  calambres,  and  the  workers  who  suffer  from 
them  are  called  calamhristes. 

In  the  moderate  cases  the  muscular  power  of  the  patient  is  preserved. 
Letulle,  however,  says  that  he  has  noticed  in  many  patients  paresis  of  the 
muscles  which  are  aflected  by  the  tremor.  In  exceptional  cases  we  may 
see  true  mercurial  paralysis,  localized  to  the  upper  limbs,  striking  the 
extensors  by  preference,  and  then  extending  to  the  lower  limbs.  These 
paralyses,  which  are  always  flaccid,  are  not,  as  a  rule,  accompanied  by 
muscular  atrophy  or  by  changes  in  the  reflexes.  They  are  incomplete  and 
transient,  and  have  a  peripheral  origin  due  to  degenerative  lesions  of  the 
nerves. 

Just  as  cases  of  saturnine  hysteria  have  been  noticed,  so  mercury  in 
some  individuals  may  also  give  rise  to  nervous  troubles  which  resemble 
those  of  ordinary  hysteria  in  every  particular.  This  mercurial  hysteria 
(Letulle)  can  only  be  diagnosed  by  the  aid  of  conmiemoratives. 

The  troubles  of  professional  hydrargyrism  are  usually  limited  to  the 
above-named  affections,  and  after  appropriate  treatment  nearly  all  are  prone 
to  disappear,  or  at  least  to  improve,  if  they  are  not  too  inveterate  and  if  the 


THK  IXTOXICAT[()\S  209?. 

workman  gives  up  hirt  tnidf.  Sometiines  they  grow  worse  :  tho  maxillae 
necrose,  the  iiitenoctual  faculties  are  blunted,  and  a  general  weakness 
supervenes,  which  renders  the  sufferer  impotent.  Tardieu  has  thus  described 
the  condition  of  these  patients  :  "  They  stoj)  indoors  bv  the  side  of  the  fire, 
huddled  up  on  a  chair  like  children  of  tender  age.  Many  of  them  cannot 
dress  themselves  or  eat  without  assistance.  Their  look  becomes  dull,  and 
at  the  same  time  they  can  only  articulate  a  few  vague  and  confused  sounds." 

Lastly,  digestive  troubles  supervene,  and  are  characterized  by  persistent 
loss  of  appetite,  by  constipation,  or  by  uncontrollable  diarrhoea.  The  gums 
swell  and  bleed  at  the  least  touch,  the  face  is  swollen,  the  extremities  become 
oedematous,  ecchymotic  patches  appear  on  different  parts  of  the  body,  and 
haemorrhages  occur  from  the  various  canals.  Mercurial  cachexia  thus 
arises.  In  many  points  it  resembles  the  cachexia  of  scurvy.  It  often  ends 
in  collapse  and  death. 

Diagnosis. — No  one  symptom  of  hydrargyrism  is  pathognomonic.  The 
presence  of  several  symptoms,  the  course  of  events,  and  the  history  alone 
allow  a  diagnosis  to  be  made.  Each  of  these  troubles,  if  taken  alone,  may 
be  confounded  with  similar  ones  due  to  many  causes.  We  have  already 
seen  the  varieties  of  stomatitis  with  which  the  mercurial  form  may  be  con- 
founded. The  mercurial  tremor  very  closely  resembles  that  of  disseminated 
sclerosis,  in  that  it  is  not  present  during  repose,  but  only  appears  with  move- 
ment, and  increases  in  proportion  as  the  patient  reaches  his  desired  object. 
In  disseminated  sclerosis  we  find  also  disturbance  of  sight  and  of  speech, 
with  permanent  contractures,  and  sometimes  also  mental  disorders  which 
are  not  found  in  hydrargyrism. 

Hydrarg3rrLsm,  which  commences  on  the  abdomen,  groin,  and  anterior 
surface  of  the  thighs,  and  is  sometimes  accompanied  by  sore  throat  and 
fever,  may  be  confounded  with  scarlatina.  The  existence  of  vesicles  on  the 
surface  of  the  erythema  is  not  always  a  sufficient  element  in  diagnosis,  as 
there  exists  a  variety  of  scarlatina  which  is  also  accompanied  by  a  vesicular 
eruption.  The  slight  elevation  of  temperature,  the  absence  of  generaliza- 
tion, and  especially  the  history,  wiU  give  the  diagnosis. 

For  a  long  while  many  svphilitic  troubles,  and  especially  changes  in  the 
bones,  were  attributed  to  mercurial  treatment.  Apart  from  necrosis  of  the 
maxillae,  mercury  has  no  action  on  the  osseous  system.  The  nervous 
troubles,  such  as  myehtis  and  encephalopathy,  were  formerly  attributed  to 
the  influence  of  mercury.  At  the  present  time  these  discussions  have  only 
a  historical  interest,  and  the  excellent  effects  produced  by  mercurial  inunc- 
tion in  these  conditions  give  the  lie  to  all  controversy.  The  therapeutic 
administration  of  mercury  has,  however,  its  limits,  and  in  some  cases 
examination  for  the  presence  and  the  quantity  of  mercury  in  the  urine  may 
be  most  useful. 


2094  TEXT-BOOK  OF  MEDICINE 

Treatment. — This  must  be  :  (1)  Hygienic  or  preventive — that  is  to  say, 
we  must  attempt  to  ventilate  as  well  as  possible  workshops  and  mines 
(Proust),  to  diminish  the  number  of  working-hours,  and  by  cleanliness  to 
check  the  causes  of  poisoning.  The  workmen  should  be  made  to  bathe 
frequently,  and  also  to  brush  their  teeth  daily,  stomatitis  beiag  much  less 
frequent  in  individuals  who  take  this  precaution.  (2)  Persons  must  be 
removed  from  the  morbid  cause,  the  secretion  of  uriae  must  be  assisted, 
and,  in  order  to  favour  the  elimination  of  the  mercury,  iodide  of  potassium 
must  be  administered.     Hydrotherapy  and  electricity  produce  good  effects . 

m.  LEAD-POISONING. 

iEtiology. — The  causes  of  lead-poisoning  are  most  varied.  All  workers 
who  handle  lead  or  its  compounds  are  more  or  less  exposed.  Those  who 
are  employed  in  mines,  in  white-lead  and  in  red-lead  works,  house-painters, 
workmen  engaged  in  scraping  moulds  for  artificial  ice  (Kenon  and  G-eraudel), 
in  the  setting  of  false  pearls  (Apert),  in  the  making  of  frosted  glass,  type- 
setters, and  glaziers,  etc.  The  symptoms  of  lead-poisoning  are  also  caused 
by  the  use  of  cosmetics  and  face-paints.  The  preparations  of  lead  enter  the 
economy  by  the  digestive  tract,  by  the  respiratory  tubes,  by  the  mucous 
membranes,  and  by  the  skin. 

Accidental  poisoning,  if  we  do  not  pay  attention  to  it,  may  be  the  un- 
known cause  of  many  morbid  symptoms.  Bread  or  meats  cooked  with 
wood  painted  with  red  lead,  preserved  foods,  pastry  covered  with  tinfoil, 
water  conveyed  by  lead  pipes,  rain-water  which  has  remained  for  a  long 
whUe  in  leaden  cisterns,  seltzer-water,  doctored  wines,  rooms  which  have 
been  ireshly  painted  with  white  lead,  are  aU  causes  to  be  carefully  looked 
for. 

Description. — In  many  persons  lead  impresses  a  general  deterioration 
upon  the  economy  before  showing  itself  by  local  manifestations.  Thia 
dyscrasia  chiefly  depends  upon  changes  in  the  blood.  In  saturnine  anaemia 
the  number  of  red  corpuscles  is  diminished  by  50  per  cent.  We  may  .find 
only  2,300,000  per  cubic  millimetre  (Malassez).  The  corpuscles  are  also 
altered  in  quality.  The  skin  is  of  a  pale  yellow  colour ;  the  patient  is  wasted ; 
the  pulse  is  smaU,  slow,  and  polycrotic.  On  examination  of  the  mouth,  we 
find  at  the  edge  of  the  gums  a  bluish  line  (lead  line),  which  results  either 
from  deposit  of  metallic  dust  in  the  capillaries  of  the  gum  or  from  the 
elimination  of  the  lead  by  the  salivary  glands.  The  breath  is  usually  foetid. 
We  may  note  also  the  patches  described  by  Gubler  as  a  kind  of 
tattooing  of  the  cheeks,  and  situated  at  the  level  of  the  small  and  large 
molars.     Let  us  mention  also  inflammation  of  the  parotid  glands. 

Lead-colic  is  one  of  the  most  frequent  manifestations  of    acute  and 


THE  INTOXICATIONS  209.' 

chronic  lead-poisoning.  It  is  sometimes  preceded  by  dyspeptic  troubles, 
loss  of  appetite,  and  constipation  ;  at  other  times  it  appears  suddenly.  The 
pain  may  occupy  every  part  of  the  abdomen,  and  may  radiate  to  the  loins 
and  to  the  testes.  The  pain  is  continuous,  and  is  increased  from  time  to 
time  by  attacks  which  cause  the  patient  great  suffering.  His  face  is  pale 
and  pinched  ;  he  tries  every  possible  jjosition  to  quiet  the  pain,  and  he  some- 
times succeeds  in  doing  so  by  squeezing  the  painful  region.  The  belly  is 
hard  and  retracted,  the  constipation  is  absolute,  vomiting  is  frequent,  and 
the  urinary  secretion  is  diminished.  The  apyrexia  is  complete,  and  the 
pulse  is  hard  and  slow.  On  percussing  the  liver  we  find  a  diminution  in 
size  (Potain),  which  probably  depends  upon  the  contraction  of  the  hepatic 
vessels.  A  subicteric  tint  of  the  skin  is  often  present.  On  auscultation,  a 
systolic  murmur  is  frequently  heard  at  the  base  of  the  heart.  Lead-colic 
has  a  duration  of  some  weeks.  It  is  due,  according  to  some  writers,  to 
painful  spasms  of  the  muscular  layers  of  the  intestine  ;  according  to  others, 
to  neuralgia  of  the  lumbar  plexus. 

Troubles  of  the  Nervous  System. — The  general  sensibility  is  frequently 
altered.  Anaesthesia,  analgesia,  and  hypersesthesia  are  frequent.  Sometimes 
there  is  a  notable  delay  in  the  perception  of  sensations  (Brouardel).  The 
anaesthesia  may  occur  in  patches ;  it  may  be  disseminated  over  the  whole 
body,  or,  on  the  other  hand,  it  may  be  localized  to  one  side  (saturnine 
hemiansesthesia).  Lead-colic  is  frequently  accompanied  by  cutaneous 
hyperaesthesia,  arthralgia,  and  myalgia. 

The  special  senses  are  sometimes  affected,  but  the  amblyopia  and 
amaurosis  are  generally  transient. 

The  visual  troubles  are  not  frequent.  They  are  generally  late,  and  of 
various  kinds.  In  some  cases  the  amblyopia  is  due  to  the  appearance  of  a 
central  scotoma,  similar  to  that  of  alcoholic  amblyopia,  and  without  lesions 
of  the  fundus  oculi.  More  commonly  we  find  optic  neuritis  or  neuro- 
retinitis,  which,  after  a  certain  period,  ends  in  atrophy  of  the  optic  nerve 
(amaurosis).  In  other  cases  albuminuric  retinitis  (Hirschberg,  Leber)  or 
uraemic  amaurosis  (Gunsburg)  develops,  and  is  consecutive  to  nephritis. 
Sometimes  the  oculo-motor  muscles  are  affected  by  paralysis,  especially  the 
external  rectus  (Schroeder). 

The  motor  troubles  are  very  important  (paralyses,  tremors,  pseudo- 
tabes). Lead-palsy  has  its  seat  of  election  in  the  extensor  muscles  of  the 
hands  and  fingers.  According  to  Duchenne  (of  Boulogne),  it  attacks  in 
succession  the  extensor  communis  digitorum,  the  extensor  indicis,  the 
extensor  minimi  digiti,  and  the  two  radial  extensors.  The  supinator  longus 
is  almost  always  spared,  which  is  not  the  case  in  musculo-spiral  paralysis. 
Gaucher  has,  however,  published  cases  in  which  the  supinators  were  affected. 

Lead- palsy  of  the  extensors  is  almost  always  bilateral.     The  fingers  are 


2096  TEXT-BOOK  OF  MEDICINE 

flexed  upon  the  hand,  the  hand  is  flexed  upon  the  wrist,  and  the  movements 
of  extension  are  abolished.  The  paralysis  of  the  extensors  is  complicated 
by  the  dorsal  tumour  of  the  wrist  (Gubler).  The  tumour  is  indolent,  and 
is  probably  due  to  inflammation  of  the  synovial  sheaths.  It  disappears 
upon  the  cure  of  the  paralysis. 

Lead-palsies  have  been  carefuUy  studied  in  the  remarkable  treatise  of 
Dejerine-Klumpke.  They  usually  are  localized,  and  may  assume  the  fol- 
lowing types  :  (1)  Remak's  antibrachial  type.  This  is  the  most  common 
form,  and  afiects  the  extensor  muscles  of  the  fingers  and  of  the  wrist. 
(2)  Superior  or  brachial  type.  The  paralysis  afiects  the  muscles  of  the 
Duchenne-Erb  group — namely,  the  deltoid,  the  biceps,  the  brachialis  anticus, 
and  the  supinator  longus.  (3)  Aran-Duchenne  type.  The  paralysis  afiects 
the  muscles  of  the  hand,  the  thenar  and  the  hypothenar  eminences,  and 
the  interossei,  and  simulates  progressive  muscular  atrophy  the  more  closely 
in  that  the  palsy  of  these  groups  of  muscles  is  always  accompanied  by  atrophy 
in  lead-poisoning.  (4)  Inferior  or  peroneal  type.  This  is  a  rare  form,  in 
which  the  paralysis  chiefly  afiects  the  peronei  muscles  and  the  extensors  of 
the  toes,  while  the  tibialis  posticus  is  usually,  but  not  always,  afiected. 

In  some  cases  the  palsies  are  not  localized  to  groups  of  muscles.  They 
tend  to  become  general,  and  the  generalization  is  slow  or  rapid.  Although 
it  may  in  the  slow  forms  invade  all  the  muscles  of  the  trunk,  it  is,  neverthe- 
less, more  marked  in  the  muscles  of  the  limbs,  especially  in  the  extensors 
of  the  fingers  and  of  the  wrist.  In  the  rare  cases  in  which  lead-palsy  rapidly 
becomes  general  it  shows  an  ascending  or  a  descending  course,  and  may 
invade  en  hloc  m  a  few  days  the  muscles  of  the  legs,  of  the  abdomen,  and 
of  the  thorax,  as  well  as  the  intercostal  muscles  and  the  diaphragm,  so  that 
the  paralysis  only  spares  the  muscles  of  the  head  and  of  the  neck.  In  spite 
of  the  apparent  gravity  of  these  rapid  paralytic  forms,  improvement  super- 
venes rapidly,  and  termination  by  death  is  the  exception. 

In  lead-palsy  the  electrical  contractility  is  rapidly  lost,  before  the 
voluntary  power ;  in  musculo-spiral  paralysis  a  frigore  the  electrical  con- 
tractility is  usually  preserved.  The  muscles  afiected  by  lead-palsy  have  a 
tendency  to  atrophy. 

The  tremor,  so  well  described  by  Lafont,  chiefly  afiects  the  hands.  It 
has  little  tendency  to  become  general.  It  is  usually  preceded  by  muscular 
weakness,  and  difiers  from  the  alcoholic  tremor  in  that  it  increases  with 
fatigue,  and  becomes  more  marked  towards  the  end  of  the  day.  This 
tremor  is  often  only  a  hysterical  one  produced  by  saturnism. 

The  muscular  atrophy  is,  as  a  rule,  limited  to  the  paralyzed  muscles. 
In  some  cases,  however,  muscular  atrophy  of  saturnine  origin  may  exist, 
and  become  general,  without  being  complicated  by  paralysis.  I  have  seen 
such  a  case  with  Geofiroy.     The  muscular  atrophy  sometimes  assumes  in 


TllK   INTOXICATIONS  2097 

the  hiuid.s  ilit!  Araii-DiKliL'iuu!  type,  so  that  the  tliagriosiB  can  only  be  made 
from  the  sBtioiogy  and  from  the  trade  of  the  ])atient. 

Recent  writers  have  noted  (Debove,  Achard,  Letulle)  the  existence  of 
hysteriform  attacks,  which  appear  both  in  men  and  women,  but  chiefly  in 
long-standing  cases.  This  saturnine  hysteria  is  identical  as  regards  its 
symptoms  with  ordinary  hysteria,  and  most  of  the  cases  of  saturnine  hemi- 
aneesthesia  must  be  explained  in  this  way.  Saturnism,  as  a  provoking  agent, 
like  syphilis  and  hydrargyrism,  would  thus  prepare  the  organic  soil  for  the 
development  of  the  neurosis  in  predisposed  persons  (Charcot).  Saturnine 
apoplexy  is  most  often  a  manifestation  of  this  symptomatic  hysteria.  It 
often  commences  in  a  sudden  fashion,  and  simulates  an  attack  of  apoplexy 
of  organic  origin.  It  leaves  behind,  as  a  rule,  motor  hemiplegia  and  sensory 
hemianoesthesia,  which  is,  as  it  were,  the  sign  of  hysteria. 

Let  us  note  also,  among  the  exceptional  motor  troubles,  hemichorea 
(Ra}auond)  and  pseudo-tabes  (Leval,  Piquechef). 

The  cerebral  troubles  in  lead-poisoning  are  more  serious  than  those 
just  described,  and  are  designated  by  the  name  of  saturnine  encephalopathy 
or  cerebro-spinal  saturnism  (Jaccoud).  According  to  the  predominance 
of  special  symptoms,  ^v^ite^s  have  described  delirious,  convulsive  and 
comatose  forms.  The  cerebral  troubles  are  frequently  ushered  in  by  pro- 
dromata,  such  as  headache,  vertigo,  squint,  insomnia,  hallucinations,  and 
tendency  to  excitement  or  to  depression.  The  condition  is,  as  a  rule,  a  late 
trouble  of  chronic  lead-poisoning,  and  is,  I  believe,  frequently  associated 
with  urremia.     Mosny  has  noted  the  occurrence  of  meningitis. 

The  delirious  form  presents  no  special  characteristics.  The  delirium  is 
sometimes  quiet,  sometimes  noisy,  and  accompanied  by  hallucinations. 
The  delirium  is  always  mobile,  and  its  duration  is  variable.  In  the  con- 
vulsive form  the  convulsions  may  be  partial  and  local  or  general,  and  like 
those  of  an  attack  of  epilepsy.  This  saturnine  epilepsy  sometimes  simulates 
the  ordinary  form  to  perfection.  The  precursory  aura  and  the  attacks  of 
vertigo  are,  as  a  rule,  wanting,  but  the  attack  may  end  in  apoplexy.  The 
comatose  form  is  rarely  primary  ;  it  usually  follows  one  of  the  preceding 
forms.  Saturnine  encephalopathy  is  sometimes  fatal  after  a  few  days.  In 
the  mixed  form  delirium  and  convulsions  often  precede  coma. 

The  condition  called  general  paralysis  in  these  cases  is  considered  by 
certain  aUemsts  as  identical  with  Baillarger's  disease.  Other  authors  think 
that  it  is  a  general  pseudo-paralysis,  which  differs  from  the  true  form  by  its 
sudden  onset  and  its  recovery  under  the  influence  of  treatment  favouring 
the  elimination  of  the  lead.  Its  history  is  connected  with  that  of  saturnine 
encephalopathy. 

Writers  have  tried  to  explain  this  encephalopathy  by  the  presence  of 
special  lesions  in  the  brain  (Renaut).     The  cerebrum  is  anaemic,  yellowish, 


2098  TEXT-BOOK  OF  MEDICINE 

and  firm  to  tlie  touch,  giving  the  sensation  of  marsh-mallow  paste.  Chemical 
analysis  reveals  the  presence  of  lead.  These  lesions  may,  however,  exist 
during  life  without  saturnine  encephalopathy.  As  a  matter  of  fact,  the 
tendency  is  to  consider  the  encephalopathy  as  symptomatic  either  of 
atheroma  of  the  cerebral  vessels,  or  of  hysteria,  or  particularly,  let  me 
repeat,  as  a  ursemic  manifestation. 

Gout. — The  attack  of  gout  very  closely  resembles  the  ordinary  form. 
It  commences  in  the  same  manner  with  fever.  It  usually  appears  during 
the  night,  and  the  pain  is  locahzed  to  the  big  toe  or  to  both  toes,  more  rarely 
to  the  tibio-tarsal  joint,  to  the  knee,  or  to  the  fingers.  The  attack,  which 
is  very  painful,  improves  towards  the  morning.  Slight  perspiration  appears, 
and  the  patient  faUs  asleep.  The  gouty  region  is  swoUen,  tender,  shining, 
and  streaked  with  dilated  veins.  The  pains  become  quite  as  severe  again 
during  the  night,  so  that  we  find  slight  improvement,  followed  by 
paroxysms,  as  long  as  the  attack  of  gout  has  not  ended.  During  the 
attack  of  saturnine  gout,  as  in  the  ordinary  disease,  the  uric  acid  con- 
tained in  the  urine  may  be  in  excess.  The  serous  fluid  from  a  blister  applied 
during  an  attack  over  the  diseased  joint  contains  uric  acid  in  both  cases. 
In  saturnine  gout,  as  in  the  genuine  disease,  we  find  tophi  in  the  neigh- 
bourhood of  the  joints,  tendons,  tendon  sheaths,  and  subcutaneous  cellular 
tissue.  These  concretions  develop  in  the  cartilages  of  the  ear.  They  are 
numerous  in  the  neighbourhood  of  the  smaU  joints,  which  they  help  to 
deform,  and  are  found  in  the  serous  bursse  of  the  knee  and  of  the  elbow, 
where  they  may  acquire  the  size  of  a  nut.  These  uratic  deposits  may  become 
inflamed,  forming  abscesses,  and  giving  exit  to  whitish  chalky  matter. 
The  tophi  in  saturnine  gout  appear  early,  so  that  in  gout  due  to  lead,  as  in 
the  ordinary  disease,  the  organism  seems  to  be  impregnated  with  uric  acid 
and  urate  of  soda. 

From  this  description  it  is  evident  that  saturnine  gout  and  diathetic 
gout  have  very  great  analogies,  and  yet  they  present  differences  which  I 
must  mention,  and  upon  which  GaUard  has  rightly  iosisted.  In  ordinary 
gout  the  attack  is  really  the  first  episode  of  the  gouty  diathesis,  and  is  often 
preceded  years  previously  by  other  manifestations  of  this  diathesis,  such  as 
gravel,  renal  colic,  asthma,  haemorrhoids,  eczema,  or  migraine.  Nothing  of 
the  kind  is  seen  ia  gout  due  to  lead-poisoning.  The  articular  disease  and 
the  concretions  are  gouty  manifestations  which  do  not  depend  upon  a 
general  diathetic  condition.  Saturnine  gout  appears  to  be  of  a  more  in- 
vading character  than  the  common  form,  and  although  it  may  remain 
localized  to  the  big  toe  after  a  first  attack,  it  is  rare  i£  it  does  not  show  a 
tendency  in  the  following  attacks  to  invade  the  other  joints,  such  as  the  knees, 
elbows,  shoulders,  and  vertebrae.  The  duration  of  the  attacks  is  longer  in 
saturnine  gout,  the  anaemia  is  more  rapid,  and  the  cachexia  is  earher. 


THK   INTOXICATIONS  2099 

The  pathogonosia  of  saturnine  j^out  is  still  a  matter  of  theory.  Saturnine 
urica3mia  is,  perhaps,  due  to  hy}jeractivity  of  the  furiciinn  of  the  cells  of  i}\t' 
organism  under  the  influence  of  the  lead  (Lecorche). 

Nephritis. — Renal  lesions,  which  may  end  in  chronic  nephritis  of  an 
int^^rstitial  nature,  are  sometimes  associated  with  lead-poisoning.  For 
purposes  of  description  I  shall  class  the  symptoms  of  saturnine  nephritis  in 
several  groups. 

In  the  first  group  I  place  those  patients  who  only  have  albuminuria, 
without  other  symptoms  of  nephritis.  The  albuminuria  is  not  severe.  It 
may  be  transient  or  intermittent,  but  it  is  usually  accompanied,  sooner  or 
later,  by  symptoms  of  Brightism,  although  it  may  comprise  the  whole  lesion 
of  the  kidney.     In  such  a  case  it  is  not  very  formidable. 

In  the  second  group  I  shall  place  the  more  numerous  patients  who  suffer 
from  Brightism,  with  or  \vithout  albuminuria,  the  symptoms  being  pol- 
lakiuria,  cryaesthesia,  dead  fingers,  itching,  buzzing  in  the  ears,  epistaxis, 
electrical  shocks,  and  cramps  in  the  calves.  These  "  minor  s}Tnptoms  of 
Brightism,"  which  are  so  frequent  when  looked  for,  may  not  be  accompanied 
by  albmninuria — at  least,  for  a  time.  I  have  had  under  my  care  in  hospital 
patients  who  came  back  months  or  years  apart,  and  who  sometimes  presented 
symptoms  of  albuminuria,  with  or  without  the  minor  s}Tnptoms  of  Brightism, 
and  at  other  times  these  symptoms  with  or  without  albuminuria.  The 
evolution  of  chronic  saturnine  nephritis  is  very  slow.  If  it  is  properly 
treated,  it  may  not  end  in  uraemia. 

In  a  third  group  I  shall  place  those  patients  who  are  threatened  with 
severe  symptoms  of  uraemia,  such  as  violent  headache,  intense  dyspnoea 
of  every  kind  (dyspnceic  uraemia),  vomiting,  and  gastric  intolerance  (gastric 
uraemia),  and  every  kind  of  nervous  uraemia,  etc. 

Saturnine  nephritis  is  rarely  accompanied  by  oedema,  or,  if  it  be,  the 
oedema  is  late.  On  the  other  hand,  the  arterial  tension  is  always  raised,  the 
temporal  artery  is  tortuous  and  distended,  the  heart  is  hypertrophied,  and 
the  gallop  rhythm  is  present  (Potain). 

These  patients  sometimes  succumb  through  the  kidney,  and  we  then 
find  the  lesions  of  the  small  contracted  kidney.  Much  histological  and 
experimental  research  has  been  undertaken  m  order  to  explain  the  patho- 
genesis of  saturnine  nephritis.  As  early  as  1863  Ollivier,  in  an  important 
work,  studied  this  disease.  He  caused  it  experimentally,  and  found  traces 
of  lead  in  the  urine  and  in  the  kidney.  He  explained  the  albuminuria  and 
the  nephritis  by  the  presence  and  by  the  elimination  of  the  lead. 

In  1881  Charcot  and  Gombault  made  anatomical  and  experimental 
researches  with  the  object  of  showing  that  saturnine  nephritis  is  an  epithelial 
cirrhosis,  the  glandular  element  being  the  first  afiected,  and  giving  rise  to 
the  lesions  of  the  connective  tissue,  which  are  secondary.     This  point  of  view 


2100  TEXT-BOOK  OF  MEDICINE 

has  since  been  severely  attacked,  and  in  a  recent  thesis  Paviot,  reviewing 
the  question  from  the  anatomical  and  experimental  point  of  view,  arrives 
at  opposite  conclusions.  In  the  fourth  case  of  saturnine  nephritis,  which 
forms  the  basis  of  his  work,  "  we  find,"  he  says,  "  the  same  irregularity  of 
distribation.  The  saturnine  intoxication  does  not  spread,  either  along  the 
epithelial  system  or  along  the  vascular  system,  but  afiects  the  interstitial 
tissue  at  many  diSerent  points  in  the  labyrinthine  spaces,  preserving,  how- 
ever, with  a  somewhat  regular  constancy  its  predominance  in  the  neigh- 
bourhood of  the  hilum  and  often  of  the  pyramids  of  Ferrein."  The  experi- 
mental and  also  the  histological  researches  of  Paviot  difier  absolutely  from 
those  of  Charcot  and  Gombault,  for  "  in  any  case,"  he  says,  "  the  renal 
epithelia  have  not  been  found  to  be  primarily  and  solely  diseased.  The 
sclerosis  has  often  been  met  with,  apart  from  any  alteration  of  the  tubules, 
and,  on  the  other  hand,  it  is  never  isolated." 

Prevost  and  Binet,  in  1889,  in  a  most  comprehensive  monograph,  state 
the  result  of  their  experimental  researches  upon  lead-poisoning.  They 
slowly  produced  chconic  poisoning  in  rats  and  guinea-pigs.  Post  mortem 
the\'  found  that  the  lesions  of  the  kidney  were  the  more  marked  in  propor- 
tion to  the  length  and  to  the  slowness  of  the  poisoning.  The  kidneys  were 
fibrous,  cystic,  and  diminished  in  size,  interstitial  nephritis  being  the  chief 
lesion.  The  kidneys  contained  much  lead.  The  comparative  examination 
for  lead  in  the  difierent  viscera  proved  that  the  lead  introduced  into  the 
organism  accumulates  in  the  kidneys.  In  spite  of  the  accumulation  of  the 
metal  in  the  kidney,  the  urine  of  the  animals  under  experiment  eliminates 
generally  but  little  lead,  and  this  fact  coincides  with  the  condition  in  man 
when  sufiering  from  lead-poisoning.  The  presence  of  lead  ia  the  urine  is, 
indeed,  difficult  to  recognize  even  when  the  patient  is  put  upon  iodide  of 
potassium,  with  the  object  of  converting  the  lead  fijsed  in  the  economy  into 
the  slightly  soluble  iodide  of  lead. 

We  have,  therefore,  abundant  data  as  to  the  pathogenesis  and  the 
nature  of  saturnine  nephritis,  but  I  must  insist  again  upon  certain  con- 
siderations of  importance.  The  patient,  as  we  have  said,  is  often  gouty,  or, 
at  any  rate,  he  often  suffers  from  iiricsemia.  He  may,  therefore,  have 
gouty  nephritis,  just  like  a  gouty  patient  has.  The  examination  of  the 
kidney  in  both  cases  reveals  traces  of  urate  of  soda.  It  must,  therefore,  be 
admitted  that  the  patient  has  many  reasons  for  haA-ing  diseased  kidneys. 
He  is  threatened  by  an  intoxication  (saturnism),  and  also  by  an  auto- 
intoxication (uricaemia).  These  two  processes  may  be  in  his  case  distinct 
or  combined,  but  finally  they  often  end  in  the  lesions  of  the  kidneys  which 
cause  the  nephritis  just  described. 

In  the  midst  of  this  morbid  complex  one  fact  is,  nevertheless,  somewhat 
astonishing — namely,  that  the  iiricsemic  process,  which  in  the  patient  with 


TlIK   IXTOXrCATIOXS  2101 

lead-poisoning  is  an  importuiit  element  in  nejihritifi,  does  not  rause  renal 
lithiasis  and  its  complications  (renal  colic,  hsnmaturia,  pyelo-nephritis,  etc.), 
which  arc  so  frequent  in  persons  of  the  gouty  diathesis. 

Parotiditis. — Hypertrophy  of  the  parotid  glands  is  frequent  in  lead- 
poisoning  (Crontes,  Achard,  Claisse  and  Dupre).  The  parotid  region  is 
swollen  on  both  sides,  but  it  is  painless  both  spontaneously  and  on  palpa- 
tion. Parotiditis,  though  essentially  a  chronic  disease,  may  become  acute 
as  the  result  of  angina,  of  stomatitis,  or  of  treatment  with  iodides.  The 
swelling  is  sometinios  limited  to  the  submaxillary  glands,  and  the  parotids 
are  free. 

The  lesions  of  saturnine  parotiditis  have  been  carefully  studied  by  Apert. 
The  condition  is  one  of  simple  h\q3ertrophy,  with  catarrh  of  the  excretory 
ducts  and  periglandular  fibrosis.  Apert  has  not  found  lead  in  the  gland 
upon  chemical  examination.  In  his  experiments  Renon  found  lead  in  the 
salivary  glands  of  guinea-pigs  poisoned  with  white  lead. 

Course — Diagnosis. — The  saturnine  dyscrasia  decreases  or  increases 
according  as  the  sufferer  is  free  from  or  exposed  to  the  toxic  cause.  Lead 
colic  is  often  one  of  the  initial  symptoms.  The  palsies,  tremors,  and  en- 
cephalopathy are,  on  the  other  hand,  later  symptoms.  Nevertheless,  we 
see  some  sufferers  \yith.  tremor,  and  others  with  paralysis  of  the  extensors, 
who  have  never  had  acute  symptoms  of  colic. 

At  length  the  patient  becomes  cachectic  ;  the  ansemia,  the  weakness,  and 
the  wasting  progress,  and  the  complications  become  more  formidable. 

The  diagnosis  is  easy  in  the  case  of  colic  and  in  paralysis  of  the  extensors. 
The  diagnosis  of  the  other  troubles  will  be  rendered  easy  by  the  trade  of  the 
patient,  the  attacks  which  he  has  previously  suffered,  and  the  presence  of 
the  lead-line  on  the  gums. 

Under  the  name  of  saturnine  asthrha  writers  appear  to  have  confounded 
cardiac  dyspnoea  following  arterio-sclerosis  of  the  heart,  ursemic  dyspnoea 
resulting  from  interstitial  nephritis,  and  attacks  of  dyspnoea  caused  by 
bronchitis  from  inhalation  of  lead-dust.  Lastly,  essential  asthma  may 
perhaps  be  caused  by  lead-poisoning  in  a  predisposed  individual. 

Pathological  Anatomy. — Lead  is  found  in  the  blood  and  in  the  organs, 
especially  in  the  liver  and  the  kidney.  The  vessels  are  rigid,  constricted, 
and  affected  with  arterio-sclerosis.  They  are  sometimes  atheromatous. 
The  heart  is  often  hypertrophied.  The  muscles  are  diminished  in  size,  and 
the  microscope  reveals  simple  atrophy,  or  atrophy  with  or  without  connec- 
tive proliferation  and  fatty  infiltration  (Gombault).  But  the  starting-point 
of  lead-palsy  is  a  periaxial  segmentary  neuritis,  which  has  been  recognised 
and  reproduced  experimentally  by  Gombault.  This  peripheral  neuritis  has 
been  carefully  worked  out.  The  poison  attacks  the  peripheral  nerves.  The 
spinal  cord  was  diseased  in  only  five  cases,  and  these  lesions  were  diffuse. 
IL  133 


2102  TEXT-BOOK  OF  MEDICINE 

Treatment. — The  treatment  of  lead-colic  aims  at  removing  the  pain 
and  the  constipation.  The  former  may  be  lessened  by  injections  of  morphia 
or  by  cataplasms  containing  laudanmn,  while  the  latter  should  be  treated 
by  repeated  purgatives  (senna,  sulphate  of  soda,  etc.). 

With  the  object  of  eliminating  the  poison,  sulphur  and  vapour  baths 
may  be  prescribed,  and  iodide  of  potassium  given,  since  Gubler  states 
that  it  favours  the  disassimilation  of  the  albuminates  of  lead.  The  con- 
tinuous current  is  employed  for  the  palsies.  Tonics  should  be  used  for  the 
anaemia. 

Prophylactic  treatment  consists  in  preventing  by  every  possible  means 
the  causes  which  favour  the  absorption  of  lead. 

IV.  PHOSPHOKUS-POISONING. 

Acute  and  chronic  forms  of  phosphorus-poisoning  must  be  distinguished. 

1.  Acute  Poisoning. — This  form  is  seen  as  the  result  of  criminal  poison- 
ing, of  attempts  at  suicide,  or  of  an  accident.  Phosphorus  from  matches  is 
the  usual  agent.  A  dose  of  3  to  5  grains  is  almost  always  sufficient  to  cause 
death.  Each  match-head  contains  about  ^  grain  of  phosphorus,  and  fifty 
heads,  therefore,  represent  a  fatal  dose.  Rat-paste  may  be  swallowed  by 
animals  eaten  for  food,  thus  rendering  their  flesh  poisonous  to  man. 

In  children  the  symptoms  run  their  course  in  a  day,  or  even  in  a  few 
hours ;  in  the  adult  the  progress  is  slower.  In  the  fijst  phase,  which  lasts 
some  hours,  the  patient  feels  a  soapy  taste  in  the  mouth,  and  the  breath  is 
sometimes  phosphorescent  in  the  dark.  The  characteristic  phenomena  con- 
sist of  pains  in  the  throat  and  guUet,  vomiting  of  food  and  bile,  and,  in  rare 
cases,  of  blood ;  while  the  vomit  is  luminous  in  the  dark,  and  gives  off  a 
strong  odour  of  phosphorus.  The  belly  is  distended  and  painful,  and  the 
patient  suffers  from  diarrhoea,  which  may  be  luminous  or  hsemorrhagic. 

This  first  period  of  digestive  disturbance  generally  lasts  from  one  to  two 
days,  and  is  succeeded  by  a  deceptive  remission,  which  may  last  for  a  few 
days. 

The  second  period  is  more  characteristic,  and  declares  itseK  by  the 
syndrome  of  icterus  gravis,  so  that  phosphorus-poisoning  has  been  looked 
upon  as  an  experimental  reproduction  of  acute  yellow  atrophy  Jaundice, 
the  cardinal  symptom,  appears  about  the  third  or  the  fourth  day  The 
urine  is  scanty  and  rich  in  bile-pigment.  It  contains  leucin  and  tyrosin. 
and  is  almost  always  albuminous. 

As  in  icterus  gravis,  nervous  phenomena  and  haemorrhages  may  be  the 
chief  features.  In  the  first  case,  we  find  more  or  less  general  paia,  fibrillary 
contractions,  hypereesthesia,  photophobia,  delirium,  and  hallucinations.  In 
this  nervous  form  the  phase  of  excitement  gives  place  to  a  period  of  depres- 


TITK  INTOXICATIONS  2108 

sion,  whicli  ends  in  (M)ma  or  in  collapse.  The  liajinorrhagic  form  is  charac- 
terized by  epistaxis,  hajrnatemesis,  nielajna,  hajraaturia,  large  and  multiple 
petechia),  and  in  most  cases  ends  in  collapse. 

Pathological  Anatomy. — Wimn  death  supervenes  rapidly,  practically 
no  lesions  are  found.  At  the  end  of  two  or  three  days  the  autopsy  revealfi 
acute  fatty  degeneration  of  the  organs.  It  is  especially  marked  in  the  liver, 
which  is  yellow,  soft,  pasty,  and  almost  diffluent. 

The  cells  are  loaded  with  fat,  and,  according  to  Cornil,  this  steatosis 
commences  from  six  to  eight  hours  after  the  intoxication.  Tlici  cells  of  the 
liver  refuse  to  act,  whence  the  icterus  gravis. 

The  kidneys,  the  heart,  the  vessels,  and  the  stomach  are  affected  with 
steatosis.  The  cells  of  the  tubuli  contorti  are  loaded  with  fat,  the  fibres  of 
the  heart  lose  their  striation,  and  the  epithelium  of  the  pepsin  glands  is 
charged  with  fat-drops.  The  gastric  mucous  membrane  sometimes  shows 
small  ulcerations,  said  by  Cornil  and  Ranvier  to  be  due  to  the  phosphoric 
acid  formed  in  situ. 

More  or  less  general  haemorrhages  may  be  found  in  the  various  organs. 

In  toxicology,  in  order  to  cause  the  production  of  phosphorescent 
glimmers,  the  organs  must  be  previously  acidified,  as  alkaline  matters  do 
not  shine  in  the  dark.  Some  days  after  poisoning  this  examination  becomes 
very  delicate. 

Treatment. — If  the  physician  is  called  at  once  to  a  case  of  poisoning,  he 
should  employ  emetics  and  lavage  of  the  stomach.  Turpentine,  adminis- 
tered continuously  in  doses  of  from  90  to  120  minima  daily,  is  an  excellent 
antidote. 

2.  Chronic  Poisoning. — This  form  is  frequently  seen  in  maitch-makers, 
especially  in  those  who  steep  the  wood  in  the  phosphorus  paste  or  who 
perform  the  sorting.  iUcoholism,  long  hours  in  badly  ventilated  workshops, 
neglect  of  personal  hygiene,  and  dirty  hands  favour  intoxication. 

Phosphorus  necrosis  of  the  jaws  and  certain  general  troubles  mark 
chronic  poisoning.  They  are  seen  after  months  or  even  after  years  of  work, 
according  to  the  individual.  The  necrosis  may  affect  both  jaws,  but  shows 
a  predilection  for  the  inferior  maxilla. 

The  researches  of  Roussel  and  Magitot  have  shown  that  there  was 
previous  dental  caries,  followed  by  penetration  of  the  poison  to  the  bone. 
Pain  in  the  teeth  is  followed  by  symptoms  of  alveolo-dental  periostitis  ;  the 
cheeks  become  swollen,  abscesses  form,  and  the  resulting  necrosis  of  the 
bone  may  be  very  extensive.  The  necrosis  may  extend  to  the  bones  of  the 
face,  and  even  to  the  base  of  the  skull.  It  can  be  arrested  by  early  surgical 
treatment. 

Necrosis  proves  fatal  in  one  case  out  of  every  two.  When  it  is  of  long 
duration,  it  is  complicated  by  cachexia,  albuminuria,  and  oedema. 

133—2 


2104  TEXT-BOOK  OF  MEDICINE 

Grave  ansemia,  with  vomiting  and  diarrhoea,  may  also  result  from  chronic 
phosphorism. 

Courtois-Suffit,  who  for  several  years  has  had  charge  of  the  match- 
makers at  the  Pantin-Aubervilliers,  has  published  a  profound  and  critical 
study  of  the  troubles  of  phosphorism  in  workmen,  and  finds  them  less  grave 
and  less  numerous  than  has  been  hitherto  supposed.  "  If  we  except  necrosis 
of  the  maxillae,  which  is  most  certainly  due  to  the  direct  influence  of  the 
vapours  of  white  phosphorus,  which  gain  an  entrance  by  reason  of  ordinary 
dental  caries,  we  find  that  phosphorus  has  no  specific  action  upon  the 
general  health.  It  is  difficult — or,  rather,  impossible — to  distinguish  in  the 
pathological  condition  of  the  workmen  what  depends  upon  the  toxine  itself 
from  what  depends  upon  bad  hygiene,  anaemia,  starvation,  and  the  most 
ordinary  pathological  and  toxic  causes." 

The  replacement  of  white  phosphorus  by  the  sesquisulphate,  which  is 
harmless,  will  cause  the  disappearance  of  all  troubles  (Courtois-Suffit). 

V.  ARSENICAL  POISONING. 

Many  years  ago  arsenic  was  the  chief  poison  employed  by  criminals. 
Since  the  researches  of  OrfiJa  showed  how  to  determine  the  presence  of 
arsenic  in  the  organs,  the  number  of  cases  of  poisoning  has  markedly  dimin- 
ished, and  at  the  present  time  crimiaal  poisoning  by  phosphorus  is  much 
more  frequent. 

It  is  necessary  to  distinguish  acute  and  subacute  from  chronic  poisoning. 

1.  Acute  and  Subacute  Poisoning. — Arsenious  acid  is  the  compound 
nearly  always  employed.  In  the  pure  state  it  is  almost  without  taste,  and 
as  it  is  almost  insoluble  it  is  most  often  ingested  in  the  form  of  a  powder. 
A  fatal  dose  varies  much  in  individuals,  and  according  as  vomiting  is  or  is 
not  present.     The  mean  fatal  dose  is  from  1  to  2  grains. 

Tolerance  of  the  poison  is  readily  established,  so  that  the  mountaineers 
of  Styria  and  the  Tyrol,  in  order  to  fit  themselves  for  their  climbs,  are  accus- 
tomed to  take  as  much  as  2  or  3  grains  of  arsenious  acid  daily.  This  habit 
creates  a  craving  for  the  drug,  and  arsenic-eaters  cannot  give  up  the  drug 
without  experiencing  signs  of  poisoning. 

Clinically,  we  must  distinguish  acute  from  subacute  poisoning. 

Symptoms  of  Acute  Poisoning. — Arsenic,  if  swallowed  in  large  doses, 
causes  symptoms  within  an  hour.  An  acrid  feeling  in  the  mouth  and 
epigastric  pains  open  the  scene.  They  are  followed  by  symptoms  of  gastro- 
enteritis, with  nausea,  vomiting  of  food  and  bile,  diarrhoea  containing 
epithelial  masses,  and  rice-water  stools,  so  that  the  syndrome  may  resemble 
an  attack  of  Asiatic  cholera. 

The  heart  beats  quickly,  the  respiration  becomes  laboured,  the  skin  is 


tup:   IXTOXTf'ATloXS  2105 

covered  with  sweat,  the  face  is  cyanosed,  the  urine  is  scanty,  the  patient 
suffers  from  muscular  cramps,  and  often  dies  from  syncope. 

The  nervuus  form  differs  from  the  gastro-intestinal  one.  Delirium,  con- 
vulsions, and  paralysis  follow  the  headache,  vertigo,  and  hyperaesthesia  of 
the  onset,  and  death  often  comes  on  with  syncope. 

Latent  cases,  in  which  death  supervened  in  a  few  hours  without  agony, 
after  some  vomiting,  have  been  noted,  as  well  as  incomplete  poisoning,  when 
the  dose  of  the  poison  was  insufficient.  Sore  throat  and  coryza  may  be  the 
only  symptoms,  or,  after  some  slight  disturbances,  eruptions,  desquamation, 
and  swelling  of  the  skin  of  the  scrotum  supervene  (Brouardel).  Con- 
valescence is  always  slow.  In  case  of  recovery  the  poison  may  be  found  in 
the  urine  for  six  weeks. 

Subacute  Poisoning. — This  form  is  seen  when  the  poison  is  absorbed  in 
insufficient  and  intermittent  doses.     It  causes  digestive  and  nervous  troubles. 

The  digestive  troubles  consist  in  vomiting,  which  becomes  worse  after 
each  dose  of  the  poison,  in  salivation,  and  in  a  bitter  taste  in  the  mouth. 

The  nervous  troubles  consist  in  paralyses,  which  appear  as  a  rule  at  the 
end  of  a  few  weeks,  and  have  all  the  characters  of  peripheral  paralyses 
(Brissaud,  Brouardel  and  Pouchet).  They  are  chiefly  motor,  and  affect  the 
extensors.  They  are  accompanied  by  atrophy,  abolition  of  the  reflexes, 
and  pains  in  the  limbs.  They  may  present  the  picture  of  pseudo-tabes. 
With  rare  exception  they  recover  very  rapidly. 

The  lesions  are  chiefly  found  in  the  digestive  tract.  The  stomach  shows 
ecchymotic  patches,  and  is  covered  with  a  thick  mucus,  and  sometimes  con- 
tains grains  of  arsenic  in  the  form  of  a  powder.  The  mucous  membrane  of 
the  intestine  is  swollen,  and  studded  with  a  psorenteric  eruption.  Steatosis 
is  found  in  most  of  the  organs,  such  as  the  liver,  kidneys,  heart,  and  muscles. 
Toxicological  examination  with  Marsh's  apparatus  shows  after  sublimation 
traces  of  the  poison  in  the  viscera,  in  the  nails,  and  in  the  hairs. 

2.  Chronic  Poisoning. — This  form  is  usually  due  to  the  patient's  occupa- 
tion. It  is  seen  in  labourers  who  extract  the  arseniferous  mineral,  and  in 
the  employes  in  certain  aniline  dye-works,  or  in  manufacturers  of  green  arsenic 
(Scheele's  green  and  Schweinfurth's  green).  The  making  of  paper  coloured 
with  green  arsenic,  or  even  living  in  rooms  covered  with  this  paper,  may 
cause  symptoms.  The  intoxication  may  be  of  alimentary  origin,  and  it  is 
sometimes  difficult  to  find  the  cause,  so  complex  may  the  aetiology  be. 

The  changes  chiefly  affect  the  skin,  the  respiratory  passages,  and  the 
nervous  system. 

The  cutaneous  lesions  are  multiple.  In  addition  to  erythemata,  accom- 
panied or  not  by  papules  and  urticaria,  we  find  vesicular  and  bullous 
eruptions,  which  may  reach  the  size  of  a  hen's  egg,  and  become  general  over 
the  whole  body.     I  must  also  note  the  appearance  of  pustules  and  ulcera- 


2106  TEXT-BOOK  OF  MEDICIKE 

tions,  and  especially  of  melanosis  and  keratosis.  The  melanosis  may  be 
general.  The  skin  takes  on  a  speckled  appearance  and  the  pigmentation 
is  most  marked  on  the  trunk  (Mathieu).  It  may  also  occur  in  isolated  spots 
and  patches.  The  keratosis  afiects  the  palms  of  the  hands,  the  soles  of  the 
feet,  and  the  orifices  of  the  sweat-glands.  It  results  from  the  hyper- 
idrosis  consecutive  to  the  employment  of  arsenic,  which  brings  the  poison 
into  prolonged  contact  with  the  integument  (Brouardel). 

Chronic  coryza,  with  muco-puiulent  secretion,  chronic  angina,  attacks  of 
asthma,  and  chronic  bronchitis,  comprise  the  changes  in  the  respiratory 
passages.  The  coryza  may  end  in  ulceration  of  the  mucous  membrane  and 
in  the  destruction  of  the  septum  and  of  the  turbinate  bones  (Cartaz). 

The  nervous  troubles  are  sometimes  revealed  by  paralysis,  which  com- 
mences with  pains  or  with  changes  in  the  general  sensibility.  The  patient 
notices  that  he  walks  with  greater  difficulty  and  cannot  clearly  feel  the 
ground.  The  paresis  and  the  paralysis  are  marked  in  the  muscles  of  the 
feet  and  in  the  extensor  communis  digitorum.  The  upper  arms  are  often 
afiected.  The  forearms  are  flexed,  and  the  fingers  are  kept  in  palmar 
flexion. 

The  paralyzed  muscles  are  more  or  less  atrophied,  but  the  reaction  of 
degeneration  is  exceptional  (Brouardel).  The  duration  of  these  paralyses 
is  very  long.  Improvement  may  not  commence  for  some  years,  and 
recovery  is  rarely  followed  by  restitutio  ad  integrum.  Brouardel  has  been 
able  to  produce  arsenical  paralysis  in  the  guinea-pig  and  rabbit. 

Treatment. — In  the  case  of  acute  and  rapid  poisoning  the  stomach 
must  be  emptied  by  emetics  or  by  lavage.  In  less  rapid  cases  of  poisoning 
peroxide  of  iron  should  be  taken,  because  it  forms  insoluble  and  harmless 
arsenite  of  iron.  Magnesium  hydrate,  which  forms  arsenite  of  magnesia, 
may  be  given.     Stimulants  are  indicated  in  case  of  threatening  collapse. 

VI.  POISONING  BY  OPIIBI,  MORPHLl,  AND  COCAINE. 

Opium. — ^Acute  poisoning  by  opium  is  very  frequent.  Laudanum  is 
often  employed  in  suicide,  and  the  therapeutical  use  of  opium  is  hable  to 
cause  numerous  accidents.  Young  children — especially  the  new-born — are 
peculiarly  sensitive  to  opium,  and  a  single  drop  of  laudanum  is  sometimes 
sufficient  to  cause  death.  In  the  adult  the  fatal  dose  is  about  15  grains 
(Hoflmann). 

The  poisoning  maybe  lightning-like  when  it  follows  the  absorption  of  huge 
doses  of  opium,  and  the  patient  becomes  comatose  from  the  first.  Death 
supervenes  rapidly  in  a  few  hours — sometimes  in  half  an  hour.  Convulsions 
and  delirium  are  not  seen.     The  pupils  are  dilated  (Tardieu). 

As  a  rule,  the  course  is  less  rapid,  and  the  patients,  who  are  at  first 


THK   INTOXICATKJNS  2107 

excited,  complain  of  iieadache  and  j)ulsati(ni  in  the  temi)le8.  The  heart 
beats  violently  ;  the  pulse  is  rapid.  The  skin  is  often  covered  with  patches 
of  erythema  and  purpura.  The  tongue  and  throat  are  red  and  dry.  Nausea 
and  vomiting  appear.  The  urine  is  suppressed,  and  the  constipation  is 
absolute.  Delirimn  and  restlessness  are  present,  and  we  notice  a  symptom 
which  is  practically  pathognomonic  of  tliis  disease — contraction  of  the 
pupils  or  absolute  myosis.  After  some  hours  the  restlessness  ceases,  and 
gives  place  to  complete  depression.  The  coma  lasts  for  a  more  or  less 
lengthy  period,  though  it  may  be  interrupted  by  convulsions,  and  death 
speedily  takes  place.  It  is  announced  by  dilatation  of  the  pupils  and  by 
relaxation  of  the  sphincters. 

Chronic  poisoning  by  opium  is  extremely  rare  in  France  and  in  Europe, 
but  very  frequent,  on  the  other  hand,  in  China,  Japan,  Annam,  Tonkin, 
where  opium  is  smoked,  and  in  Asia  Minor,  Persia,  and  Turkey,  where  opium 
is  eaten.  The  symptoms  in  this  intoxication  reveal  themselves  by  organic 
decay  and  complete  decrepitude. 

The  treatment  in  acute  poisoning  consists  in  removing  the  poison  from 
the  stomach  (emetics,  lavage).  The  patient  should  be  stimulated  by  coffee, 
given  by  the  mouth  or  by  the  rectum. 

Morphine. — Morphinism  is  seen  under  the  following  conditions  :  An 
individual  who  is  suffering  from  an  incurable  and  painful  affection  gets  into 
the  habit  of  reUeving  his  sufferings  with  morphia.  The  means  of  reUef 
become  later  a  necessity,  so  that  the  patient  who  cannot  do  without  injec- 
tions of  morphia  gradually  increases  the  doses,  and  becomes  a  morphino- 
maniac.  Some  persons  seek  in  morphia  oblivion  from  their  troubles  and 
griefs,  or,  finding  the  drug  to  be  a  mental  stimulant,  proceed  to  the  abuse 
of  the  poison  and  to  morphinism.  Many  morphinomaniacs  are  neuro- 
pathies, and  it  is  very  often  because  the  patient  is  a  neuropathic  that  he 
becomes  a  morphinomaniac.  The  quantity  of  morphia  taken  daily  is  very 
variable.     It  may  amount  to  several  grains. 

The  symptoms  of  morphinism  take  a  certain  time  to  appear,  and  it  is 
only  after  six  or  eight  months  that  the  morphinomaniac  shows  a  peculiar 
look.  The  face  is  pale,  covered  with  early  wrinkles,  and  sometimes  of  an 
earthy  colour.  The  pupils  are  contracted  ;  the  will  is  enfeebled.  Insomnia 
is  the  rule.  The  mouth  is  dry  and  the  thirst  is  acute.  The  appetite  may 
be  lost  or  exaggerated.  Digestion  is  slow,  but  nausea  and  vomiting  are 
absent,  though  pjrrosis  is  sometimes  present.  Injection  of  morphia  often 
causes  a  sensation  of  epigastric  constriction  well  known  to  the  sufferers. 
The  constipation  is  obstinate  and  the  beUy  is  distended.  Palpitation  is 
frequent.  The  pulse  is  irregular  and  intermittent.  The  genital  faculties 
are  weakened.  In  women  menstruation  may  be  disturbed,  and  there  is  a 
tendency  to  abortion.     The  urine  sometimes  contains  sugar  or  albimiin. 


2108  TEXT-BOOK  OF  MEDICINE 

The  skin  is  at  length  covered  with  indurated  nodules,  crusts,  abscesses,  and 
ulcers — lesions  due  to  the  use  of  dirty  syringes  and  septic  solutions. 

Psychical  and  mental  troubles  are  common.  Morphinism  aggravates 
injuries  and  retards  recovery.  The  morphinomaniac  may  be  seized,  either 
during  an  intercurrent  disease  or  through  the  poison  itself,  with  delirium 
tremens  and  maniacal  excitement  similar  to  that  seen  in  alcoholism. 

The  only  treatment  is  to  leave  of!  the  drug ;  but  how  can  this  be  properly 
carried  out  ?  The  injection  of  morphia  becomes  such  an  imperative  need 
that  the  patient  would  rather  give  up  all  the  world  than  the  drug.  A 
morphinomaniac  who  is  sad,  duU,  prostrate,  and  restless,  if  he  have  not  had 
his  injection  of  morphia  for  some  time,  becomes  gay,  talkative,  and  ani- 
mated as  soon  as  the  injection  is  given.  The  morphinomaniac  craves  for 
the  injection,  and  will  give  up  drink,  food,  and,  in  fact,  everything  else. 
Whether  he  be  at  the  theatre  or  spending  an  evening  with  his  friends,  he 
always  finds  means  to  give  himself  an  injection.  For  fear  of  being  without 
morphia,  he  lays  in  a  sometimes  enormous  stock,  and  takes  the  greatest 
precautions  to  keep  some  of  it  in  his  wardrobe,  in  the  drawers  of  his  desk^ 
and  in  his  pockets.  He  keeps  several  syringes  and  spare  needles.  The 
morphinomaniac  who  is  under  treatment  and  is  prevented  from  taking  his 
morphia  demands  the  most  careful  watching,  as  he  always  succeeds,  by 
bribes  or  otherwise,  in  procuring  the  drug.  He  hides  it  in  his  bed  or  in  his 
boots,  and  when  he  cannot  inject  it  under  the  skin  he  takes  it  in  some  other 
way.  I  have  seen  a  patient  in  an  attack  of  maniacal  excitement  eat  morphia, 
of  which  he  had  an  enormous  stock. 

We  can  understand  how  difficult  treatment  must  be  in  persons  who  would 
willingly  submit  to  it,  but  who  cannot.  The  morphia  must  not  be  sup- 
pressed suddenly,  for  this  course  exposes  the  patient  to  violent  delirium, 
obstinate  diarrhoea,  and  collapse.  For  two,  three,  or  six  months,  if  necessary, 
the  dose  should  be  diminished  very  gradually  every  week. 

Cocaine. — Cocaine,  even  in  small  doses,  may  cause  death  when  the 
patient  is  not  accustomed  to  the  drug.  When  the  doses  are  progressive,  a 
fatal  termination  is  never  seen ;  but  we  find  certain  troubles,  described 
under  the  name  of  "  chronic  cocainism." 

In  acute  poisoning  following  injections  given  to  produce  analgesia 
(opening  of  abscesses,  removal  of  teeth),  the  patient  experiences  almost  at 
once  very  distressing  preecordial  angina.  The  heart  beats  violently ;  the 
pulse  becomes  small  and  thready.  At  the  same  time  nausea  and  vomiting 
come  on,  and  the  patient,  who  is  pale,  anxious,  and  weak,  feels  as  though 
his  life  were  slipping  from  him  and  death  were  at  hand.  Sometimes  the 
muscles  of  the  face  and  of  the  neck  are  affected  by  convulsions,  which  in 
grave  cases  simulate  an  attack  of  epilepsy,  and  may  terminate  fatally.  In 
general  these  troubles  do  not  last  long,  and  recovery  is  rapid. 


THE  LNTOXICATIONS  2109 

The  troul»lt's  of  chrtuiic  poisoning  are  chi(;fly  intellectual,  and  give  rise 
tu  fulie  cocdlniqac.  The  delirium  is  of  the  hallucinatory  type  (Saury). 
The  patients  think  that  they  have  under  their  skin  small  bodices,  insects, 
or  little  animals,  which  prick  them  ceaselessly,  and  which  they  are  always 
trying  to  extract.  Hallucinations  of  sight,  hearing,  smell,  and  taste  are 
common.  Sometimes  delirium  of  persecution  is  also  present.  Loss  of 
memory  and  of  \vill-power  is  very  frequent.  Acceleration  and  irregularity 
of  the  pulse,  profound  sweats,  and  diarrhcea  are  also  .seen.  The  wasting  is 
rapid  and  constant.     Genital  impotency  is  usual. 

Intoxication  by  morphia  may  be  associated  with  cocainism,  especially 
in  hereditary  neuropathies,  who  become  toxicomaniacs. 

Subcutaneous  injections  of  ether  and  infusion  of  coffee  should  be  given 
for  acute  poisoning.  The  treatment  of  chronic  cocainism  demands  the 
gradual  suppression  of  the  drug. 

VII.  POISONING  BY  TOBACCO. 

Tobacco  owes  its  toxicity  to  an  alkaloid,  nicotine,  and  to  other  dangerous 
compounds,  such  as  prussic  acid  and  pyridine  bases,  which  are  given  off 
in  the  smoke. 

Poisoning  by  pure  nicotine  is  extremely  rare.  A  few  drops  suffice  to 
cause  sudden  death.  When  death  is  less  sudden,  it  is  preceded  by  burning 
in  the  throat,  violent  pains  in  the  stomach,  diarrhoea,  convulsions,  and 
coma.  The  autopsy  reveals  no  lesions,  and  chemical  analysis  alone  leads 
to  the  discovery  of  the  poison  in  the  organs. 

Tobacco  may  cause  acute  poisoning.  The  mixture  of  tobacco  with  the 
food,  enemata  of  tobacco  formerly  employed  in  intestinal  occlusion,  the 
direct  application  of  tobacco-leaves  to  the  skin  for  the  cure  of  obstinate 
ulcers,  are  causes  of  intoxication.  The  toxic  dose  is  uncertain  ;  it  appears 
to  be  about  an  omice.  The  following  symptoms  occur  :  A  short  time  after 
the  absorption  of  the  poison  the  patient  suffers  from  burning  in  the  throat 
and  oesophagus,  the  stomach  becomes  painful,  and  vomiting,  with  or  without 
diarrhoea,  appears.  Vertigo,  intense  headache,  great  restlessness,  and  cold 
sweats  occur.  The  patients  fall  into  a  state  of  coma,  and  die  from  syncope 
or  from  asphyxia,  after  suffering  from  convulsions. 

Chronic  poisoning  by  tobacco  is  seen  in  smokers,  in  those  who  chew 
tobacco,  and  in  workmen  who  manipulate  it.  Nearly  all  the  systems  are 
affected.  Loss  of  memory,  especially  for  words,  tremor,  and  vertigo 
are  common  symptoms.  As  regards  neuralgia,  let  me  mention  brachial 
and  scapular  neuralgias  and  cardio-aortic  neuralgia  (tobacco  angina). 
Hysteria  has  also  been  noted  (Gilbert).  As  regards  the  digestive  system 
let  me  mention  dental  caries,  stomatitis  (smoker's  patches),  chronic  pharyii- 


2110  TEXT-BOOK  OF  MEDICINE 

gitis  and  disturbed  digestion,  accompanied  by  acid  eructations.  Tobacco 
acts  on  the  nerves  of  the  heart  by  producing  painful  palpitation  and  inter- 
mittence.  Genital  troubles  are  by  no  means  rare  in  the  workpeople  employed 
in  tobacco  factories  (slight  or  absolute  impotence,  abortion). 

Let  me  note,  lastly,  changes  in  the  senses  of  taste  and  smell,  catarrh 
of  the  Eustachian  tube,  and  a  form  of  amblyopia  special  to  smokers  (Gale- 
zowski  and  Martin). 


VIII.  CARBONIC  OXIDE  POISONING. 

Carbonic  oxide  gas  is  an  active  poison,  which  rapidly  causes  death  by 
its  direct  action  on  the  blood.  It  becomes  fixed  with  the  hsemoglobin, 
and  drives  out  the  oxygen  of  the  blood,  in  order  to  form  a  more  stable  com- 
pound than  oxyhsemoglobin.  The  oxygen,  brought  to  the  blood  by 
respiration,  cannot  act  upon  the  red  corpuscles,  which  become  incapable  of 
hsematosis. 

^Etiology. — Poisoning  by  oxide  of  carbon  is  very  rarely  criminal.  It 
is  nearly  always  the  result  of  suicide  or  of  accident.  The  charcoal  stove 
(a  very  frequent  means  of  suicide) ;  the  use  of  fixed  stoves,  in  which  the  flue 
of  the  stove  is  shut,  in  order  to  keep  the  heat  longer ;  the  use  of  movable 
stoves,  in  which  the  draught  is  defective,  are  the  commonest  causes  of  this 
poisoning.  Let  us  also  mention  the  danger  of  blast  furnaces,  coke  furnaces, 
plaster  and  tile  furnaces,  and  foundries,  in  which  the  metallic  oxides  are 
reduced  by  charcoal.  Carbonic  oxide  is  also  formed  in  explosions  due  to 
fire-damp,  in  conflagrations  (as  at  the  Opera  Comique),  and  in  public 
carriages  heated  with  "  briquettes."  It  enters  into  the  composition  of 
gas,  which  largely  owes  its  toxicity  to  this  fact. 

Symptoms. — ^During  sleep  poisoning  may  take  place  without  causing 
any  symptoms.     Coma  and  death  rapidly  result. 

If  the  patient  is  awake,  the  onset  of  the  poisoning  is  marked  by  headache, 
vertigo,  and  visceral  troubles.  The  patient  suffers  from  pulsation  in  the 
head  and  temples,  and  sometimes  from  vomiting.  The  limbs  become  weak 
and  walking  is  impossible.  Dyspnoea  appears,  and  is  accompanied  by 
acceleration  of  the  heart  and  by  peripheral  cyanosis.  Coma  comes  on  in  a 
very  short  while,  and  death  rapidly  ends  the  scene.  It  is  sometimes  pre- 
ceded by  a  period  of  violent  convulsions. 

Recovery  is  possible  in  cases  of  slight  poisoning.  It  results  at  the  end 
of  a  few  days,  after  obstinate  headache,  which  disappears  gradually.  In 
severe  cases,  cerebral  softening,  dementia  (Labord.e),  and  paralysis  (Rendu, 
Brissaud)  are  often  seen.  The  paralysis  may  be  total,  or  be  limited  to 
one-half  of  the  body  (Laroche,  Rendu).  It  is  very  rarely  general,  and  death 
is  exceptional.     The  extensor  muscles  are  the  most  afiected.     Tl^e  teD,don. 


THK   INTOXICATIOXS  2111 

reflexes  are  usually  exaggerated.  Anujstliesia  is  the  rule.  Trophic  troubles, 
bedsores  (Venieuil),  and  eruptions  of  herpes  (Leudet,  Rendu)  may  also  be 
seen. 

Poisoning  by  carbonic  oxide  may  be  chronic.  The  chief  symptoms  con- 
sist of  antrmia,  lassitude,  ana}.sthosia  or  paralysis,  tracheal  cough  (Lan- 
cereaux  and  Aul)ort),  and  glycosuria  (Ollivier). 

Pathological  Anatomy. — The  body  in  carbonic  oxide  poisoning  remains 
well  preserved,  putrefaction  developing  with  extreme  slowness.  On  opening 
the  body,  the  blood  is  fluid  and  of  a  peculiar  clear  red  colour.  On  section, 
all  the  organs  show  this  colouring,  which  in  the  lungs  may  be  scarlet.  No 
other  lesions  are  apparent.  The  reaction  of  the  blood  with  the  spectro- 
scope is  characteristic.  In  the  normal  condition,  when  blood  is  treated  by 
a  reducing  agent,  such  as  sulphide  of  ammonia,  the  two  absorption  bands 
of  the  spectrum  unite  into  a  single  band,  which  is  the  absorption  band  of 
reduced  haemoglobin.  When  the  blood  contains  carbonic  oxide,  the 
addition  of  ammonium  sulphide  has  no  action  on  the  two  normal  absorption 
bands,  and  their  fusion  is  never  seen. 

Treatment. — Pure  air,  artificial  respiration,  inhalations  of  oxygen,  and 
rubbing  with  stimulants,  form  the  basis  of  treatment.  Transfusion  of  blood 
may  give  good  results. 

IX.  INTOXICATION  BY  CARBON  BISULPHIDE. 

Poisoning  by  carbon  bisulphide  was  first  noted  in  France  by  Delpech 
(1856). 

etiology. — The  ingestion  of  common  sulphide  of  carbon  in  large 
doses  is  exceptional.  It  is  usually  the  result  of  accident  or  of  suicide. 
The  pure  drug  has  been  used  in  therapeutics  for  diseases  of  the  skin  (itching, 
chronic  ulcers,  and  sluggish  wounds)  and  for  gastro-intestinal  infections 
(dilatation  of  the  stomach,  typhoid  fever,  and  cholera).  It  has  been 
prescribed  in  affections  of  the  respiratory  tract  in  the  form  of  vapours 
and  of  injections.  These  methods  of  treatment  are  rarely  accompanied 
by  serious  troubles,  because  pure  sidphide  of  carbon,  free  from  hvdro- 
sulphides  and  sulphuretted  hydrogen,  is  much  less  toxic  than  the  commercial 
product; 

The  poisoning  is  nearly  always  of  professional  origin,  arising  from  the 
handling  of  the  tube  during  its  manufacture,  and  especially  in  the  vulcaniza- 
tion of  objects  with  indiarubber.  It  is  also  seen  in  perfumeries,  where  the 
sulphide  is  used  to  isolate  the  essences  of  flowers ;  in  the  factories  where 
camphor  and  various  aromatic  products  are  made ;  and,  lastlv,  in  vane- 
growing  countries,  where  it  is  used  for  the  treatment  of  phylloxera. 

The  symptoms  chiefly  appear  in  neuropathic  persons,  especially  women 


2112  TEXT-BOOK  OF  MEDICINE 

(Delpech).     The  question  of  age  is  of  no  importance.     Want,  alcoholism, 
and  excesses  of  all  kinds  have  an  undoubted  influence. 

Symptoms. — The  acute  accidental  intoxication  must  be  distinguished 
from  the  chronic  professional  form. 

1.  Acute  Intoxication. — The  patient  shows  muscular  relaxation,  the 
face  is  pale  and  moist,  the  lips  bluish  and  covered  with  froth,  the  eyelids 
closed,  the  pupUs  dilated  and  insensitive  to  light,  whUe  the  conjunctivae 
show  no  reflex.  The  breathing  is  stertorous,  and  the  breath  has  a  charac- 
teristic odour  (Douglas).  As  soon  as  the  poison  is  taken,  the  sufferer 
experiences  a  sharp  burning  in  the  mouth,  oesophagus,  and  stomach,  with 
eructations,  nausea,  and  vomiting,  foetid  and  black  diarrhoea.  The  urine, 
which  is  rather  scanty,  is  brownish  or  sometimes  bloody.  The  pulse  is 
irregular,  intermittent,  and  quick.  The  respiration  is  rapid  and  laboured, 
and  the  face  is  covered  with  sweat.  The  nervous  phenomena  are  never 
absent — headache,  tremor,  general  restlessness,  followed  by  somnolence 
and  tendency  to  syncope.  The  liver  may  be  congested  and  hypertrophied. 
The  general  health  is  profoundly  affected. 

2.  Chronic  Intoxication. — The  symptoms  appear  suddenly,  or  after 
prodromata,  such  as  violent  and  persistent  frontal  headache. 

Digestive  troubles,  stomatitis  (Rendu),  a  constant  taste  of  sulphide 
of  carbon  in  the  mouth,  a  blackish  line  upon  the  gums,  salivation,  nausea, 
vomiting,  and  diarrhoea  are  seen.  Persistent  cough,  attacks  of  dyspnoea  and 
epistaxis  have  been  noted.  The  hands  which  are  "  soaked  "  in  the  sulphide  of 
carbon  are  swollen,  painful,  and  covered  with  eczema.  The  skin  of  the  limbs 
and  of  the  thorax  sometimes  shows  blackish  spots  and  irregular  maculae, 
probably  produced  by  an  iron  pigment  (Kiener  and  Engel).  The  urinary 
system  is  rarely  affected.  Such  is  not  the  case  with  the  genital  functions, 
which  pass  through  phases  of  excitation  and  depression.  In  women 
menorrhagia  and  abortion  are  frequent. 

The  nervous  system  is  always  affected  in  chronic  poisoning,  and  three 
chief  varieties  of  nervous  disorder  have  been  described — psychical  troubles, 
symptoms  which  resemble  hysteria,  and  peripheral  neuritis. 

Among  the  psychical  troubles  I  may  quote  a  form  of  drunkenness  in 
fresh  workers,  and  especially  in  women.  Perversion  of  character,  neuras- 
thenia, dementia  (BaU),  mania,  and  lypemania  (Bonnet)  are  seen.  These 
different  varieties  may  be  lasting  or  transitory  (Raymond). 

The  hysteria  produced  by  sulphide  of  carbon  is  shown  either  by  hemi- 
anaesthesia,  anaesthesia  of  the  cornea  and  pharynx,  or  by  hemiplegia,  para- 
plegia, monoplegia,  glosso-labial  hemispasm,  headache,  insomnia,  and 
tremors.  These  troubles  commence  suddenly,  and  are  often  preceded  by  an 
aura,  which  in  man  takes  the  form  of  troublesome  itching  in  the  region  of 
the  scrotum. 


Till-:   INTOXIC'ATJONS  2113 

Tho  iKMiiitis  hiis  not  any  spocific  charactors  (Rayiiiorid).  The  localiz.'i- 
tion  of  the  paralysis  to  the,  upper  extremities  (hipcrids  upon  tho  contact  with 
the  poison.  The  flexors  of  the  fingers  are  chiefly  affected,  and  the  sensi- 
bility is  blunted  in  tho  zone  of  the  musculo-spiral  and  median  nerves.  In 
the  lower  limbs  the  paralysis  takes  the  paraplegic  form,  but  it  is  limited  to 
the  muscles  of  the  feet,  and  chiefly  to  the  extensors. 

The  paralysis  is  flaccid,  with  reaction  of  degeneration.  The  atrophy  is 
slight,  and  the  tendon  reflexes  are  weakened.  Walking  is  still  possible. 
Sensibility  is  affected.  At  lirst  the  limbs  are  painful  ;  later,  hyposesthesia, 
ansesthesia,  or  hyperesthesia  is  seen.  We  find  in  exceptional  cases  signs 
of  pseudo-tabes  (Babes,  Stadelmann),  with  motor  inco-ordination,  lightning 
pains,  plantar  anaesthesia,  and  abolition  of  the  patellar  reflexes.  In  one 
case  Rendu  found  contractures  of  the  jaw,  the  neck,  the  vertebral  column, 
the  legs,  and  the  arms.  These  contractures  were  independent  of  hysteria. 
The  nervous  troubles  usually  recover  in  this  form  of  poisoning. 

The  diagnosis  of  the  acute  and  chronic  troubles  produced  by  sulphide  of 
carbon  is  easy,  as  the  trade  of  the  patient  at  once  attracts  attention.  The 
exact  distinction  from  hysterical  and  toxic  manifestations  is  sometimes 
more  difficult. 

Treatment. — The  removal  of  the  poison  is  the  essential  condition  in 
treatment.  Prophylaxis  will  be  assured  by  thorough  ventilation  of  work- 
shops, hygienic  measures,  and  the  mechanical  prehension  of  objects  soaked 
in  sulphide  of  carbon.  In  chronic  poisoning,  electricity^  tonics,  stimulants, 
and  inhalations  of  oxygen  should  be  employed. 

X.  PELLAGRA. 

Pellagra  is  a  general  disease,  characterized  by  cutaneous  erythema  of 
the  parts  which  are  uncovered,  and  by  nervous  and  digestive  troubles. 

etiology. — Pellagra  exists  in  an  endemic  or  in  a  sporadic  condition. 
The  endemic  condition  is  met  with  in  different  countries  :  in  France,  where 
it  is  very  rare  at  the  present  time,  after  having  been  fairly  common  in 
Les  Landes  and  on  the  frontier  of  the  Pyrenees  ;  in  Spain,  where  it  is  chiefly 
found  in  Asturia  and  Galicia  ;  in  Italy,  which  furnishes  a  considerable  nimi- 
ber  of  cases  in  the  plains  of  Lombardy  and  Venetia.  In  the  sporadic  con- 
dition pellagra  is  met  with  everywhere  :  in  Vienna,  Westphalia,  and  Greece. 
In  France  it  has  been  found  in  Paris,  in  the  districts  of  the  Allier,  Sologne, 
Normandy,  the  Rhone  (Bouchard),  and  the  Marne  (Landouzy). 

Sex  has  no  predisposing  influence,  but  pellagra  is  more  common  in  adults 
and  in  children  than  in  elderly  persons.  It  is  neither  contagious  nor 
hereditary  (Bouchard).  Some  authors  admit  a  parasitic  origin  in  pellagra. 
The  pathogenic  agent  (bacillary  schizomycetes)  is  said  to  occur  on  decayed 


2114  TEXT-BOOK  OF  MEDICINE 

maize,  and  to  have  been  found  in  the  viscera  and  in  the  brain  substance  of 
patients  (Majocchi) ;  but  "  this  opinion  must  be  confirmed  by  further 
researches  "  (Gaucher  and  Barbe). 

Pellagra  is  probably  caused  by  defective  nourishment.  Writers  have 
assigned  a  very  great  part  to  the  emplojonent  of  damaged  maize  (Balardini, 
Roussel).  A  fungus  is  said  to  develop  in  the  interior  of  the  grain,  and  to 
cause  a  disease  ia  maize  known  as  le  verdet,  and  the  granules  of  this  afiection 
are  said  to  produce  profound  cachexia  ia  animals  (Balardini,  Lombroso). 
PeUagra,  however,  may  be  met  with  in  persons  who  do  not  use  maize 
(Hameau,  Bouchard,  GLntrac).  It  develops,  on  the  other  hand,  in  those 
who  are  poor  and  live  upon  inferior  food.  Accordingly,  want,  insufficient 
nourishment,  digestive  troubles  among  lunatics  and  alcoholics,  are  most 
often  the  cause  of  pellagra  (Hardy,  Gaucher).  The  cutaneous  erythema 
in  a  patient  with  pellagra  is  in  part  produced  by  the  sun's  rays,  and  especially 
by  the  chemical  or  violet  rays  (Bouchard). 

Symptoms. — The  disease  commences  with  lassitude  and  prostration, 
accompanied  by  headache,  diarrhoea,  and  sometimes  by  nausea  and  vomit- 
ing ;  then,  towards  the  month  of  March  following,  the  dorsal  surface  of  the 
hands  becomes  of  a  bluish-red  tint,  which  is  more  or  less  dark,  and  accom- 
panied by  violent  itching.  The  dorsal  surface  of  the  two  last  phalanges  is 
almost  always  spared  (Raymond).  The  redness  usually  stops  on  the  dorsal 
surface  of  the  wrist,  though  it  sometimes  invades  the  forearm  as  far  as  the 
elbow.  The  erythema  may  be  also  situated  on  the  dorsal  surface  of  the 
feet,  on  the  neck,  on  the  upper  part  of  the  chest,  and  in  women  and  children 
on  the  face.  After  from  ten  to  twenty  days,  desquamation,  which  takes 
place  in  greyish  layers,  and  more  rarely  in  furfuraceous  scales,  supervenes. 
At  the  same  time  the  erythema  fades,  the  skin  becomes  brown  and  pigmented 
with  small  patches,  which  grow  larger  as  the  result  of  fresh  attacks  of  ery- 
thema, so  that  the  seats  of  election  of  the  eruption  finally  assume  a  dark 
brown  tint  (Brocq).  After  some  time  the  skin  atrophies,  and  resembles 
closely  the  dry,  wrinkled  skin  of  certain  elderly  and  cachectic  persons. 

In  addition  to  the  cachectic  lesions  very  marked  digestive  troubles 
are  found ;  the  lips  and  the  mucous  membrane  of  the  mouth  are  red,  inflamed, 
and  swoUen.  The  gums  are  sometimes  fungous  and  bleeding.  The  tongue 
is  red,  smooth,  and  sometimes  covered  by  aphthous  ulcerations.  Gas- 
tralgia,  nausea,  and  pyrosis  are  present,  and  may  be  accompanied  by  loss 
of  appetite,  or  more  usually  by  boulimia.  Diarrhoea  is  practically  constant, 
with  or  without  intestinal  hsemorrhages. 

The  nervous  troubles  consist  in  frontal  headache,  neuralgia,  rachialgia, 
formication,  buzzing  in  the  ears,  and  gradual  weakness  of  hearing  and  of 
sight.  The  lower  limbs  are  often  paretic  (Hameau).  The  paralysis  becomes 
marked  and  reaches  the  upper  limbs.      Cramps,  tetaniform  contractures, 


rilK   INTOXICATKJNS  2115 

and  cpUeptiforiii  convulsions  are  present  in  some  cases.  The  mental 
troubles  may  simulate  those  of  general  paralysis  (Baillarger),  and  we  often 
find  lypemania,  which  sometimes  leads  to  suicide,  especially  by  drowning 
(Strambio). 

The  duration  of  pellagra  varies  from  some  months  up  to  twenty  years. 
Recovery  is  possible  when  the  disease  develops  in  young  persons,  and  when 
it  is  treated  in  time.  A  fatal  ending  is  very  common,  and  is  due  to  suicide, 
pulmonary  complications  (hypostatic  pneumonia,  tuberculosis),  or  to 
cachexia.     The  prognosis  of  pellagra  is,  therefore,  very  grave. 

Diagnosis. — The  erythema  of  pellagra  is  distinguished  from  other 
pellagroid  er}-themata  by  the  fact  that  intestinal  troubles  and  mental 
changes  are  absent  in  the  latter.  Pellagroid  erythema  is  a  benign  affection, 
which  often  improves,  while  pellagra  is  subject  to  periodical  recrudescences 
at  different  seasons  (Janselme).  Nevertheless,  certain  pellagroid  erythemata 
may  be  only  one  of  the  forms  of  pellagra  (Gaucher).  Pellagrous  erythema 
is  readily  distinguished  from  eczema  on  the  back  of  the  hands,  which  is 
more  general  and  moist,  and  it  will  not  be  confounded  with  the  solar  ery- 
thema, which  is  not  accompanied  by  general  troubles. 

Pathological  Anatomy. — The  lesions  are  excessively  varied  and  but 
little  characteristic.  We  find  general  atrophy  of  all  the  viscera,  especially 
appreciable  in  the  spleen ;  steatosis  of  the  liver ;  brownish  pigmentation  of 
the  pancreas  and  of  the  kidneys  ;  frequent  general  hj^ersemia  of  the  mucosa 
of  the  digestive  tube  ;  interstitial  gastritis ;  and  ulcerative  enteritis.  The 
spinal  cord  is  often  affected  (Bouchard),  and  the  posterior  columns  of  GoU 
show  shght  sclerosis.  Degeneration  and  atrophy  of  the  posterior  group  of 
the  cells  in  Clarke's  column  have  been  found  (Tuczek,  Marie).  The  meninges 
are  sometimes  slightly  injected  and  adherent.  Let  me  quote  diminution 
in  thickness  of  the  epidermis  and  disappearance  of  the  papillae  as  the  chief 
lesions  of  the  skin  (Raymond). 

Treatment. — Abundant  nourishment,  tonics,  protection  of  uncovered 
parts  from  the  rays  of  the  sun,  and  the  exhibition  of  arsenic  (Lonibroso), 
are  the  means  usually  employed  in  pellagra. 


APPENDIX   ON   THERAPEUTICS 

I.  TREATMENT  OF  SYPHILIS— MERCURY— HECTINE— 
EHRLICH'S  606— WASSERMANN'S  REACTION. 

Experience  has  taught  us  that  syphiUs  plays  a  considerable  part  in  pathology. 
Foumier  can  claim  a  large  share  of  this  idea.  The  more  we  study  syphilis,  the  more 
often  do  we  find  it — either  apparent  or  hidden,  acquired  or  hereditary.  We  must  there- 
fore be  able  to  recognize  it. 

While  in  many  morbid  conditions  we  are  in  doubt  when  it  is  a  question  of  deter- 
mining the  cause  of  the  pathogenesis  of  the  affection,  with  syphilis,  on  the  other  hand, 
even  in  doubtful  cases,  it  is  possible  for  us  to  find  the  true  cause,  thanks  to  the  efficacy 
of  treatment,  and,  indeed,  this  treatment  is  often  a  true  therapeutic  triumph. 

A  patient  is  suffering  from  severe  headache,  with  symptoms  of  meningitis,  from 
epileptiform  convulsions,  from  Jacksonian  epilepsy,  or  from  stertor  and  coma.  It 
is  evident  that  the  motor  convolutions  are  affected,  and  the  situation  is  serious.  A 
correct  pathogenic  diagnosis,  however,  allows  us  to  affirm  or  to  suspect  the  syphilitic 
nature  of  the  lesion,  and  we  at  once  institute  specific  treatment.  In  a  few  days  the 
symptoms  improve,  and  in  a  few  weeks  the  patient  is  cured. 

A  patient  has  been  suffering  for  some  months  from  symptoms  of  pulmonary  phthisis  : 
fever,  night -sweats,  haemoptysis,  wasting,  and  cavities  in  the  lung.  The  situation  is 
very  grave,  and  the  prognosis  is  bad.  In  this  case,  however,  a  correct  diagnosis  proves 
or  causes  suspicion  that  the  lesion  of  the  lung  is  syphilitic.  Specific  treatment  is 
prescribed.  In  a  few  weeks  the  symptoms  improve,  and  in  a  few  months  the  patient 
is  well. 

A  patient  has  suffered  for  a  year  or  for  eighteen  months  from  Cruveilhier's  ulcus 
simplex  :  acute  pain  at  the  xiphoid  and  spinal  points,  gastric  intolerance,  vomiting 
of  food,  hsematemesis,  wasting,  and  cachexia.  The  customary  remedies  have  been 
employed  without  success,  and  we  fear  perforation  of  the  stomach,  or  other  complica- 
tions. As  a  last  resort  we  think  of  surgical  intervention.  A  correct  diagnosis,  however, 
leads  us  to  hope  that  the  condition  is  due  to  sjrphilitic  ulceration  of  the  stomach.  We 
employ  specific  treatment.  In  a  fortnight  the  symptoms  improve,  and  in  a  few  weeks 
the  patient  recovers. 

A  patient  has  been  suffering  for  fourteen  years  from  severe  trigeminal  neuralgia. 
Treatment  has  failed ;  large  doses  of  morphia  merely  lessen  the  pain  for  a  time ;  the 
situation  becomes  intolerable,  and  beginning  at  the  end  of  our  resources,  we  discuss 
the  question  of  surgical  intervention.  Accurate  diagnosis  of  the  pathogenesis,  however 
again  leads  us  to  think  that  the  neuralgia  is  possibly  syphilitic.  We  employ  specific 
treatment.    In  three  weeks  the  pains  improve,  and  in  two  months  the  patient  is  cured. 

In  the  treatment  of  syphilis  mercury  and  iodide  of  potassium  are  the  two  specific 
drugs.  Speaking  generally,  it  is  customary  to  employ  mercury  in  the  early  stages  of  the 
disease,  and  to  give  the  preference  to  iodide  for  the  tertiary  troubles.  I  consider  that 
iodide  is  often  useless,  and  the  chief  point  in  the  treatment  of  syphihs  (secondary 
and  tertiary  troubles)  is  to  employ  mercury.  It  is  with  mercury  alone  that  I  have 
obtained  a  cure  in  grave,  inveterate  tertiary  syphilis. 

2116 


AITENDLX    ON   TIIKRAI'KUTICS  1!1L7 

In  what  form  nnd  in  what  ilosus  must  wo  udminiHtfir  irmrctiry  ?  As  ft  matlt^r  of  fin't, 
wo  hftvo  only  to  take  our  olioiio  from  amongat  tho  many  proparations— Hiich  as  pills 
of  protoiodicio  of  niorciiry,  mnoiirial  jiills,  Van  Swieten's  solution,  morcurial  inunctionH, 
or  injections  of  morciiry. 

Tlie  pills  of  protoiociido  are  given  by  Fournier  at  the  onset  of  Hy()hilis,  in  dijses  of  ono 
or  two  pills  daily.  Enoli  pill  contains  a  grain  of  tho  protoiodido,  and  i  giain  of  opium. 
This  modicino  sometimoa  gives  rise  to  colic  or  to  diarrhoea,  but  it  is  none  the  loss  an 
excellent  remedy. 

1  prefer  to  use  injections  of  biniodide  of  mercury.  Like  many  other  methoda  used 
in  therapeutics,  the  hypodermic  method  of  treating  syphilis  at  first  found  partisans 
and  opponents.  The  latter  are  becoming  less  numerous.  Physicians  at  first  proposed 
either  solutions  of  bichloride  of  mercury,  with  the  addition  of  sodium  chloride,  or  of 
ammonium  chloride,  or  combinations  of  the  sublimate,  wth  peptones.  As  the  first 
attempts  were  not  satisfactory,  because  the  injections  were  very  painful,  and  because 
peptonate  of  mercury  did  not  keep,  tho  cyanide  and  the  sozoiodolate  of  mercury 
were  employed.  Attention  was  then  turned  to  special  preparations,  such  as  grey  oil 
and  suspension  of  calomel  in  vasehn.  These  drugs  have  advantages  and  disadvantages 
which  need  mention. 

The  grey  oil,  for  which  several  formulae  have  been  proposed,  like  the  suspension  of 
calomel  in  vasehn,  requires  a  somewhat  delicate  manipulation.  In  fact,  with  these 
preparations  we  do  not  know  the  exact  quantity  of  the  active  substance  injected  under 
t  he  skin,  and  even  while  a'^lmitting  that  the  mixture  is  as  homogeneous  as  possible 
(tliis  is  always  a  difficult  matter  to  obtain),  the  dose  must  be  changed,  for  the  weight 
of  the  drops  is  equally  variable.  Further,  this  method  is  not  free  from  the  foUovnug 
complications  :  Intense  pain  :  redness  and  induration  around  the  scat  of  the  injection  ; 
nodes  which  remain  so  painful  for  a  long  time  that  absolute  rest  is  necessary  ;  abscesses 
which  supervene  in  spite  of  ever)^  antiseptic  precaution  ;  fever,  malaise,  lassitude, 
and  gastric  disturbances  ;  stomatitis  and  slight  sahvation  for  the  fii'st  two  or  three  days 
after  the  injection. 

For  the  pain,  which  is  almost  constant  after  the  injection  of  grey  oil,  injections  of 
cocaine  have  been  advised  ;  but  the  improvement  produced  does  net  last — the  patients 
soon  complain,  and  some  refuse  a  fresh  injection. 

Although  the  grey  oil  and  the  suspension  of  calomel  in  vasehn  have  drawbacks, 
they  are  none  the  less  endowed  with  great  activitj^  two  or  three  small  injections  being 
sufficient  to  make  up  a  complete  treatment.  The  benefits  of  this  method  are  no  longer 
recognized.  Writers  on  svphihs  have  extoUed  the  effects  of  this  method  in  very  severe 
cases  where  other  methods  of  administering  mercury  have  failed.  They  are  useful 
when  patients  cannot  take  pills,  and  they  may  replace  with  advantage  the  inunction  of 
mercury,  but  they  are  by  no  means  free  from  inconvenience. 

Accordingly,  physicians  have  tried  to  perfect  this  mode  of  treatment  by  using  a 
preparation  constant  in  its  effects  and  free  from  the  foregoing  accidents.  With  this 
end  in  view,  Panas  has  employed  a  solution  of  biniodide  of  mercury  in  sterihzed  oUve 
oil.     In  my  opinion  the  aqueous  solution  is  preferable. 

Aqueous  Solution  of  Biniodide  of  Mercury. — The  injection  of  oil  is  not  always  well 
borne  locally.  It  is  sometimes  very  painful,  and  some  patients  refuse  to  submit  to  it. 
It  also  has  the  inconvenience  of  leaving  painful  nodules.  Lastly,  if  we  desire  to  inject 
a  large  dose  of  the  biniodide  of  mercurj^  (^  grain),  the  oily  solution  is  imsuitable,  since 
it  only  contains  h  grain  in  110  minims.  For  these  reasons  I  emploj^  the  aqueous 
solution,  which  is  much  less  painful,  leaves  practically  no  nodules,  and  permits  the 
injection  of  'arge  doses  of  the  active  substance. 

The  watery  solution  of  biniodide  of  mercury  contains  distilled  water,  the  mercurial 
salt,  and  a  small  quantity  of  dried  iodide  of  sodium.  In  order  to  prepare  the  solution, 
the  two  salts  should  be  put  in  a  small  quantity  of  water,  so  that  the  biniodide  is  added 

n.  134 


2118  TEXT-BOOK  OF  MEDICINE 

to  a  concentrated  alkaline  solution  of  the  iodide.  The  percentage  of  the  solution  is 
arbitrary.  We  may  take  it  up  to  §  centigramme  per  cubic  centimetre,  which  is  the 
minimum,  and  we  may  employ  solutions  of  1,  2,  3,  or  4  centigrammes  of  biniodide  of 
mercury  per  cubic  centimetre  of  water.  It  is  evident  that  the  solutions  are  the  more 
painful  the  more  concentrated  they  are.  With  ^  centigramme  per  cubic  centimetre 
pain  is  absent^  and  with  1  centigramme  per  cubic  centimetre  it  is  trifling. 

In  giving  an  injection,  every  aseptic  precaution  must  be  taken.  The  syringe  is 
boiled,  and  the  skin  is  cleansed  with  alcohol  or  with  ether,  followed  by  perchloride  of 
merciury.  The  injection  should  always  be  given  by  pushing  the  needle  deeply  into 
the  cellular  tissue  of  the  loins  or  of  the  buttocks.  The  hquid  is  slowly  injected.  The 
needle  is  withdrawn,  and  a  small  dressing  of  sterihzed  wool  is  placed  over  the  puncture. 
After  each  injection  the  syringe  should  be  cleaned  with  ether  and  alcohol,  and  placed  in 
cold  water,  which  is  brought  to  the  boil. 

When  the  symptoms  are  moderate,  it  suffices  to  inject  dsiily  from  4  milligrammes 
to  1  centigramme  of  the  biniodide.  Twelve  to  fifteen  consecutive  injections  are  given, 
and,  as  a  rule,  improvement  takes  place  after  six  or  seven  injections.  The  injections 
are  then  stopped  for  about  from  twelve  to  fifteen  days.  Several  successive  series  may 
be  given,  if  it  be  deemed  necessary. 

In  severe  cases,  where  the  treatment  must  be  thorough  and  quick,  the  dose  of  bin- 
iodide is  increased.  This  can  be  easily  accomphshed  Avith  a  watery  solution.  A  solu- 
tion containing  2  or  3  centigrammes  of  biniodide  per  cubic  centimetre  is  prepared, 
and  3  or  4  centigrammes  are  injected,  either  in  a  single  dose  or  in  two  doses. 

This  intensive  treatment  should  be  employed  in  cerebral  syphihs,  £^  action  is  neces- 
sary before  the  lesions  become  irremediable.  I  have  also  had  occasion  to  prescribe  it 
in  rebeUious  cases  of  ulcerative  syphilis  of  the  throat,  in  syphilis  of  the  aorta,  etc. 
Consecutive  series  of  ten  injections  are  employed,  and  we  must  not  be  discouraged  if 
we  have  to  continue  the  series  for  several  months.  Tabe^  and  general  paralysis  do  not 
react  to  these  measures. 

I  have  given  more  than  15,000  injections  of  biniodide  of  mercury,  but  I  have 
never  seen  the  least  trouble  ;  in  my  opinion,  no  preparation  of  mercmy  can  be 
compared  with  it.  The  administration  is  doubtless  more  compHcated  than  that  of 
other  mercurial  preparations  ;  it  is  more  simple  for  the  patient  to  take  pills  or  Gibert's 
syrup  than  to  give  mercmial  injections,  but  we  are  recompensed  by  the  results  obtained. 
In  the  first  place,  we  know  exactly  what  dose  is  absorbed,  which  we  never  do  with 
inimction  of  mercury ;  in  the  second  place,  this  preparation  is  rarely  inefEectual.  I 
may  say  that  in  most  cases  injections  of  mercury  are  sufficient,  without  the  addition 
of  iodide  of  potassium. 

I  was  formerly  in  the  habit  of  giving  the  iodide,  even  in  very  large  doses,  thinking 
that  it  was  superior  tc  mercury  in  tertiary  syphilis.  With  further  experience,  I  have 
given  up  this  opinion.  The  longer  I  hve,  the  less  do  I  prescribe  iodide  of  potash.  The 
remarkable  recoveries  from  tertiary  syphihs  reported  in  my  chnical  lectures  at  the 
Hotel-Dieu  and  in  the  present  work  have  been  obtained  in  most  cases  by  mercury 
alone. 

The  treatment  of  syphilis  is  therefore  simpKfied  in  the  great  majority  of  cases  ; 
instead  of  prescribing  iodide  of  potassiimi,  which  is  hable  to  produce  iodism  ;  instead 
of  prescribing  Gibert's  syrup.  Van  Swieten's  solution,  or  mercury  in  piUs,  which  may 
upset  the  digestive  organs  ;  instead  of  ordering  mercurial  inunctions,  in  which  the  dose 
is  difficidt  to  regulate,  I  am  content  to  give  injections  of  biniodide  of  mercury,  which, 
with  proper  precautions,  do  not  cause  local  troubles  or  symptoms  of  poisoning,  and 
which  give  excellent  results. 

Nevertheless,  I  do  not  say  that  iodide  of  potassium  should  never  be  used  in  the 
treatment  of  syphilis.  It  may  be  useful  in  some  cases.  In  syphilitic  lesions  of  the 
aorta,  in  syphilitic  arteritis  of  the  brain  and  of  the  Hmbs,  iodide  of  potassimn  may  be  of 


APPENDIX    nX     111  i;i;AI'KUTICS  2110 

servieo.  In  such  a  cnso  morcury  and  potassium  iodido  should  ho  givrn  altnmatfly ; 
twplve  to  liftoon  injections  of  the  biniodidc  aro  given,  and  iodido  of  potassium  is  then 
taken  for  a  fortnight. 

Lot  mo  add  a  few  words  as  to  possiblo  mishaps.  In  some  ca-sos  wo  think  tliat  the 
disoaso  is  conquered,  the  symptoms  having  disappeared,  and  yet  they  return.  We 
must  never  forget  that  syphilis  is  naturally  obstinJito,  and  doe.s  not  alwaj-s  yield  easily. 
I.<et  us  not  mistake  for  a  definite  cure  what  is  only  a  tran.sient  improvement.  In  this 
ease  the  treatment  must  be  recommenced. 


HECTINE. 

At  the  present  time,  two  preparations  of  arsenic  are  occupying  the  attention  of  the 
medical  world  :  the  one  is  hectine,  the  other  is  Ehrlich's  606. 

Hectiue  is  used  in  solution,  the  dose  being"  10  to  20  centigrammes  in  a  gramme 
of  distilled  water.  According  to  Hallopeau,  it  gives  excellent  results  in  tlie  abortive 
treatment  of  syphilis.  "  The  injections  are  given  in  the  chancre  or  in  its  immediate 
neighbourhood,  by  preference  in  the  track  of  the  lymphatics.  They  give  rise  to  some 
pain  and  to  slight  induration,  which  disappears  in  a  few  days.  They  should  be  given 
daily  in  doses  of  20  centigrammes,  varying  the  site  of  injection  ;  in  chancres  of  the  glans 
and  of  the  corona  we  may  inject  as  high  up  as  the  root  of  the  thif^h.  The  injections 
should  be  continued  until  the  primary  induration  has  disai>peai-ed.  The  inconveni- 
ence, experienced  by  the  patient  from  intervention  at  such  short  intervals,  is  largely 
compensated  by  the  probability  of  escaping  treatment  again  later,  and  by  the 
possibility  of  aborting  the  disease.  The  local  treatment  of  the  chancre  also  acts  upon 
the  hyperactive  treponemata  in  the  surrounding  cellular  tissue,  in  the  Ij-mphatics  and 
in  the  sateUite  glands. 

In  a  recent  communication,  Hallopeau  has  quoted  several  cases,  in  which  the 
abortive  treatment  of  syphilis  was  instituted  by  means  of  injections  of  hectine, 
together  with  20  inti-a-gluteal  injections  of  2  centigrammes  of  benzoate  of  mercury, 
while  15  grains  of  potassium  iodide  were  given  by  the  mouth.  The  results  were  very 
favourable.  "  We  cannot  prophesy  absolutely  as  to  the  future,  but,  if  the  results  are 
constant,  and  if,  after  a  certain  time,  Wassermann's  test  is  repeatedly  negative,  we 
shall  be  correct  in  stating  that  this  remedy  is  definitely  curative.  In  any  case, 
treatment  with  hectine  is  free  from  risk." 

The  foregoing  remarks  apply  to  the  use  of  hectine  at  an  early  stage,  when  the 
chancre  is  present.  No  data  are  at  hand  regarding  curative  results  in  an  advanced 
stage  of  the  disease. 

EHRLICH'S   606. 

At  the  present  time  it  is  scarcely  possible  to  speak  definitely  regarding  606 
(arseno-benzol)  as  a  therapeutic  agent.  In  spite  of  the  many  statistics,  regarding  the 
results  obtained  by  606,  exact  data  are  lacking,  and  the  question  wiU  not  be  decided 
until  all  the  returns  are  to  hand.  We  know  that  arseno-benzol  is  very  efBcacious, 
but  there  is  still  much  to  be  learnt  as  to  the  best  method  of  administration,  the 
dose  to  be  prescribed,  the  cases  in  which  it  is  contraindicated,  and  the  accidents 
that  may  result  in  special  instances. 

Several  methods  of  injection  have  been  advocated.  Intramuscular  injections  were 
so  painfid  that  the  jjatient  was  compelled  to  remain  in  bed  for  several  days,  being 
unable  to  walk  or  to  sit  down.  Volk  dissolved  4<)  centigrammes  of  606  in  10  i>er  cent, 
emulsion  of  paraflin  in  olive  oil ;  in  over  a  hundred  gluteal  injections  pain  did  not  once 
occnr. 

The  dose  varies  from  40  to  60  centigrammes.  The  injection  is  frequently  followed 
by  fever,  tachycardia  and  nausea.    Some  writers  advise  one  large  dose,  others  recommend 

134—2 


2120  TEXT-BOOK  OF  MEDICINE 

rejDeated  small  doses.     Opinions  are  divided  as  to  the  relative  merits  of  intramuscular 
and  intravenous  injections. 

Tlie  results,  obtained  witli  606,  are  often  remarkable.  Chancres  disappear 
rai^idly.  Cutaneous  syphilides  disintegrate  more  slowly  than  mucous  patches,  which 
vanish  in  a  few  days.  In  early  malignant  syphilis  the  results  are  very  satisfactory, 
as  well  as  in  the  tertiary  lesions.  Bonnier  reports  a  case  of  a  patient  suffering  from 
such  severe  lesions  of  the  larynx  that  tracheotomy  appeared  imperative ;  in  three  days 
the  lesions  disappeared  in  a  remarkable  fashion.  In  one  of  Wolff's  cases,  a  tuberculo- 
ulcerative  sypliilide  of  the  nose  disappeared  in  two  weeks. 

In  early  hereditary  syphilis,  the  infant  should  be  suckled  by  an  infected  woman 
(mother  or  wet  nurse),  who  has  been  treated  with  arseno-beuzol. 

How  does  the  drug  act?  Under  its  influence,  the  treponemata  disappear  in  48 
hours  from  the  chancre,  and  from  the  secondary  lesions,  but  in  several  instances  they 
have  reappeared,  some  weeks  or  months  later,  with  fresh  specific  manifestations. 

"  Wassermann's  reaction  gives  similar  results.  On  this  j)oint,  Lange  has  examined 
268  persons  treated  with  arseno-benzol :  153  cases,  in  which  the  reaction  was  positive, 
became  negative  at  the  end  of  four  to  five  weeks,  this  lapse  of  time  depending  on  the 
initial  strength  of  the  reaction ;  18  cases  were  negative  before  treatment ;  13  cases 
remained  negative ;  5  again  became  positive ;  97  cases  remained  positive  in  spite  of 
the  injection;  some  cases,  which  were  neg'ative  before  the  injection,  became  strongly 
positive  after  it,  with  a  gradual  decrease  to  the  negative  again  ;  54  were  not  modified 
after  three  weeks ;  8  (2  adults  and  6  children)  died,  with  a  positive  though  less 
marked  reaction,  either  from  pre-existent  diseases  (pernicious  antemia,  chronic 
nephritis,  miliary  gummata  in  the  liver,  gummata  of  the  heart,  syphilitic  ulceration 
of  the  intestine),  or  from  intercurrent  maladies  (infantile  diarrhoea);  24  patients 
showed  a  diminution  in  the  strength  of  the  reaction  five  weeks  later.  One  case 
of  severe  laryngeal  syphilis  showed,  in  spite  of  a  second  injection,  a  strongly  positive 
reaction  at  the  end  of  six  weeks.  We  see,  therefore,  that  no  fixed  rule  obtains  in 
these  findings." 

Clinically,  we  can  also  note  dissimilar  results.  Some  cases  are  favourably 
influenced  by  606,  others  are  rebellious  to  it.  And  even  in  cases  favourably 
infliienced,  relapses  are  not  uncommon.  Some  authorities  hoped  that  this  drug  would 
be  so  effe^jtive  as  to  cui-e  syphilis  at  once;  it  was  the  therapia  sterilisans  magna, 
obtained  by  a  single  injection  of  40  or  50  centigrammes.  Unfortunately,  606  is  far 
from  killing-  sypliilis  at  one  stroke.  Remy  speaks  of  a  case  treated  immediately  after 
the  appearance  of  the  chancre  ;  mucous  patches  appeared  some  weeks  later. 

Many  instances  of  recurrence  have  been  published.  Four  of  Bering's  patients 
with  chancres  showed  secondary  symptoms  six  to  eight  weeks  after  the  injection. 
Wechselmann  reports  six  cases  of  chancre,  in  which  the  roseola  appeared  in  spite  of 
606.  In  two  cases  the  rash  disappeared  in  a  few  days,  under  the  infliience  of  the  drug. 
In  two  other  cases  a  second  injection  was  necessary  ten  weeks  after  the  first  injection. 
Bering  has  seen  three  cases  of  recurrence  in  tertiary  syphilis.  Frankel  and  Gronven 
consider  that  a  single  dose  is  never  sufficient.  They  advise  an  injection  of  40  centi- 
grammes, two  weeks  later  a  second  of  70  centigrammes,  and  then,  after  two  weeks,  a 
third  of  80  centigrammes  to  1  gramme.    They  would  even  give  as  much  as  1  g"r.  20. 

Reisser  and  Gennerich  g'o  so  far  as  to  advise  the  combination  of  mercurial 
preparations  with  the  arseno-benzol.  This  suggestion  has  some  merit,  but  606  thereby 
loses  much  of  its  prestige. 

Further,  606  may  cause  accidents :  thus,  in  addition  to  high  fever,  profuse  sweat- 
ing, vomiting",  arrythmia  and  syncope,  death  has  occurred  after  the  injection  of  606. 
On  this  point,  Ehrlich  says  :  "  I  have  always  discountenanced  injections  in  persons 
suffering  from  grave  affections  of  the  nervous  system,  but  yet  such  cases  have  been 
given  injections  in  spite  of  my  advice.     The  fatal  result  is  explained :  (1)  by  a  local 


Ali'KNDlX   (»X   TIlKIIAriX'TlCS  2121 

reaction  of  til t«  syi)liili1iL'  iiiHltnilions  .surroumliiiff  nerves  nepessarv  to  fxistciife ;  (2) 
by  liyiitTSfUsiliility  of  tlif  urjj-aiiisui  to  toxic  ajreiits,  u  fact  lou^'  since  ustahiislicd  in  tin* 
case  of  iocliu**  and  of  mercury  in  syphilitic  persons;  {'-l'  by  defective  techuic,  inii)erfect 
asepsis,  abscesses.  I  have  also  j)rotested  ajrainst  inje<;tiou.s  in  persons  with  vascular 
lesi«)ns.    Sarajevos  died  from  rupture  of  an  aneurysm." 

The  contraindications,  therefore,  are  numerous.  Moreover,  we  mu.st  remember, 
says  Balzer,  that  the  many  reports  published  upon  (jtMj  are  lacking'  in  detail  as 
reg-ards  the«e  unfortunate  cases.  In  fatal  cases,  every  po.ssible  detail  should  be  jj^iven 
so  tliat  the  profession  may  have  full  knowledg-e  of  their  sijrnificance.  The  recognition 
of  these  oases  is  just  as  important  as  that  of  the  most  favourable  cases. 

In  short,  we  liave  in  tit>(>  a  drug"  which  will,  with  proper  huudlinjr,  render  great 
services.  Nevertheless,  it  does  not  prevent  recurrences,  and  the  jjatient  is  exposed  to 
grave  dangers,  when  the  (b*ug  is  not  jirescribed  with  due  caution.  On  the  whole, 
liowever,  it  has  given  remarkable  re.sxilts  in  many  syphilitic  manife.stations.  When 
the  indications  and  the  coutra-indications  have  been  definitely  fixed,  ar.seno-benzol  will 
take  its  ])roper  i)lace  with  mercury,  so  that  the  mercurial  preparations  and  arseno- 
beuzol  will  lend  each  other  mutual  aid. 

WASSERMANN'S    REACTION. 

Wassei-mann  conceived  the  idea  of  applying  to  the  diagnosis  of  syphilis  Bordet  and 
Gengou's  method  of  the  deviation  of  the  complement. 

As  it  is  not  j^ossible  to  cultivate  and,  consequently^  to  obtain  the  treponema  in  a  fine 
state.  Wassermann  uses,  as  an  antigen,  the  liver  of  a  syphUitic  foetus,  which  usually 
contains  many  treponemata.  The  first  investigations  gave  much  promise.  But  it  was 
soon  found  that  the  reaction  was  not  specific,  and  that  it  occurred  when  a  rabbit's 
heart,  and  even  glycocholate  or  ta\u-ocholate  of  soda  were  employed  as  an  antigen. 
This  result  proved  that  the  Wassermann  reaction  is  not  biological  and  due  to  the 
presence  of  svi)hilitic  antibodies,  but  that  it  is  a  chemical  reaction,  i)robably  dependent 
upon  lipoid  substances  (Levaditi). 

In  secondary  syphilis,  Wassermann's  reaction  is  very  often  positive.  As  the  interval 
after  infection  increases,  it  becomes  less  constant. 

In  the  parasyphilitic  nervous  affections,  it  is  usually  negative  with  blood-serum, 
although  it  is  fairly  often  positive  with  cerebro-si^inal  fluid. 

It  may  also  be  observed  in  hereditary  syphilis  and  in  experimental  syphilis  in 
monkeys.  In  certain  cases,  however,  it  is  absent,  and  no  explanation  of  this  fact  is 
forthcoming.     It  may  also  be  absent  after  antisyphililic  ti-eatment. 

Fui-thermore.  the  reaction  is  not  specific  ;  it  has  been  obtained  in  leprosy,  malaria, 
scai'latina,  and  jaundice  ;  it  supervenes  after  chloroform  anaesthesia.  The  indications, 
furnished  by  the  reaction,  must  be  accepted  with  caution,  when  we  are  intei-preting 
the  results. 

Several  simplifications  of  the  Wassermann  methods  have  been  proposed ;  thus, 
rabbit's  serum  immunized  against  human  corpuscles  has  been  employed  instead  of  an 
anti-sheep  ha^molytic  serum.  Yamanonchi  considers  this  method  more  delicate,  be- 
cause human  serum  contains  a  natural  amboceptor  to  sheeps  corpuscles ;  this  ambo- 
ceptor may  cause  haemolysis  even  though  s}i)hilis  be  present. 

Noguchi.  in  order  to  simplify  the  test  in  practice,  prepares  filter-papers  impreg- 
nated with  the  antigen,  amboceptor  and  complement.  These  papers  are  said  to  keep 
well,  and  can  be  readily  made  active  by  soakjng  in  normal  solution. 

Further  details  are  unnecessary,  because  the  most  expert  investigators  agree  that 
the  original  method  is  the  most  reliable,  since  in  ever}"  modification  positive  reactions 
can  be  obtained  in  cases  which  are  not  sj^jhilitic. 

Brief  reference  may  here  be  made  to  certain  recent  attempts  to  find»a  cutaneous 
reaction  in  syphilis,  similar  to  Von  Pu-quet*s  cutaneous  reaction  in  tuberculosis.     An 


2122  TEXT-BOOK  OF  MEDICINE 

extract  called  "sypliiline  "  has  been  employed ;  it  is  prepared  in  the  following  manner : 
the  dried  liver  from  a  case  of  congenital  syphilis  is  triturated  in  a  mortar,  and  next 
heated  with  10  per  cent,  honillon-glycerin  at  115°  C.  for  fifteen  minutes.  The  extract 
is  filtered,  reduced  hy  evaporation  at  65°  C,  and  diluted  with  two  parts  of  serum. 
One  drop  is  used  for  injection. 

Fontana  has  employed  it  in  67  cases,  51  syphilitic  and  16  non-syphUitic.  Of  the 
51  syphilitics,  27  gave  a  positive  reaction  (a  true  infiltration  of  the  skin)  in  twenty- 
four  hours.  In  the  non-syphilitic  cases  only  2  reacted.  It  is  i^ossible  that  with  a 
more  perfect  technic[ue,  better  results  may  be  obtained. 

II.  ARSENICAL  TREATMENT— CACODYLATE  OF  SODA. 

Three  preparations  of  arsenic  have  been  chiefly  in  vogue  :  Fowler's  solution,  pills 
of  arsenious  acid,  and  solution  of  arseniate  of  soda. 

Fowler's  solution  is  composed  of  arsenious  acid,  carbonate  of  potash,  and  distilled 
water.  The  dose  for  an  adult  is  from  2  to  8  drops  daUy.  We  may  commence  with 
2  drops  in  a  Uttle  water  after  breakfast  and  after  dinner,  carefully  increasing  the  dose 
by  1  drop  daily,  until  the  maximum  is  reached,  when  we  go  back  again  gradually  to 
the  initial  dose.  Fowler's  solution  has  the  drawback  that  it  is  not  always  well  borne, 
and  often  provokes  cramps  in  the  stomach. 

The  piUs  or  granules  of  arsenious  acid  are  composed  as  follows  (Trousseau) : 

Arsenious  acid  . .  .  .  . .  . .  . .     25  centigrammes. 

Starch  . .  . .  . .  . .  . .  . .  . .     5  grammes. 

Syrup  . .  . .  . .  .  .  .  .  . .  . .     q.s. 

These  ingredients  are  carefully  mixed  into  a  piU  mass,  which  is  divided  into  100 
pills,  so  that  each  pill  contains  2J  milligrammes  of  arsenious  acid.  Trousseau  gave 
to  this  preparation  the  name  of  "  pilules  de  Dioscorides."  One  pill  is  given  to  an  adult 
before  the  two  chief  meals.  Their  exhibition  is  continued  for  a  fortnight,  and  then 
suspended  for  a  week,  this  order  being  maintained  as  long  as  their  use  is  considered 
necessary,  and  according  to  the  tolerance  of  the  digestive  organs. 

An  excellent  preparation  is  the  solution  of  arseniate  of  soda.  The  following  is 
Trousseau's  formula : 

Distilled  water  . .  . .  . .  . .      100  grammes. 

Arseniate  of  soda      . .  . .  . .  . .     5  centigrammes. 

Tincture  of  cochineal  .  •  . .  . .     q.s.  to  colour  the  solution. 

We  prescribe  daily  at  the  commencement  of  the  two  chief  meals  a  teaspoonful  of 
this  solution,  which  represents  2^  milligrammes  of  arseniate  of  soda.  This  preparation 
is  excellent.  I  have  often  noticed  that  arseniate  of  soda  is  better  tolerated  than  arsenious 
a  aid. 

A  fresh  preparation — ^namely,  cacodylate  of  soda — has  recently  been  introduced. 

The  name  cacodyl  (KaKos,  bad)  is  given  to  an  "  organic  mineral  compound,  in 
which  arsenic  enters  into  molecular  combination  with  an  organic  radical."  The 
intervention  of  Gautier  in  his  communications  to  the  Academic  de  Medecine  has  caused 
the  speedy  inclusion  of  cacodylate  of  soda  among  our  therapeutic  measures.  Its  good 
effects  have  been  witnessed  on  aU  sides,  and  the  frequent  use  which  I  have  made  of  it 
permits  me  to  give  my  personal  opinion  upon  this  subject. 

Cacodylate  of  soda  may  be  given  in  three  ways :  in  a  mixture,  in  enemata,  and  in 
subcutaneous  injections. 

Cacodylate  of  soda  may  be  given  in  a  mixture  in  daily  doses  of  5  centigrammes,  but 
the  administration  of  cacodylate  of  soda  by  the  mouth  is  not  free  from  inconveniences. 
Tn  the  digestive  canal,  says  Gautier,  the  cacodylate  of  soda  may  be  converted  into 


ATTKNDIX  ON  TURRAPRl'TK  s  2123 

oxido  of  caooilyl,  wliii-li  jo^t'S  oil  a  cliiimct^Mirttic;  alliacoous  odour.  It  may  cauBo 
opigastrio  pain  and  ronal  oonm^tion,  witli  albuminuria.  "  (Jn  tho  other  iiund,"  sayB 
Gauticr,  "  wlinu  tbo  drug  is  givori  liypodorraically,  I  liavo  not  noticed  albuminuria, 
albaeoous  odour  of  tho  broatb,  or  inlostinal  trnuhlo.s." 

For  my  part,  whtm  1  wi.slj  to  give  a  preparation  of  arsonic  \>y  tho  mouth,  I  prcHcribo 
the  sokition  of  ar-^i^niato  of  soda.  ai-oonUng  to  the  formula  ahoady  jipven.  I  reserve 
the  cacodylato  for  injoitii)U.s. 

Manufacturera  now  make  storili/.od  glas.s  capsules,  each  containing  5  centigrammes 
of  caoodylate  of  eoda,  dissolved  in  1  c.c.  of  water.  Wo  can  keep  capsules  indefinitely, 
without  any  change  in  the  solution.  When  we  desire  to  use  tho  drug,  the  point  of  the 
capsule  is  broken,  and  the  tJuid  is  drawn  into  the  syringe,  which  has  been  previously 
sterilized. 

A  daily  injection  of  from  3  to  5  centigrammes  of  cacodylate  is  given  for  eight,  ten, 
or  twelve  days  in  succession.  Tho  treatment  is  stopped  for  a  week,  and  it  is  then 
repeated  as  before  for  as  long  as  may  be  necessary. 

It  is  certain  that  this  tonic  method  of  treatment  is  to  be  preferred.  It  is  applicable 
to  all  patients  who,  for  various  causes,  are  suffering  from  amemia,  neurasthenia,  weak- 
ness, or  wasting.  Persons  sutlering  from  tuberculosis,  diabetes,  or  cachexia  derive 
benefit.  Sometimes  the  result  is  surprising.  After  from  twelve  to  fifteen  injections 
the  patient  becomes  fat,  and  bis  strength  and  colour  return.  Arrhenal  has  been  extolled 
by  Gautier  in  malaria. 


III.  INJECTIONS  OF  ARTIFICIAL  SERUM. 

In  the  first  place,  what  is  meant  by  artificial  serum  ?  Artificial  sera  are  saline  solu- 
tions, which  contain  one  or  more  of  the  normal  salts  of  the  blood  in  various  proportions. 
Some  sera  are  concentrated,  and  others  are  weak.  Among  the  former  we  may  quote 
that  of  Cheron,  which  has  the  following  composition 


Crystalline  carbolic  acid 
Chloride  of  sodium 
Sulphate  of  soda 
Phosphate  of  soda  . . 
Distilled  water 


1  gramme. 

2  grammes. 
8 

4        „ 
100    „ 


It  is  injected  hj'podermically  in  small  quantities  of  from  5  to  10  grammes.  At  the 
present  day  we  employ  dilute  sera.     Hay  em's  serum  has  the  following  composition  : 

Chloride  of  sodium  . .         . .         . .  . .     5  grammes. 

Sulphate  of  soda        . .  . .         . .         . .         . .     10    „ 

Sterilized  water  .  .  . .  . .  . .  . .      1  litre. 

The  addition  of  sulphate  of  soda  is  now  considered  superfluous,  and  solutions  of 
chloride  of  sodium  are  alone  employed.  The  percentage  composition  of  these  solutions  is 
of  much  importance.  Physicians  have  for  a  long  time  employed  a  solution  of  7-5  parts  per 
1,000,  which  was  the  "  indifferent  "  or  "  physiological  "  solution  of  histologists.  Malassez 
has  shown  that  this  solution  causes  marked  changes  in  the  red  corpuscles,  and  has 
proposed  a  solution  of  10  parts  per  1,000.  This  conclusion  has  been  confirmed  by 
researches  upon  human  blood-serum,  and  authorities  are  agreed  in  considering  that 
the  serum  of  human  blood  corresponds,  from  the  point  of  view  of  its  "  molecular 
concentration,"  to  a  solution  of  chloride  of  sodium,  with  a  percentage  of  9  to  10  parts 
per  1,000. 

This  artificial  serum  is  prepared  as  follows :  9A  grammes  of  pure  salt  are  dissolved 
in  1  Utre  of  distilled  water.     This  solution  is  filtered  through  wool  into  a  flat-bottomed 


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TEXT-BOOK  OF  MEDICINE 


The  neck  of  the  flask  is  plugged  with  a  tampon  of  cotton-wool.  The  flask  is 
then  placed  in  the  autoclave  at  a  temperature  of  115°  C.  for  ten  minutes.  The  sHght 
concentration  caused  by  steriUzation  reduces  the  percentage  of  the  solution  to  9-5  per 
1,000.  Flasks  thus  prepared  are  easily  kept.  It  is  necessary  to  cover  the  neck  with  a 
cap  of  indiarubber,  in  order  to  avoid  the  concentration  which  would  take  place  in  time. 

An  injection  may  be  given  with  various  apparatus.     One  apparatus  consists  of  a 
two-way  flask,  into  which  the  serum  is  introduced.     One  of  these  two  glass  tubes  is 

connected  with  an  indiarubber  tube,  armed  with  a 
needle,  which  is  introduced  into  the  tissues,  while  the 
other  glass  tube  is  connected  with  a  pump.  This 
apparatus  has  several  drawbacks.  In  the  first  place, 
it  is  difficult  to  graduate  the  force  of  the  injection  ;  in 
the  second  place,  it  may  happen  that,  for  want  of 
attention,  the  air,  instead  of  fluid,  is  injected  into  the 
tissues.  Extensive  emphysema  may  thus  arise.  I 
have  twice  witnessed  this  accident. 

Carrion-Haillon's  apparatus  appears  to  me  to 
fulfil  the  principal  indications.  Its  management  is 
simple.  With  this  apparatus  the  injection  of  serum 
takes  place,  so  to  say,  automatically  and  slowly,  under 
conditions  of  rigorous  asepsis. 

This  apparatus  is  composed  of  a  large  receiver, 
which  will  hold  from  250  to  500  grammes  of  serum. 
This  receiver  is  closed  up  by  a  stopper,  and  is  con- 
nected to  an  indiarubber  tube,  furnished  with  a 
needle. 

The  injection  of  serum  is  given  as  foUows  :  Before 
introducing  the  needle  into  the  chosen  region  (cellular 
tissue  of  the  abdomen  or  of  the  buttocks),  we  exhaust 
the  air  contained  in  the  tube  and  in  the  needle. 
For  this  purpose  we  turn  the  glass  tube,  which  is 
passed  through  the  stopper,  so  that  the  position  F  is 
changed  to  the  position  O.  These  two  letters,  which 
are  engraved  upon  the  stopper,  indicate  that  the  tap 
is  closed  at  F  and  open  at  O.  The  open  tap  allows 
the  air,  which  is  purified  by  a  plug  of  wool,  to 
exercise  pressure  on  the  fluid.  The  chp  which  closes 
the  indiarubber  tube  is  then  removed,  and  the  hquid 
flows  out  from  the  needle.  The  flow  is  stopped  by 
means  of  the  chp,  and  the  apparatus  is  suspended 
either  from  the  wall  or  from  the  head  of  the  bed. 
The  atmospheric  pressure  on  the  serum  depends  upon 
the  height  at  which  the  apparatus  is  suspended. 
The  needle  is  introduced  into  the  cellular  tissue  of  the 
region  which  has  previously  been  rendered  aseptic,  the 
clip  is  let  go,  and  the  injection  of  serum  takes  place  very  slowly.  An  injection  of 
250  grammes  takes  about  twenty  minutes.  We  may  thus  give  further  injections  in 
the  same  day,  either  by  using  a  series  of  receivers  or  by  recharging  the  same  recei  ver 
with  serum  kept  in  a  sterih'zed  flask. 

The  enormous  pad  of  oedema  produced  by  the  injection  of  the  serum  into  the  cellular 
tissue  is  fairly  rapidly  absorbed. 

The  injection  of  serum  is  given  in  the  above  manner.     If,  however,  the  serum 
is  not  at  hand,  as  may  happen  to  physicians  in  the  country  and  in  small  towns,  it  is 


Fig.  97. — Apparatus  for 
Injection  of  Serum. 


APPENDIX  ON  THERAPEUTICS  2125 

easy  to  niako  an  injection  on  the  spot,  in  the  following  manner :  9J  granimee  of  pure 
salt  are  put  into  1  litre  of  water — Hltorcd,  if  possible.  The  solution  ia  boiled  for  half  an 
hour,  and  the  loss  of  fluid  duo  to  evaporation  is  made  up  by  the  addition  of  boiled 
water.  In  this  way  we  obtain  an  aseptic  solution,  which  contains  9-5  grammes  of  salt 
per  1,0U(). 

The  therapeutic  indications  for  large  injections  of  serum  are  very  numerous,  and  are 
repeatedly  mentioned  throughout  the  ])age3  of  this  work. 

Profuse  hivmoniiages  (epistaxis,  metrorrhagia,  ha-matemeses  of  exulceratio  simplex 
and  of  ulcus  simplex,  etc.)  may  bo  elToctively  treated  by  largo  injections  of  serum. 
Surgeons  also  give  prophylactic  injections  before  operating  upon  ana;mic  or  debilitated 
persons. 

At  first  sight  largo  injections  of  serum  do  not  ajjpear  to  be  logical  in  cases  of  hiemor- 
rhage.  Thus,  in  a  patient  suffering  from  severe  hjematemesis  due  to  exulceratio  simplex 
wo  might,  a  priori,  fear  tliat  the  rise  of  blood -pressure  due  to  the  injection  of  serum 
would  interefere  with  the  formation  of  the  clot.  Such  is  not  the  case.  This  question 
has  been  discussed  imder  Exulceratio  Simplex. 

Large  injections  of  serum  may  be  beneficial  in  toxic  and  infectious  diseases  (typhoid 
fever,  adynamic  pneumonia,  poisoning,  etc.),  since  they  favour  diuresis  and  elimination 
of  toxines.  They  have  given  good  results  in  maUgnant  jaundice.  On  account  of  the 
chloride  of  soda  wliich  they  contain,  injections  of  serum  should  be  prohibited  in  Bright's 
disease,  and  in  all  diseases  accompanied  by  oedema. 

We  see,  therefore,  from  this  rapid  survey  the  importance  of  injections  of  serum, 
and  the  many  indications  for  their  use.  The  quantity  of  serum  injected  varies  in 
different  cases.  Injections  of  100,  200,  300,  400,  or  500  grammes  may  be  given.  In 
fact,  cases  occur  in  which  2  htres  may  be  injected,  di\nded  into  four  or  five  injections, 
in  the  twenty-four  hours. 

For  a  long  while  I  have  been  accustomed  to  add  a  little  benzoate  of  caffein  to  the 
injection  of  artificial  serum — 5  to  10  centigrammes  per  litre  of  serum.  Although  this 
dose  of  caffein  is  very  small,  it  has  a  beneficial  effect  upon  the  heart  and  the  kidneys. 
The  mixture  is  readily  made  at  the  time  of  the  injection  by  pouring  a  few  drops  of  a 
solution  of  benzoate  of  caffein  of  known  strength  into  the  receiver. 


IV.— TEEATMENT  WITH  SUPEEHEATED  ATE— GANGEENE— 
AETHEITIS— NEUEALGIA— GANGEENE  OF  THE  LIMBS— 
GONOCOCCAL    AETHEITIS. 

The  sero-thermo-generator. — This  ajjparatus,  made  by  Gceffe,  supplies,  by  means  of 
an  eleoti'ical  ciu-rent,  a  jet  of  air  which  can  be  directed  uj)on  gangrenous  tissues,  and 
can  be  raised  to  any  temperature  up  to  700^  C.  I  have  sugge.sted  the  name  of  £ero- 
tliermo- generator  for  this  apj^aratus.  It  is  readily  poi-table,  and  can  be  used  either  with 
the  constant  or  with  the  alternating  cuiTent. 

The  electric  ciuTent  serves  a  double  jjurpose ;  on  the  one  hand  it  drives  a  rotary 
pump  which  can  supply  50  litres  of  air  i^er  minute ;  on  the  other  hand,  it  can  heat  to 
an  exceedingly  high  temperature  a  platinum  wire,  coiled  up  in  a  cylinder  of  fireproof 
material.  The  air,  circulating-  round  the  wire,  is  heated  to  the  rt'nuii-ed  degi-ee ;  it 
escapes  from  a  tubular  orifice  at  the  end  of  the  heating  npparatus  which  is  held  by  the 
operator,  and  is  played  like  a  jet  of  water  upon  the  sloughing  tissues.  The  operator 
keeps  the  jet  about  2  to  6  inches  from  the  tissue.  The  healthy  area  around  the  slough 
is  protected  by  moi.st  compresses. 

The  air  supply  and  the  temperataire  are  regulated  independently,  so  that  we  can 
obtain  an  air  supply  of  15  to  50  litres  i)er  minute,  aud  any  temperature  up  to  700°  C. 
Fui'ther,  the  temperature  can  be  varied  by  increasing  or  diminishing  the  air-supply. 


2126 


TEXT-BOOK  OF  MEDICINE 


while  the  temperatiu-e-regtilator  is  not  altered.  A  pyi-ometer  shows  the  temperature 
of  the  air-douche.  With  practice,  we  can  adjust  the  regulators  without  referring  to 
the  pyrometer. 

Treatment  of  gangrene  of  the  limbs. — The  following  case*  gives  an  idea  of  the  treat- 
ment of  gang-rene  by  douches  of  superheated  air  : 

On  September  14,  1909,  I  saw,  with  Dr.  Darras,  a  man,  sixty-four  years  of  age, 
whose  left  leg  and  foot  had  just  become  g-angrenous.  The  toes  were  violet-coloured. 
The  foot  and  the  leg-  up  to  within  two  fingers'  breadth  of  tlie  knee  had  a  livid  tint. 
The  calf  showed  two  ecchymoses.  The  foot  was  quite  cold.  No  oedema  present.  The 
g'angrene  had  set  in  two  days  before  with  severe  pain  ;  it  was  due  to  obliteration  of  the 
arteries  of  the  lower  limb ;  there  was  no  pulse  in  the  dorsalis  pedis,  tibial  and  popliteal 
arteries ;  the  pulse,  though  weakened,  could  be  felt  in  the  femoral  vessels. 

The  urine  contained  much  g-lucose  and  acetone.  The  man  had  suffered  from  diabetes 
for  twenty  years;  so  that  it  appeared  natural  to  classify  the  case  as  one  of  diabetic 
gang-rene ;  and,  although  obliterating-  arteritis  is  not  seen  in  diabetes  unless  atheroma 
is  also  present,  yet  we  made  a  diag-nosis  of  diabetic  g-angrene. 

Examination  of  the  urine  (September  14) : 

Amount  in  24  hours     ..  ..  ..         2200  c.c. 


Specific  gravity 
Grlucose  .. 
Acetone  .. 
Albumin 


1031 

82  grammes  in  24  hours. 
31 
U 


The  man  was  almost  comatose,  the  pulse  was  wretched  and  the  rate  was  140, 
the  gangrene  was  spreading  every  hour.  Amputation  was  out  of  the  question.  As 
reg-ards  the  g-eneral  condition,  our  efforts  were  directed  to  supporting  the  strength  and 
to  checking-  the  diabetes.  Rig'id  antidiabetic  regime  was  ordered.  The  yolk  of  eggs 
beaten  up  in  broth  rich  in  meat  juice,  and  Vichy  water  were  given.  Milk  was 
proscribed.  Injections  of  2  to  3  centigrammes  of  cacodylate  of  soda  were  ordered. 
Antipyrine  with  soda  bicarbonate  was  given.  To  induce  sleep,  we  used  veronal  40 
centigrammes,  and  injections  of  morphine  1  centigramme. 

The  gangrene  was  treated  with  a  douche  of  hot  air  twice  daily  to  the  dying- 
tissues.  The  temperature  of  the  air  varied  from  200°  to  600°  C.  We  thus  tried  to 
prevent  secondary  infection  and  absorption  of  the  toxic  products. 

The  treatment  began  on  September  14,  with  two  douches  daily  at  a  temperature  of 
300°  C.  to  the  sloughing  areas,  and  85°  to  100°  over  the  surrounding  tissue.  The 
distance  of  the  jet  was  5  to  10  centimetres ;  each  seance  lasted  half  to  three-quarters 
of  an  hour.     The  treatment  did  not  cause  pain. 

After  a  week,  the  suffering  was  less  acute,  the  toes  and  the  foot  had  a  blackish  tint, 
and  the  leg  was  purple.  No  blebs  were  present,  the  gangrenous  tissue  did  not  oose, 
the  gangrene  remained  dry  and  odourless.  The  fever  was  nil ;  the  patient  beg-an  to 
take  food ;  he  slept  for  some  hours,  and  the  sugar  tog-ether  with  the  acetone  rapidly 
diminished. 

Urinary  analysis,  September  27  : 

Quantity  in  24  hours  ..  ..  ..     2-200  c.c. 


Specific  gravity 
Glucose 
Acetone 
Albumin 


1014 

3J  grammes  in  24  hours. 

Q3 

'-'4  »  J! 

i 


The  air  douches  were  continued  twice  daily  at  300°  and  400°.     On  October  17,  the 
gangrenous  tissues  were  blackish,  dry,  reduced  in  size  and  odourless. 


Communication  a  I'Academie  de  Medecine,"  seance  du  Midi,  15  Fevri«r,  1910. 


APrENDIX  ON  TllKKAI'EUTlCS  2127 

Tli«  nil-  (luiu-h(>  iioi  only  uttm-Us  llie  Hurfaco  <ir  llm  lissufs,  but  also  infiltrates 
ihom;  no  tissues  I'si-iijies  ils  action;  it.  does  not  cautoriw*  tlio  tiHsiios  like  thf>  actual 
ouut«<ry  tUw's,  Init  cooks  ami  drios  tlicni  ;   in  othor  words,  it  muniniifinH  tliein. 

Ou  Novfiubor  17  tho  apparatus  noodcd  repairs,  and  tlie  Hi'-anooH  woro  Hnspended  for 
I'orty-oiKl't  hours.  The  jran^'-rene  at  once  became  moist  and  foul  BW(dlintr.  After 
Novembor  I'J  two  douches  were  apiin  friven  daily,  at  teniperaturea  of  'U)(P  to  r,iHP. 
The  p-anpreue  became  dry  and  odourless,  while  a  line  of  deninrcation  appeared  below 
the  knee.  In  time  the  dead  tis.sne  ]»ecame  separated  from  the  liealthy  flesh.  The 
patient  piiiietl  stren^ith,  and  took  food  well. 

Urinary  analysis: 

Quantity  in 'Jl  hours  ,.  ..  ..  ..  2100  grammes 

Specific  V-nivity        1009 

Glucose  . .  . .  . .  . .  absent. 

Acetone  . .  . .  . .  .  •  absent. 

All)umin         . .  . .  . .  . .  4'>  centi^ammes. 

On  December  21  Legueu  amputated  tliroug-L  the  thig-li  at  tlie  junction  of  the 
upper  and  middle  thirds.  The  man  made  an  excellent  recovery,  and  was  sent  home  on 
January  17,  1910.  The  stump  was  supple  and  well  formed;  the  appetite  was  good; 
the  ui-tne  contained  neither  sugar  nor  acetone. 

The  microscopic  examination  is  shown  in  Fig.  98. 


v-a.cJi'i.'o--  ■ 


X 


A  .JS--^     r  LI 


II 


Fig.  98. — Arteritis  Obliteraxs  or  the  Popliteal  Artery,  Diabetic  Gangrene 

WiTHOtTT  Infection. 

In  the  centre,  the  artery. — A.  clot  undergoing  organization  with  new  formation  of 
vessels  (c).  LI,  internal  elastic  limiting  layer. — Mesarterium  invaded  by  hyaUne 
degeneration,  especially  marked  at  II.  Y,,  satellite  vein,  with  organized  clot, 
partially  obliterating  tlie  lumen  (d).  New  formed  capillaries  in  the  clot. — Y;,  Y3, 
satellite  veins  with  endoplilebitis.  Note  the  absence  of  lymphangitis  and  the 
absence  of  embryonic  infiltration,  as  much  in  the  elements  as  in  the  connective 
sheath  of  the  vascular  system. 

It  is,  perhaps,  surprising  that  the  vitality  of  the  stump  allowed  healing  by  first 
intention,  although  the  femoral  artery  was  completely  blocked.  The  nutrition,  how- 
ever, was  carried  on  by  some  arteries  which  had  not  been  compressed  in  the  athero- 
matous process. 

The  amputated  portion  was  examined  at  the  H6tel-Dieu.     The  arteries  of  the  leg 


2128  TEXT-BOOK    OF   MEDICINE 

and  foot  coiild  not  be  found  in  the  mummified  tissues.  The  popliteal  artery  was 
obliterated  by  the  lesions  of  arteritis,  and  by  an  adherent  clot. 

As  the  preceding  figure  shows,  the  lumen  of  the  artery  had  quite  disappeared ;  the 
centre  of  the  vessel  was  occupied  by  a  clot,  everywhere  adherent  to  the  endarterium. 
The  clot  was  but  little  organized,  some  new-formed  vessels  ran  through  it,  and  a  little 
adult  connective  tissue  was  present.  The  endarterium  was  thickened  ;  foci  of  hyaline 
degeneration  were  present.  The  internal  elastic  lamina  was  not  recognizable  at  many 
points.  Centres  of  hyaline  and  atheromatous  degeneration  were  found  in  the  mesar- 
terium.  The  vena  comes  of  the  artery  was  aifected  with  granulating  endophlebitis ; 
an  organized  clot  filled  the  entire  lumen  of  the  vessel. 

The  arteritis  came  under  the  heading  of  senile  and  diabetic  arteritis  obliterans.  It 
is,  however,  strange  that  the  histological  examination  revealed  no  trace  of  infection, 


V 

H  r 

\. 

A  , 

IJ 

M  - 

- 

II 

— .        _ 

L  . 

'^  fc  tb-o  vjujiio  ^ 

Fig.  99. — Arteritis  0-BLitekans  of  the  Posterior  Tibial  Artery.     Diabetic 

GrANGRENE   WITH   InEECTION. 

The  artery  occupies  the  middle  of  the  figure.  A  shows  the  lumen  filled  with  organized 
clot,  traversed  by  three  bands  of  fibrous  tissue  (T).  Between  the  bands  the  parts 
of  the  clot  in  process  of  organization  are  invaded  by  embryonic  cells. — C,  new- 
formed  capillaries  in  the  clot. — LI,  internal  elastic  layer,  separated  at  some 
points,  and  almost  destroyed  at  others. — H,  foci  of  hyaline  degeneration. — M, 
mesarterium  infiltrated  with  embryonic  cells.  Y,  vena  comes,  the  walls  invaded 
by  embryonic  cells.  The  embryonic  infiltration  has  invaded  the  perivascular  con- 
nective tissue  ;  the  infiltration  is  most  marked  around  the  foci  of  lymphangitis  (L). 

lymphangitis  and  embryonic  infiltration  being-  absent.  In  order  to  grasp  the  value  of 
this  negative  fact,  we  must  compare  this  case  with  one  of  infective  diabetic  gangrene 
in  a  man  aged  sixty- four  years. 

This  case  was  one  of  gangrene  of  the  foot  following  arteritis  obliterans.  The 
gangrene,  after  being  dry  for  three  months,  became  moist  and  very  offensive.  At  this 
time  we  had  not  the  apparatus  for  using  superheated  air.  The  g'angrene  invaded  the 
malleoli,  and  the  situation  became  rapidly  worse  ;  the  oedema  spread  to  the  leg",  blebs 
appeared,  the  j)ain  was  intolerable,  the  foetor  was  excessive,  the  appetite  failed,  the 
temperature  rose,  the  j^atient  wasted  visibly,  and  was  becoming  infected.  Amjjuta- 
tion  was  performed  through  the  middle  third  of  the  thigh,  and  in  three  weeks  the 
stump  healed  perfectly. 

The  condition  of  the  vessels  is  shown  in  Fig.  99. 

The  dorsalis  pedis  was  much  thickened.     On  section  its  lumen  was  obliterated  by 


AITKNDIX  ON  Til KlIAl'ia TICS  2129 

pranulntioiis  of  ciuhirierilis  and  by  a  fibrinous  clot.  The  anterior  tibial  artery  was 
iHTiiu'iiblt"  in  its  \ii)jM'r  part.  The  obliteration  of  the  ves.s»'l  was  duo  to  endarteritis 
and  to  a  stnititit'd  an<l  or^'anized  dot.  Athi>romatous  and  hyaline  nju.s.ses  were  present 
in  tJie  me.sarlerimii.  'J'he  emlarferium  of  the  po.sterior  tiliial  art^-ry.  where  it  pas.ses 
behind  the  niallfoius,  wils  completely  destr<)yed.  The  inesartcriuni  contained  ])atche8 
of  atheroma  and  of  hyaline  ti.ssue.  The  blocking  of  the  vessel  wiw  due  almost 
enlirely  to  a  clot  of  fibrin,  or^'anized  and  adherent  to  the  internal  elastic  lamina.  The 
clot  was  traversed  by  bands  of  tibrous  tissue ;  a  section  .showed  new-formed  vessels, 
but  no  blood  corpuscles. 

The  most  intere.sting-  feature  was :  The  presence  of  elements  of  recent  dat«  in 
addition  to  the  chronic  process  of  atheroma.  Inliltration  of  embryonic  cells  was 
everywhere  pre.sent :  in  the  walls  of  the  artery,  in  the  connective  tissue  around  the  veins, 
in  the  lymphatics  and  in  the  lymph  spaces.  The  lymphatic  vessels  were  so  packed 
that  it  was  difficult  to  find  on  section  anything  except  embryonic  cells.  The  cells 
decreased  in  numbers  in  proportion  as  the  sections  were  made  higher  up  in  the  course 
of  the  vessels. 

Tliis  infiltration  had  most  probably  started  from  the  centres  of  the  gangrenous 
lymphangitis,  as  an  ascending  infection.  Letulle,  an  authority  on  this  question, 
said,  after  examining  the  histological  preparations :  "  We  tind  in  thera  a  new  condition 
of  vei-y  great  interest."  It  is  probable  that  the  outbreak  of  moist  infecting  gangrene 
which  appeared  coincided  with  these  attacks  of  lymphangitis. 

On  comparing  the  histological  findings  of  these  two  cases,  we  find  that  the 
difference  is  fundamental.  In  each  case  the  obliterating  lesions  in  the  vessels  are 
identical ;  but  in  the  case  treated  with  superheated  air.  the  gangrene  remained  dry, 
and  did  not  cause  infection.  In  the  second  case,  on  the  contrary,  the  gangrenous  in- 
fection threatened  the  patient's  life,  and  the  histological  examination  showed  the 
infective  process. 

It  is  then  logical  to  conclude  that  frequent  douches  of  air  render  gangrene  harm- 
less, prevent  secondary  infection  with  infective  lymphangitis  and  toxic  absorption, 
and.  by  mummifying  the  sloughs  without  danger  to  the  economy,  give  the  surgeon 
time  to  choose  his  opportunity,  in  ca.se  an  operation  is  deemed  necessary. 

These  considerations  apply  equally  to  all  forms  of  gangrene,  in  the  treatment  of 
which'there  are  two  phases — a  phase  in  which  the  dead  tissues  are  sterilized  by  super- 
heated air,  and  a  surgical  phase,  which  consists  in  separating,  at  the  proper  time,  the 
dead  from  the  living  tissues. 

In  limited  gangrene,  superheated  air  may  bring  about  recoveiy  without  the  need 
for  surgical  intervention,  as  in  the  case  of  an  aged  man  who  was  in  the  St.  Christopher 
ward,  suffeiing  from  diabetes  and  gangrene  of  the  right  big  toe.  The  gangrene  was 
moist.  Superheated  air  was  emi^loyed  daily  ;  the  pain  rapidly  diminished,  cicatrization 
occurred,  and  recovery  followed  after  fifty  applications. 


TREATMENT   OF   GONOCOCCAL  ARTHRITIS. 

Several  cases  of  gonococcal  artkritis  have  been  treated  with  superheated  air  at  the 
H'*'tel-Dieu.  Each  seance  lasted  from  twenty-five  to  thirty  minutes,  and  the  tempera- 
ture of  the  air  was  about  125"  C.  The  treatment  was  well  borne  by  the  patients, 
cau.sing  no  pain,  and  producing  simply  some  redness  of  the  skin,  accompanied  by 
sweating  over  the  area  treated. 

Case  I. — Girl,  seventeen  years  old.  gonococcal  vaginitis  and  arthritis.  Enoi-mous 
effusion  in  left  knee.  Walking  impos.-ible.  Joint  exquisitely  tender  to  the  touch, 
semiflexed,  and  resting  with  its  outer  surface  on  the  bed.  Salicylate  of  soda  given  : 
no  benefit.  After  five  douches,  pain  quite  gone  :  effusion  much  less.  After  nine 
douches,  walking  possible  ;  all  pain,  swelling,  and  effusion  have  disappeared. 


2130  TEXT-BOOK  OF  MEDICINE 

Case  II.— G-irl,  aged  twenty  years,  admitted  on  June  7  for  gonococcal  arthritis  of 
the  left  ankle-joint.  Joint  swoUen  and  red  ;  unbearable  shooting  paiu  in  it.  Wright's 
vaccine  given  (5,000,000,  10,000,000,  and  finally  20,000,000  gonococci) ;  no  benefit. 
June  19,  first  douche  of  hot  air.  After  fifth  seance,  spontaneous  pain  disappeared, 
patient  slept  aU  night.  After  thirteenth  douche,  free  movement  of  joint.  Patient 
discharged  on  August  5  ;  she  was  cured,  and  had  regained  perfect  movement  in 
the  affected  joint. 

CAtiE  III.— C,  nineteen  years  of  age.  Gonococcal  arthritis  of  right  ankle,  with 
periarthritis.  Joint  red,  swollen,  and  very  tender.  Ifo  movement  possible.  Sali- 
cylate of  soda  and  Wright's  vaccine  given ;  no  benefit.  After  fifth  air  douche,  joint 
less  swoUen,  paia  gone  ;  patient  can  move  the  foot.  Complete  recovery  after  sixteen 
applications. 

Summary : 

1.  Diminution  and  disappearance  of  pain. 

2.  Eemarkable  resolution  of  the  inflammation,  with  absorption  of  effusion,  in  a 
much  shorter  time  than  with  other  methods  of  treatment. 

3.  Absence  of  ankylosis  after  the  disappearance  of  the  inflammation.  Ankylosis 
has  always  been  liable  to  occur  in  gonococcal  arthritis,  and  diificult  to  avoid,  ^ro- 
thermotherapy,  by  quieting  the  pain  rapidly,  allows  the  patient  to  move  the  joint,  and 
thus  to  avoid  the  results  of  articular  stiffness.  Furthermore,  in  chronic  or  subacute 
cases  with  ankylosis,  superheated  air  gradually  brings  about  a  more  or  less  marked 
return  of  mobility,  according  to  the  degree  of  the  lesion. 

In  superheated  air  we  have  a  valuable  therapeutic  agent ;  it  may  be  used  in  com- 
bination with  other  measures.  The  treatment  is  applicable  to  all  forms  of  arthritis, 
and  especially  to  those  which  are  of  rheumatic  origin. 


v.— VACOmES— OPJGINAL    IDEAS    OF    PASTEUE— WEIGHT'S 

OPSONIC    METHOD. 

•  The  idea,  which  led  Wright  to  prepare  his  vaccines,  is  really  an  outgrowth  of  the 
original  ideas  of  Pasteur.  "  To  confer  immunity  on  an  organism,  by  means  of  an 
attenuated  and  harmless  virus  was  Pasteur's  object,  after  his  early  work  upon  the 
bacteridium  of  anthrax  had  shown  him  that  certain  conditions  of  culture  lessened  the 
virulence  of  this  pathogenic  agent "     (Armand-Delille). 

At  one  time  herds  of  cattle  and  flocks  of  sheep  were  decimated  by  anthrax. 
Pasteur,  by  means  of  heat,  attenuated  the  virulence  of  the  Bacteridium  anthracis  ;  the 
cultures  were  kept  for  some  time  at  42°  C.  and  the  animals  were  vaccinated  with  the 
attenuated  bacteridium.  The  culture  was  so  modified  as  to  produce  merely  a  mild 
infection,  and  rendered  the  animal  immune  to  subsequent  infection  by  the  most 
virulent  germs. 

Pasteur,  in  Ms  celebrated  experiment  at  PouiUy-le-Fort,  demonstrated  successfully 
the  worth  of  his  method  of  vaccination.  The  results  of  this  discovery  have  been 
widespread.  Between  1882  and  1894, 1,788,677  sheep  were  vaccinated  in  France,  and 
the  mortality  was  not  even  1  per  cent.,  while  it  was  as  high  as  10  per  cent,  ia 
unvaccinated  sheep.    In  cattle  the  same  ratios  held  good. 

Pasteur,  following  up  his  idea  of  vaccination,  asked  himself  whether  it  could  be 
applied  to  rabies.  This  question  was  beset  with  difficulties  because,  the  organism  of 
rabies  being  unknown,  it  was  impossible  to  obtain  cultures  and  to  attenuate  their 
virulence. 

Pasteur  overcame  the  difficulty  by  employing  desiccation  in  order  to  attenuate  the 
virulence.  He  took  the  spinal  cords  of  rabbits  which  had  been  kiUed  by  "  fixed  virus." 
The  term   "fixed  virus"  means  that,  by   successive  passages,  the  duration  of  the 


Ari'ENDix  OX  '1'iiki;ai'Ki;ti(s  2i:;i 

incnbation  poriod  of  nil)i»'s  whs  bmujrhi  down  to  tin  iniiiiiiiuui  ;  tliis  niiiiiiiium  i« 
obUiiiu'd  utter  iibout  a  huudi'od  piussug'os  ;  it  in,  tlitrn,  iuvariiiblo  and  aniouiitH  to  six  or 
Heven  days. 

Paatour  dried  tlie  cords  in  order  to  attenuate  their  vinilenco.  After  thirteen  or 
fourteen  days,  the  cord  los(<s  its  virulcnec,  wliii'h  varios  in\<'rscly  as  the  time  of 
desiccation.  I'asteur  vuccinatod  fifty  do^'s  with  fravrnK'nls  of  cords  thus  pnspared,  at 
first  usiuji"  the  h'ast  virulent  and  finally  the  most  virulont  cords.  The  dopn  so 
vaccinated  were  refractory  to  rabies  ;  the  bites  of  rabid  do;,'s  and  inoculation  of  the 
most  viinilent  cords  had  no  efFect  on  them. 

Pasteur  then  applied  his  method  to  the  treatment  of  rabies  in  man  with  excellent 
results ;  the  mortality,  which  in  uuvaocinated  jiersons  was  15  per  cent.,  fell  in  those 
vaccinated  to  1  ])er  cent. 

We  cannot  think  of  the  term  "  attenuation  of  virus  "  without  recalling'  the  labours 
of  that  genius,  Pasteur,  who  has  revolutionized  medical  science. 

Wrip-ht  attenuates  his  vaccines  by  heat,  the  following-  temperatures  being 
employed : 

Gonococcus         ..  ..  ..  <nO°  C. 

Stapliylococcus  ..  ..         60^  C. 

Streptococcus     . .  . .  60°  C. 

Pueiunococcus     ..  fiC  C. 

Eberth's  bacillus  ..  ..  59°  C. 

Koch's         „  ..  ..         (J(P  C. 

Let  us  take,  for  example,  the  gonococcus.  The  emulsion  of  gonococci  is  enclosed 
in  sterilized  ampnllfe  containing  one  or  more  cubic  centimetres.  Each  cubic  centi- 
metre contains  five  million  or  ten  million  gonococci  of  attenuated  virulence. 

In  the  first  place,  it  w'ill  bo  useful  to  give  a  general  survey  of  vaccines  and  of  their 
mode  of  action.  We  use  both  immunizing  and  curative  vaccines;  indeed  many 
vaccines  fulfil  both  these  functions. 

Immunizing  vaccines  are  g-iven  in  order  to  prevent  a  possible  attack  of  infection, 
the  person  vaccinated  becoming  immune  to  the  infection.  The  best  example  is  small- 
pox vaccine,  which  protects  the  vaccinated  person  against  smaU-pox  for  many  years. 
The  vaccine,  if  given  during  the  incubation  period  of  small-pox,  may  be  cui-ative  in  its 
action. 

The  vaccine  of  rabies  is  both  immunizing  and  curative.  Vaccinated  dogs  are 
immune  to  the  bites  of  rabid  animals.  When  the  vaccine  is  given  to  person.s  bitten 
some  time  previously  by  rabid  animals,  the  disease  fails  to  develop  in  those  persons. 
Intravenous  injections  have  been  successful,  even  thoug'h  symptoms  of  rabies  have 
aLready  appeared  (cases  of  Nivi  and  of  Pippi). 

It  seems  probable  that  Wright's  vaccines  belong  to  the  class  of  curative  vaccines 
rather  than  to  l^e  class  of  immunizing  vaccines. 

By  what  mechanism  does  a  vaccine  f  oreai'm  the  economy  against  possible  attacks 
of  infection,  and  how  does  a  vaccine  assist  the  economy  in  getting  rid  of  an  enemy 
which  has  already  taken  possession  ?  In  order  to  answer  these  questions  we  must 
consider  the  history  of  jjhag'ocytosis,  so  clearly  put  by  Metchuikoft",  and  disc\ass  the 
bactericidal  power  of  sera;  in  other  Avords,  we  must  touch  upon  the  problem  of 
immunity.    In  order  to  render  the  subject  more  clear,  let  us  take  two  examples  : 

The  fii'st  example  is  based  upon  an  experiment,  known  as  PfeifEer's  phenomenon. 
All  our  knowledge  in  i-egard  to  the  bactericidal  power  of  sera  and  to  immunity  is 
based  on  this  experiment.  "VV^hen  a  culture  of  cholera  vibrios  is  injected  into  the 
peritoneal  cavity  of  a  non-immunized  g'mnea-pig,  the  microbes  at  once  multiply  freely 
and  produce  fatal  peritonitis.  If  some  of  the  peritoneal  fluid  is  taken,  a  quarter  or 
half-an-hour  after   the   injection,    the   preparation   shows  many    vibrios,   i)0ssessing 


2132  TEXT-BOOK  OF  MEDICINE 

extreme  mobility  and  in  every  way  comparable  with  the  vibrios  found  in  a  brotli-ctilture. 
Plate  VIII.,  A,  shows  these  features  :  many  vibrios  and  some  polynuclear  cells. 

If  a  guinea-pig,  rendered  immune  by  injections  of  attenuated  vibrios,  is  taken,  the 
result  is  quite  different.  The  same  procedure  is  employed  as  in  the  case  of  the  non- 
immune guinea-pig,  and  the  preparation  is  then  examined.  The  bacilli  have  not 
multiplied,  and  are  not  mobile ;  many  are  grouped  en  masse ;  they  have  lost  their 
elongated  comma-shape  and  look  like  baUs.  These  points  can  be  seen  in  Plate  VIII.,  B. 
Pfeiffer's  experiment,  above  described  in  vivo,  can  also  be  performed  in  vitro.  If 
serum  from  a  non-immune  guinea-pig  and  a  fresh  culture  of  vibrios  are  mixed,  in  equal 
proportions,  in  a  little  normal  saline,  the  bacilli  develop  just  as  in  a  broth  culture.  If, 
however,  the  serum  is  taken  from  an  immunized  guinea-pig,  the  bacilli  are  promptly 
attacked  by  the  bactericidal  serum,  lose  their  mobility  and  become  grouped  en  masse. 
Some  years  later  G  ruber  performed  Pfeiffer's  experiment  with  the  Bacillus  typhosus 
instead  of  the  cholera  vibrio. 

He  injected  a  culture  of  Eberth's  bacilli  into  the  peritoneum  of  a  non-immune 
guinea-pig.     On  examining  the  serous  fluid  from  the  peritoneum,  he  found  many 
extremely  mobile  bacille,  which  remained  separate  and  did  not  show  agglutination. 
This  phenomenon  is  shovsoi  in  Plate  IX.,  A. 

When,  however,  he  took  an  immune  guinea-pig,  and  employed  the  same  technique 
as  in  the  case  of  the  non-immune  guinea-pig,  he  found  that  the  bacilli  did  not  multiply, 
and  became  agglutinated  en  masse.  Many  were  ingested  by  the  leucocytes.  These 
details  are  shown  in  Plate  IX.,  B. 

This  experiment,  like  that  of  Pfeiffer's,  can  also  be  performed  in  vitro.  Widal  has 
utilized  the  experiment  and,  as  is  well  known,  has  applied  it  most  successfully  in  the 
sero-diagnosis  of  typhoid  fever. 

In  short,  the  serum  which  destroys  the  microbe  and  the  phagocyte  which  devours 
it,  are  the  two  important  factors  that  safeguard  the  economy  and  free  it  from  the 
enemy  within  the  gate.  Aiithorities,  however,  do  not  agree  regarding  the  relative 
importance  of  these  two  factors  and  the  mechanism  of  their  mutual  action.  The 
cellular  theory  attributes  the  larger  share  to  the  phagocyte,  the  humoral  theory  assigns 
the  major  part  to  the  bactericidal  action  of  the  serum. 

The  defenders  of  the  humoral  theory  admit  that  the  phagocytes  can  ingest  and 
digest  the  microbes,  but  this  property  of  the  phagocytes,  they  say,  is  dependent  on  the 
special  action  of  certain  substances  contained  in  the  serum.  The  defenders  of  the 
cellular  theory  admit  the  bactericidal  properties  of  the  serum,  but  they  hold  that 
phagocytosis  is  spontaneous,  and  that  the  phagocytes  can  deal  with  the  microbes  with- 
out any  assistance  from  the  serum. 

At  the  present  time,  it  has  been  shown  that  phagocytosis  is  much  favoured  by  the 
existence  in  the  serum  of  substances  which  act  as  assistants.  Some  authorities, 
Wright  in  particular,  have  found  that  spontaneous  phagocytosis  is  much  less  energetic 
than  phagocytosis  associated  with  the  action  of  serum. 

The  substances  in  the  serimi  may  act  either  by  increasing  the  phagocytic  power  of 
the  leucocytes  or  by  preparing  the  microbes  for  digestion  by  attenuating  their  virulence 
and !  their  vitality.  In  any  case,  the  bactericidal  power  of  the  serum  is  of  the  greater 
importance. 

To  these  substances  Wright  has  given  the  name  of  opsonins.  Wright  and  Douglas, 
in  1903,  conceived  the  idea  of  employing,  in  the  therapetitics  of  infectious  disease,  the 
phenomenon  of  phagocytosis,  which  had  been  previously  confined  to  the  study  of 
immunity.  The  word  "  opsonin  "  is  derived  from  the  Greek  {6\i/ovec>),  "  I  prepare  ").  The 
opsonins  are  soluble  substances  found  in  normal  and  iu  immune  sera.  They  have  never 
been  isolated  from  the  serum,  and  their  existence  is  proved  by  their  property  of  inter- 
vening in  the  phenomenon  of  phagocytosis,  so  as  to  render  it  more  active ;  they  serve 
as  intermediaries  between  the  phagocytes  and  the  microbes. 


Plate  Mil. 


PFEIFi'ER's   EXVKIIIMEXT    WITH   TllK    CllOLEKA    VlBUIO. 


To  face  p.  2132 


ntutc  /A, 


GRUliEll's   Exi'EKIMEXT    WITH    EjiERTll's   BaCILLUS. 


To  face  p.  2132 


Ari'KNhlX    MX   TIII:i;aI'KUTI('S  2133 

Several  Ihcorics  liavc  Imtii  pn)|K»t'il  to  (•x)>laiii  <lii-ir  art  ion  ;  on<?  tlioory  stafi's  : 
lli«>  opsonins  cook  tlio  niicro))es  and  tlins  rfnilcr  tln-m  nion-  nMidily  inj^'t^stt-d  and 
diirt'sted  hy  tlio  pha^'ocytt's ;  tin*  ollu-r  llicory  says  :  tlii<  opsonins  art  chiofly  upon  llio 
pliav'ocylos,  ini'it-asin^-  tlioir  fnor^ry  and  n-ndcrin-.--  (lu-in  more  ablo  (o  fifrlit  tli<'  trirrniH. 

In  any  case.  pliai.'ocytosis  may  ^--o  on  without  tlio  assistance  of  tin-  opsonins,  hut  it 
(Uics  not  ac(iuin>  its  lull  power  unless  they  are  presont.  It  is  necessary  to  know  the 
tipsouie  i)ower  of  the  serum,  tliat  is,  to  mea.sure  tho  influence  of  tlio  opKoninH  of  any 
jriven  serum  duriup  tlio  process  of  phupocytosis.  P^or  this  purpose  tliree  factorn  are 
required  :  1.  leucocytes  ;  2,  an  emulsion  of  micro-org-anisms ;  3,  serum.  Let  us  suppose 
tliat  the  reader  desires  to  tiud  the  opsonic  power  of  his  own  seinuu. 

The  serum,  the  emulsion  of  orpauisms  and  the  leucocytes  (details  an  to  their  pre- 
paration are  priven  in  Greene's  '"Medical  Diag-nosis'  and  many  other  works),  being- 
mixed  in  etjual  j)roportions,  the  mixture  is  spread  out  in  a  slide  and  stained.  One 
liundred  leucocytes,  and  also  the  number  of  organisms  contained  in  the.se  leucocytes 
are  counted  ;  if  the  number  of  organisms  is  3(Mi.  it  means  that  the  senim  has  an 
opsonic  power  such  that  lOU  leucocytes  can  injest  8oO  microbes.  This  opsonic  power 
is  represented  by  the  tigiu-e  1,  wliich  is  the  standard. 

To  compare  the  opsonic  power  of  this  serum  witli  that  of  a  sick  person,  the  reader 
will  take  his  own  leucocytes,  emiilsion  of  microbes,  and  the  patient's  serum.  The 
count  is  made  as  before,  and  perhaps  150  organisms  are  found  in  the  leucocyte.s.  In 
this  case  the  patient's  serum  would  have  half  the  opsonic  power  of  the  reader's  serum, 
so  that  the  figures  would  read  :  1  and  050.  The  relation  between  these  figui-es  is 
called  the  opsonic  index.  ^ 

If  400  organisms  were  found  in  100  leucocytes  the  fignres  would  be  1  and  \"2o,  and 
the  patient's  serum  would  be  one-quarter  higher  in  opsonic  power  than  the  reader's 
seriun.     The  relation  between  1  and  1'26  would  then  be  the  opsonic  index. 

By  taking  a  series  of  observation,s,  an  opsonic  curve  is  obtained,  showing  the 
variations  in  the  opsonic  index  j\ist  as  a  temperature  cui-ve  shows  the  variations  in 
temperature. 

The  therapeutic  results  of  gonococcic  vaccine  in  arthritis,  vaginitis,  and  ui-ethritis 
have  been  discussed  under  Gonorrhoea,  where  the  reader  will  find  full  details. 

At  the  present  time,  we  have  no  exact  dosage  in  the  ajiplication  of  Wright's 
vaccine  ;  we  are  not  certain  whether  we  should  begin  with  five,  twenty,  or  a  hundred 
millions  of  gonococci,  and  whether  it  is  best  to  give  increasing  doses. 

Wright  governs  the  treatment  by  the  information  given  by  the  opsonic  index. 
This  method  is  flifficult  in  practice  and  demands  the  expenditure  of  much  time  for  each 
patient.  Other  authorities  claim  that  the  clinical  featiu-es  of  the  case  furnish  suffi- 
ciently exact  information. 

It  is  prematm-e  to  pronounce  sentence  on  the  value  of  Wright's  vaccines.  The 
cases  at  present  j)uhlished  are  not  sufficiently  numerous  or  suggestive. 

Staphylococcic  vaccine  in  boils  and  in  pustular  acne  of  the  face  has  given  undoubted 
results. 

In  any  case  Wright  has  opened  a  qaestion  of  the  most  acute  intercstw 


n.  135 


INDEX 


Abasia,  1618 

Abdominal  typhus,  Ititio 

Abortion  in  relapsing  fever,  1736;  in  small- 
pox, 1613 

Abscess  :  from  angiochoUtis,  1024  ;  appen- 
dicular, 9S4  ;  of  brain,  1376  ;  of  cerebel- 
lum, 1339 ;  fixation,  139 ;  in  glanders, 
844 ;  of  liver,  977 ;  of  lung,  122 ;  of 
ptincreas,  1061  ;  inparacholecystitis,  1025  ; 
of  parotid.  1699;  perigastric,  781;  peri- 
nephritic,  1214 ;  peritoneal,  868  ;  pulsa- 
ting, 334 ;  retropharyngeal,  584 ;  sub- 
phrenic, 704  ;  in  typhoid  fever,  1689 

Acephalocystic  cyst,  962 

Acetonaemia,  1968 

Acetone,  1968 

Acholia,  917 

Achondroplasia,  1600 

Acromegaly,  2022 

Actinomycosis,  1845  ;   of  appendix,  827 

Acute  biilb  paralysis,  1325  ;  yellow  atrophy, 
1038 

Addison's  disease,  1233 

Adenia  (Trousseau's),  1885 

Adenitis,  in  scarlet  fever,  1629  ;  tubercular, 
2011 

Adenoid  growths,  586 

Adenoma  of  kidney,  1103  ;  of  liver,  905,  950 ; 
of  stomach,  666,  723 

Adenopathy  :  mediastinal,  388  ;  scrofulous, 
2010 ;  supraclavicular,  730 ;  iu  tracheo- 
laryngeal  syphilis,  35 

Adenophlegmon  of  neck.  1638 

Adherent  pericardium,  407 

Adiposis  dolorosa,  2003 

Adrenalin  in  epistaxis,  21  ;  in  purpura,  1911 

Adrenals  in  Addison's  disease,  1238 

Adynamic  typhoid  fever,  1670 

iEgophony,  251 

.^tivo-autiimnal  fever,  1812 

Aero-thermo  generator,  2125 

Agglutination  of  Eberth's  bacillus,  1708 ; 
of  Koch's  bacUlus,  274;  of  the  pneumo- 
coccus,  124 

Agoraphobia,  1516 

Agraphia,  1370 

Air,  superheated,  treatment  with,  2125 

Albuminous  expectoration  in  pleurisy,  265 

Albuminuria :  of  adolescence,  1151  ;  in 
appendicitis,    776 ;     m    BiigLt's    disease. 


1117  ;  not  due  to  Bripht's  disease,  1160; 
in  aoute  Bright's  disease,  1088  ;  in  chronii; 
Bright's  disease,  1101,  1117;  cyclical, 
1151 ;  in  diabetes,  1969 ;  in  diphtheria, 
598  ;  in  erysipelas,  1750  ;  in  gout,  1941  ; 
in  influenza,  1774 ;  in  malaria,  1816 ; 
orthostatic,  1151  ;  in  scarlet  fever,  1633  ; 
in  typhoid  fever,  1844;  in  syphilitic 
nephritis,  1170 

Albuminuric  retinitis,  2095 

Alcoholic  neuritis,  1473 

Alcoholism,  acute,  2086  ;  chronic,  2087 

Algid  stage  in  cholera,  1769;  in  malaria, 
1812 

Alienation,  mental,  in  epilepsy,  1479 

Alopecia  in  typhoid,  1669 

Amaurosis,  hysterical,  1503  ;  toxic  in  lead- 
poisoning,  2095  ;  ursemic,  1127 

Amblyopia,  alcoholic,  2088 ;  hysterical, 
1503 ;   tobacco,  2110 

Ambulatory  typhoid,  1670 

Ammonisemia,  1124 

Amnesia  in  general  paralysis,  1406 

Ajnoeba  in  dysentery,  845 

Amphoric  breathing,  182,  385 

Ampulla,  cancer  of  Vater's,  843 

Amyloid,  disease  of  kidney,  1152  ;  of  liver, 
975 

Amyotrophic  lateral  sclerosis,  1285 

Anaemia,  1881  ;  in  ankylostomiasis,  1885  ; 
bothriocephalic,  853 ;  cerebral,  1349 :  in 
chlorosis,  1897  ;  from  haemorrhage,  1881 ; 
infantile  pseudo-leuksemic,  1890  ;  in  lead- 
poisoning,  2094  ;  in  malaria,  1815  ;  perni- 
cious, 1882  ;  primary  or  essential,  1882  ; 
in  rheumatism,  1924  ;   secondary,  1882 

Ansemic  murmurs,  1896 

Anaesthesia  in  haematomyelia,  1315 ;  in 
hemiplegia,  1357  ;  in  hysteria,  1496 ;  in 
leprosy,  1828 ;  locomotor,  1261  ;  in 
Morvan's  disease,  1275 ;  in  syringo- 
myelia, 1273 

Anarthria,  1375 

Anasarca  in  cardiac  disease,  429  ;  in  acute 
nephritis,  1088  ;  in  scarlatina,  1637 

Aneurysm  of  abdominal  aorta,  536 ;  of 
thoracic  aorta,  509 ;  of  aorta  due  to 
syphUis,  526;  arterio-venous,  511;  of 
brain,  1354 ;  syphilitic  brain,  1390 ;  of 
heart,  454  ;  of  limbs,  5U4  ;  of  Rasmussen, 
185 


2135 


135—2 


2136 


TEXT-BOOK   OF  MEDICINE 


Angina  :  acute  catarrhal,  577  ;  chronic,  585  ; 
diphtheritic,  692  ;  normal,  593  ;  toxic,  596  ; 
symptoms,  596  ;  aetiology,  544  ;  bacterio- 
logical diagnosis,  610  ;  clinical  diagnosis, 
606  ;  course,  546  ;  diagnosis,  547  ;  due  to 
micrococcus  tetragenus,  624 ;  erythe- 
matous, 577  ;  gangrenous,  631 ;  herpetic, 
602,  630  ;  pectoris,  543  ;  prognosis,  612  ; 
pseudo  diphtheritic,  620 ;  syphilitic, 
624 ;  tabetic,  537 ;  treatment,  615 ; 
tubercular,  643  ;  varieties,  601 ;  Vincent's, 
583 
Angiocholitis,  1005,  1023  ;  in  typhoid  fever, 

1688 
Anhepatia,  1975 

Ankylostoma  duodenale,  856,  1885 
Ano-rectal  tuberculosis,  830 
Anomahes  of  heart,  447 
Anopheles,  1800 
Anopsia,  cortical,  1506 
Anorexia  nervosa,  1501 
Anterior  cerebral  artery,  1353 
Anthracosis,  142 
Anthrax,   1837  ;    pulmonary  and  intestinal 

forms,  1841 
Anti-ethylin,  2090 

Antitoxin,  diphtheria,  616  ;  tetanus,  1795 
Antityphoid  serum,  1726 
Anuria,  calculous,  1201  ;   scarlatinal,  1636 
Anus,  abscess  and  fistula,  831  ;    gonorrhoea, 

2059 ;  tuberculous,  830 
Aorta,  aneurysm  of,  509,  526  ;  incompetence 
in  syphilis,  525  ;  pulsation  of  abdominal, 
536 
Aortic  incompetence  and  stenosis,  441 
Aortis  chloroticse,  1896 
Aortitis,   506 ;     with  aneurysm  in   syphilis, 

526  ;  syphilitic,  520  ;  in  tabes,  537 
Aphasia,   1361,    1369 ;   in   cerebral   tumour, 
1388  ;    diabetic,  308,  1976  ;  new  doctrine 
of,  1374  ;  syphilitic,  1394  ;  transitory,  1376 
Aphonia  :   hysterical,  1498  ;   in  acute  laryn- 
gitis, 27  ;    in  syphihtic  larjmgitis,  32  ;    in 
tubercular  laryngitis,  43 
Aphthae,  561 
Aphthous  fever,  561 
Apical  pneumonia,  131 

Apoplexy,  1349,  1355,  1467;  hysterical, 
1499  ;  in  mitral  disease,  428  ;  pulmonary 
154  ;  serous,  1469  ;  in  syphilis,  1393 
Appendicitis  :  aetiology,  766  ;  anatomy,  756  ; 
calm  treacherous  in,  778  ;  cavitj^  closed, 
761 ;  cholecystitis,  1025 ;  chronic  form, 
790 ;  course,  769  ;  diagnosis,  783  ;  em- 
pyema (subphrenic),  365  ;  kidney  in,  1090  ; 
liver  in,  981  ;  pathogenesis,  758 ;  peri- 
tonitis, 771  ;  phlebitis,  493  ;  pleurisy,  358  ; 
pregnancy,  781  ;  pseudo-,  806 ;  sj^mp- 
toms,  767  ;  toxic  forms,  775  ;  treatment, 
791 ;  vomito  negro  (ulcerative  gastritis), 
679 
Appendicular  subphrenic  empyema,  365 ; 
sabphrenic  pyo-pneumothorax,  366  ;  pleu- 
risy, 358 


Appendix,  anatomy  of,  756 
Aran-Duchenne  type  of  atrophy,  1277 ;    in 

lead-poisoning,  2096 
Arch  of  aorta,  aneurysm  of,  510 
Areolar  pleurisy,  354 

Argyll-Robertson  pupil :  in  ataxia,  1246  ;  in 
general  paralysis,  1407  ;  in  syringo-myelia, 
1274 
Arm  dead,  1112 
Arrhythmia,  431 
Arsenic,  poisoning  by,  2104  ;  treatment  with, 

2122 
Arseno-benzol,  2119 
Arterial  tension,  548 

Arteries,  119;    anatomy  of,  496;    cerebral, 
1351 ;    diseases  of,  496  ;    tuberculosis  of, 
500 
Arterio-sclerosis,  496 

Arteritis,  496  ;  of  cerebral  arteries,  1390  ; 
infective,  500 ;  syphilitic,  504 ;  toxic, 
502  ;  traumatic,  499  ;  in  typhoid  fever, 
1694 
Arthritis,  gonococcal,  2054,  2125  ;  pneumo- 
coccal, 130  ;  scarlatinal,  1638  ;  sicca,  1929 
Arthropathies,  in  hemiplegia,  1358  ;  in  tabes, 

1252 
Arthropathy,    in    dysentery,    850 ;     hyper- 
trophic pulmonary,  2026 
Ascaris  lumbricoides,  852 
Ascites,  890  ;    in  cancer  of  the  peritoneum, 
887  ;  in  Laennec's  cirrhosis,  911  ;  chylous, 
891 ;    curability  of,   922 ;    physical  signs 
of,    912 ;     saccharine,    1976 ;     tubercular, 
865 ;     varieties    of,   in    Bright's    disease, 
1122 
Ascitic   fluid,   chylous,    891 ;     haemorrhagic, 

887 
Aspergillosis,  207 
Asphyxia,  local,   1604 ;    acute  tuberculous, 

206 
Aspiration,  268  ;    in  hydatid  cyst  of  liver, 
971  ;    in  hydrocephalus,    1470 ;    in   peri- 
carditis, 406 
Association    of    Bacillus   coli   and   fmeumo- 
coccus,  878 ;    of  microbes  in  diphtheria, 
55 
Astasia,  1518 

Asthenia  (Addison's),  1233 
Asthenic  bulbar  paralysis,  1326 
Asthma,   109;    cardiac,   113,  428;    kidney, 
1110;    nasal  lesions  in,    114;    saturnine, 
2101  ;     sputum   in,    110 ;     summer    (hay 
fever),  115 
Asymmetry,  facial,  1480 
Asynergy,  cerebellar,  1289 
Asystole,  422,  462 
Ataxic  typhoid  fever,  1670 
Ataxy,  hereditary,  1266  ;    locomotor,  1243  ; 
ataxic  paraplegia,  1270  ;   ataxo-spasmodic 
paraplegia,  1271 
Atelectasis,  82 
Atheroma,  496,  1364 
Athetosis,  1359,  1528  ;  double,  1381 
Athrepsia,  753 


INDF.X 


2137 


Atrophy,  ncuto  yellow,  of   liver,   1038  ;    of 
Iner.  915  ' 
miisouiiir.  ill  livHU'ria,  1501  ;   in  infantilf 
spiiiiil   paralysis,    1295;    in  poly-neu- 
ritis, 1474;    in  rlioumatism,  1282;   in 
insular  sclerosis,  1290;    in  hereditary 
syphilis  of  medulla,  1311 
optle.  I24l»,  138G;  in  diabetes.  1961 
prt)gres8ive    muscular,    1276 ;     tyiH-     of 
Charcot-Maric.      1282  ;       progressi%-e 
nuisfular  dystrophies,  2027  ;    pseu(k>- 
hypeitri)phic    paralysis,    2039 ;     pro- 
gressive atrophic  myopathy,  2042 
imilateral,  of  face,  1601 
Attitude    in    pseudohypertrophic    muscular 
parah'sis,  2041  ;  in  paralysis  agitans,  1522 
Attitudes,  sense  of,  1249 
Aura  epileptica,  1477  ;  hysterica,  1493 
Auto-intoxication.  919 
Autolysate,  vaccine,  1730 
Avian  tuberculosis.  175 
Azoospermia,  2049 
Azoturia,  1970,  1982 
Azygos  veins,  390 

B 

Bacelli's  sign,  252 

Baciliary  dysentery,  845 

Bacillus  :  acid-resisting,  171  ;  anthrax,  1837  ; 
of  cholera,  1763  ;  chromogenic,  754  ;  colt 
communis,  765 ;  diphtheria,  588 ;  of 
dysentery,  848  ;  of  glanders,  1843  ;  icte- 
roitles  (yellow  fever),  1777  ;  of  leprosy, 
1829  ;  of  Nocard  (psittacosis),  1854 ;  of 
Pfeiffer  (influenza),  1776  ;  of  plague,  1785  ; 
pseudo-diphtheritic,  589 ;  pvccvaneus, 
1153;  of  soft  chancre  (Ducrey),"  2065 ; 
septicus,  2082  ;  of  tetanus,  1788  ;  tubercle, 
170  ;   of  typhoid,  1712 

Bact^ridia  (anthrax),  1837 

Balanitis,  1955 

Balanoposthitis,  2047 

Banti's  disease  (primary  splenomegaly),  1875 

Barlow's  disease,  1914 

Bartholinitis,  2049 

Basedow's  disease,  470 

Baths  in  measles,  1657  ;  in  scarlatina,  1644  ; 
in  typhoid  fever,  1722 

Beaded  ribs  (rosary)  in  rickets,  2020 

Beard's  disease  (neurasthenia),  1515 

Bedsores,  gluteal,  1358;  in  mvelitis,  1304; 
in  typhoid  fever,  1652 

Bellini  3  tubes,  1077 

Bell's  palsy,  1564 

Biermer's  disease,  18S2 

Bile,  composition  of,  898  ;  tests  for,  1033. 
1035 

Bile-ducts,  acute  catarrh  of,  1033  ;  cancer  of 
948  ;  obliteration  of,  1003,  1013 

Bilhaizia,  2017 

Biliary  cirrhosis  of  liver,  933,  1005  ;  endo- 
carditis, 1010;  fistulse,  1012;  (hepatic) 
colic,  995 

Bilious  remittent  fever,  1808 


Hiniixlide  of  mercury,  117 

Hirth  palsies  (spasmodic  diplegia),  1381 

Black  vomit  (vomito  iu'){ro),  tl79.  1779 

Black-watir  fever,  JSIO 

Bladder,  troubles  in  locomotor,  1254  ;  tuber- 
culosis of,  1 101 

Blepharospasm,  l.'SOS 

Blood,  characters  of  : 

in  anxiiiia,  1881  ;  in  cbloroHin,  1897  ; 
in  cholera,  1769;  in  tV)Ut,  1946;  in 
leuku'iiiia,  1.S86;  in  pernicious ana?mia, 
1884;  in  purpura,  1912;  in  rheu- 
matism. 1924  ;  in  secondary  ana»mia. 
1882;  in  typhoid  fever,  "l71(»;  in 
yellow  fever.  17S0 
clinical  examination,  1877  ;  red  cor- 
puscles, 1878  ;  varieties  of  leucocytes, 
1879 

Blood-letting  in  acute  nephritis,  1089  ;  in 
cerebral  haemorrhage,  1363  ;  in  heart  di- 
sease, 435;  in  oedema  of  lung,  167;  in 
pneumonia,  138;    in  urajmia,  1141 

Blood-pressure,  548 

Blood  tumours,  1913 

Bloodvessels,  diseases  of,  488 

Blue  line  in  lead-poisoning.  2094 

Bone,  lesions  of,  in  acromegaly,  2025 ;  in 
osteomalacia,  2021  ;  in  Paget's  disease, 
2030;  in  rickets,  2019;  in  tabes,  1252; 
in  typhoid  fever,  1 70 1 

Bonnier's  s}Tidrome,  1338 

Borborygmi,  1502 

Bothriocephalus  latus,  853 

Boulimia,  670,  1989 

Bovine  tuberculosis,  175 

Brachial  plexus,  anatomy  of,  1592 

Bradycardia,  466 

Brain,  diseases  of,  1348 ;  abscess,  1376 ; 
affections  of  bloodvessels.  1364;  anaemia, 
1349;  congestion,  1348  ;  haemorrhage  into, 
1349  ;  inflammation.  1376  ;  porencephalus, 
1379;  sclerosis,  1405;  softening,  1366; 
syphilis,  1389  ;  tubercle,  1437  ;  tumours. 
1384 

Brand's  method  in  typhoid  fever,  1722 

Bright's  disease,  1098  ;  interstitial  nephriti?, 
1102;  mixed  nephritis,  1105;  parenchy- 
matous nephritis,  1099 

Brightism,  1111;  aetiology,  1108;  albumi- 
nuria, 1118;  ascites.  1122  ;  cardiac  troubles, 
1120;  cerebral  haemorrhage,  1122;  cu- 
taneous troubles,  1123  ;  digestive  troubles, 
1120;  epistaxis,  1121  ;  haematuria.  1119  ; 
headache,  1119;  oedema.  1115;  respira- 
tory troubles,  1119;  uraemia,  1124; 
visual  troubles.  1121 

Brocas  convolution,  1373 

Bronchi,  casts  of,  102 ;  disease  of,  70 ; 
syphilis  of,  102 

Bronchial  asthma,  109 

Bronchial  glands,  tuberculosis  of,  388 

Bronchiectasis,  cerebral  abscess  in,  99 ; 
ampullary,  94  ;  endocarditis  in,  99  ;  spu- 
tum in,  97  ;   uniform,  94 


2138 


TEXT-BOOK   OF  MEDICINE 


Bronchitis,    acute,    76 ;     albumimiric,    162 
capillary,  79  ;   chronic,  91  ;   foetid,  92,  99 
membranous,     101  ;     in    measles,    1650 , 
pseudo-membranous,    100 ;    in   smallpox. 
1613  ;  in  typhoid   fever,  1691 

Bronchohths,  216 

Bronchophony, 126 

Broncho -pneumonia,  79 ;  setiology,  90 ; 
bacteriology,  85  ;  diagnosis,  89  ;  patho- 
logical anatomy,  81  ;  symptoms,  86 

Bronchorrhagia,  154 

Bronchorrhoea,  97 

Bronchostenosis,  103 

Bronzed  skin,  in  Addison's  disease,  1233  ;  in 
Basedow's  disease,  475 ;  in  cirrhosis  of 
liver,  931 ;  in  diabetes,  932  ;  in  vagabond's 
itch,  1238 

Bruits  :  d'airain,  385  ;  de  cuir  neuf ,  225  ;  de 
diable,  1897  ;  de  drapeau,  67  ;  frou-frou, 
403  ;   pericardial  bruit  de  galop,  403 

Buboes  in  plague,  1783  ;  in  simple  chancre, 
2066  ;   in  syphilitic  chancre,  2069 

Bulb  (anatomy  of),  1321 

Bulbar  paralysis,  acute,  1322;  of  cerebral 
origin,  1325  ;  pseudo-,  1325 


Cachexia  :  bothriocephalic,  853  ;  in  cancer 
of  stomach,  727 ;  exophthalmic,  475 ; 
hydatid,  965  ;  malarial,  1815  ;  mercurial, 
2093  ;  pachydermic,  2004 ;  pigmentary, 
930  ;   strumipriva,  2005 ;   virginum,  1894 

Cacodylate  of  soda,  2122 

Csecmn,  cancer  of,  828  ;  hypertrophic  tuber- 
culoma of,  816 

Caisson  disease  (hsematomyeha),  1314 

Calcareous  concretions  in  phthisis,  196  ;  de- 
generation of  arteries,  502 ;  granulosis. 
216 

Calcification  of  skin,  1598 

Calculi,  appendicular,  759 ;  bUiary,  990 ; 
pancreatic,  1061;   renal,  1192 

Calciilous  anuria,  1201 ;  appendicitis,  759 ; 
peritonitis,  1011 ;  pyelitis,  1205 ;  perine- 
phritis, 1207 

Calambres,  2092 

Canals,  biliary,  anatomy  of,  897 

Cancer  of  ampulla  of  Vater,  843 ;  of  bile- 
ducts,  948 ;  of  caecum,  828 ;  of  gall- 
bladder, 954  ;  of  heart,  458  ;  of  intestine, 
837;  of  kidney,  1186;  of  larynx,  38;  of 
liver,  948 ;  of  lung,  213  ;  of  oesophagus, 
656 ;  of  pancreas,  1059 ;  of  head  of 
pancreas,  1015  ;  of  peritoneum,  886 ;  of 
pleura,  289  ;  of  stomach,  724  ;  of  thoracic 
duct,  398  ;  transformation  of  simple  ulcer 
of  stomach  into  cancer,  717 

Capillary  pulse  in  aortic  insufficiency,  441 

Capsule,  Bowman's,  1078 ;  external,  1350 ; 
internal,  1350  ;  of  kidney,  1206 

Capsules,  suprarenal,  diseases  of,  1233 ; 
physiology  of,  1239 

Carbon,  bisulphide  of,  2111 ;    oxide  of,  2110 


Carbuncles,  in  diabetes,  1959  ;  in  plague,  1784 
Carcinosis  of  lung,  214 
Cardiac  Liver,  901 ; 
Cardiac  murmurs  : 

aortic  disease,  442  ;   in  chlorosis,  1896  ; 
in  congenital  heart  disease,  448 ;    in 
idiopathic  ansemia,   1884 ;    in  mitral 
disease,  431 ;    organic,  424 ;    in  pul- 
monary valve  disease,  446 ;    in  tri- 
cuspid valve  disease,  443 
nerves,  neuralgia  of,  541 
septa,  abnormalities  of,  447 
Cardio-fibrosis,  forms  of,  452 
Caries  of  spine  (Pott's),  1317 
Camification  of  lung,  141 
Carphologia,  1667 
Caseation  in  tubercle,  177 
Caseous  pneumonia,  198 
Casts,  in  fibrinous  bronchitis.    101  ;    renal, 

1084  ;  varieties  of,  1118 
Catalepsy,  1509 
Cataplasm,  Trousseau's,  1936 
Cataract,  1961 
Catarrh  :    acute  gastric,  662  ;    of  bile-ducts 

1048  ;    buccal,  552  ;  chronic  gastric,  665 ; 

dry,    92 ;     Kthogenous,    992 ;     nasal,     1 ; 

suffocative,  80 
Catheterism  of  oesophagus,  660 
Cavities  in  limg,  99,  178 
Cauda  equina,  diseases  of,  1311 
CeU,  giant,  172 

CeUuhtis  in  scarlet  fever,  1639 
Cephahc  tetanus,  1791 
Cerebellar  ataxy,  hereditary,  1268 
Cerebellum,  diseases  of,  1339 
Cerebral    haemorrhage,    1349 ;     localization, 

1427 ;      sinuses,     thrombosis     of,     1898 ; 

softening,    1364;     syphilis,    1389;    liere- 

ditary,   1404;    tumours,   1384;    uraemia, 

1127 ;  rheumatism,  1921 
Cerebro-cardiac  neuropathy,  1520 
Cerebro-spinal  meningitis,  1444 
Cervical  pachymeningitis,  1320 
Cervico-brachial  neuralgia,  1547 
Cervico-occipital  neuralgia,  1547 
Chalicosis,  143 
Chancre,    simple,    2064 ;     of    tonsil,    632 ; 

syphilitic,  2067  ;   description,  2068  ;   diag- 
nosis of,  2069  ;  of  tongue,  564 
Charbon,  1840 

Charcot-Leyden  crystals,  110 
Charcot's  joint,  1252 
Cheyne-Stokes  breathing,  114 ;    in  uraemia, 

1129 
Chiasma,  optic,  compression  of,  2025 
Chicken-pox  (varicella),  1621 
Children,  broncho-pneumonia,  132  ;  diabetes 

in,   1970;    diarrhoea  in,   752;    mortaUty 

from    smallpox,    1613 ;     rheumatism    in, 

1920  ;  typhoid  fever  in,  1671 
Chlorides,  retention  of,  1116 ;   treatment  by 

dechlorination,  1141 
Chloro-Brightism,  1900  ;  pathogenesis,  1906 ; 

pregnancy,  1903 


INDEX 


218'J 


Chlorosis:   amenorihoBa  in,  ISOH  ;   dyspopsia 
in,    18Ut; ;     f.^bris   allni.    ISltT  ;     hfnjt   in, 
ISJTi  ;     iminnurs  in,    IS!M>  ;     iiariDwing  of 
aorta  in,  IS!);");  phlrt^ma.sia  in,  ISys 
Cholasmin,  UrMi 
rholocyskMt.iiny,  lt»l(l 
CholocvHtitis,    H>24  ;    in  ai)j)cndicitiH,   102.') ; 

oalouloua,  1(H)7  ;   in  typhoid  fever,  1688 
Oliolocystotoray.  1010 

Cholera,  17t)l  ;  jctiology,  17(il  ;  bnotoriolnjjy, 
17<)3 ;     de-soription,    1768;     infantile, 
752  ;     pathological    anatomy,    1767  ; 
vwrietios.  1770 
roth,  1763.  1767 
sicca,  1770 
t-oxinc,  17(54 
Cholerine,  1770 
(^holcsterino  in  gall-stones,  991 
Chorda  tynipaui  (in  facial  paralysis),  1566 
Ohorditia  tuberosa,  30 

Chorea,  1523  ;   setiology,  1526  ;  in  the  aged 
1526 ;     chronic,    1520 ;     description 
1523;     diagnosis,    152S ;     electrical 
1528  ;   gravidarum,  1528  ;   post-para 
lytic,      1360;      preparalytic,      1360 
Sydenham's,  1523 
gravis,  1530  ;  death  from  complications, 
1530 ;     fatal   per   se,    1531  ;     mental 
troubles  and  prognosis,  1534 
Chorio-retinitis,  syphilitic,  1399 
Choroid,  tubercles  in,  1440 
Chromo-diagnosis,  1362 
Chylothorax,  379 
Chyluria,  1120  ;  in  filariasis,  2016 
Cicatricial  constriction  of  bowel,  839 
Ciliary  muscle,  paralysis  of,  1580 
Circulation,  collateral,  in  cirrhosis,  913  ;    in 
mediastinal  syndrome,  348  ;  in  mediastinal 
tumours,  390 
Circumflex  nerve,  affections  of,  1592 
Cirrhosis  of  liver,  904 ;    curability  of  ascites 
in,  925 
atrophic,   aetiology,  918  ;    ascites,  911  ; 
atrophy  of  liver,  915  ;  collateral  circu- 
lation, 913  ;    coiirse,  916  ;    diagnosis, 
917 ;      pathological    anatomy,     907  ; 
symptoms,  911  ;   treatment,  920 
hypertrophic  alcoholic,  922 ;    regenera- 
tion of  Liver,  922 
hypertrophic    biliary,    933 ;     diagnosis, 
939 ;     duration,    939 ;     pathological 
anatomy,  933  ;   symptoms,  937 
hypertrophic  pigmentary,  930 ; 
mixed  forms  of,  941  ;    diabetic,   1973 ; 
fatty    hypertrophic,    947 ;     malarial, 
930 ;  tubercular,  947 
Claudication,  454 
Claustrophobia,  1516 
Clavus  hystericus,  1497 
Claw-hand  [main  en  griffe),  1278 
Climate,  in3uence,  in  asthma,  112  ;  in  tuber- 
culosis, 195 
Club-foot,  1253 
Cocainism,  108 


CoccuB,  Brisou's,  621 

Connr  en  hisHiin.  455 

CiA'w,  bronchial,  217;  licpntic,  h'j3  ;  load, 
2094;    pancreatic;,  1000;   renal,  1193 

Colitis,  798 

Colon,  cancer  of,  837 

Coma  :  in  abscess  of  brain,  137H  ;  in  acute 
yellow  atrophy.  1042  ;  alcohohu,  2086  ;  in 
apoplexy,  1355 ;  in  cerebral  tumours, 
1388;  diabetic,  1968;  epileptic,  1479; 
in  lead  jioisoning,  2097  ;  in  malaria,  1811  ; 
in  tubercular  meningitis,  1440 ;  iu  tuber- 
culosis, 206  ;  in  urx'inia,  1128 

Comma  bacillus,  1763 

Common  bile-duct,  obliteration  of,  1013 

Compensation  in  valve  lesions,  422 

Compression  of  spinal  cord,  1317 

Concretions  in  tonsils,  579 

Concussion,  spinal,  1315 

Congenital  heart  affections,  445 

Congestion  of  brain,  1348  ;  of  kidney,  10'^  1  ; 
of  liver,  900;  of  lung,  118,  254;  of 
viscera,  429 

Conjugate  deviation  of  eyes,  1355 

(Conjunctivitis,  diphtheritic,  4 ;  gonorrhoeal, 
2059  ;  in  measles,  1652 

Consecutive  nephritis  (pyelitis),  1210 

Consumption,  181 

Contracted  kidney,  1102 

Contractions,  fibrillary,  1279 

Contracture,  1284  ;  in  cerebral  haemorrhage, 
1355,  1358 ;  in  facial  paralysis,  1569 ; 
hysterical,  1495 ;  paraplegia  in  infancy, 
1382 

Convalescence  in  typhoid  fever,  1669 

Convergence,  paralysis  of,  1585 

O)nvulsions,  1430  ;  epileptic,  in  alcoholism, 
2087;  in  cerebral  abscess,  1378;  in  cere- 
bral haemorrhage,  1355 ;  in  cerebral 
sjrphilis,  1400  ;  in  cerebral  tumours,  1387  ; 
in  chronic  Bright's  disease,  1105 ;  in 
Jacksonian  epilepsy,  1484  ;  in  lead-poison- 
ing, 2097  ;  in  pernicious  fevers,  1812  ;  in 
rheumatic  fever,  1922  ;  uraemia,  1127  ;  in 
whooping-cough,  107 

Co-ordination,  abohtion  of,  in  tabes,  1243 

Clornage,  bruit  de,  352 

Coronaritis,  516  ;  sj'phUitic,  534 

Corpora  quadrigemina,  lesions  of,  1586 

Corrigan's  pulse,  441 

Coryza,  acute,  1  ;  chronic,  3  ;  hepatic,  3 ; 
infantile,  3  ;  of  new-bom,  7  ;  posterior,  3  ; 
scrofulous,  3  ;    syphihtic,  7 

Cough  :  hysterical,  1501  ;  in  acute  bronchitis, 
76  ;  in  chronic  bronchitis,  92  ;  in  bronchi- 
ectasis, 97  ;  in  aspiration  of  pleural  effu- 
sions, 265  ;  in  pneumonia,  125 

Cowpox,  1616 

Coxalgia,  hysterical,  1496 

Cracked-pot  sound,  182 

CJramp  in  Bright's  disease,  1113 ;  in 
cholera,  1769  ;  in  stomach,  672  ;  writer's, 
1537 

Cretinism,  2007 


2140 


TEXT-BOOK   OF   :MEDICINE 


Crises  :  of  tabes,  clitoridean,  1247  ;  gastric 
rectal,  renal,  vesical,  and  urethral,  1244 ; 
testicular,  in  filariasis,  2016 

Crisis,  in  pneumonia,  126  ;  in  relapsing  fever, 
1735  ;  in  typhus,  1732 

Crossed  paralysis,  1253,  1357 

Croup,  47  ;    diagnosis,  52  ;    symptoms,  48  ; 
treatment,  54 
false,  56 

Crura  cerebri,  disease  of,  1321 

Crutch  palsy,  1588 

Cruveilhier's  disease,  698 

Cry,  epileptic,  1478  ;  hydrocephalic,  1439  ; 
hysterical,  1493 

Crysesthesia,  1114 

Cryoscopy  of  cerebro-spinal  fluid,  1458  ;  in 
nervous  polyuria,  1502  ;   of  urine,  1136 

Crystals,  Charcot-Leyden,  110 

Cucurbitins,  885 

Culex  ciliaris,  2015  ;   fasciatus,  1777 

Curschmann's  spirals,  110 

Cutaneous  nerve,  external,  neuritis  of,  1560 

Cyanosis,  446 

Cystitis  in  tabes,  1251 

Cystoscopy,  1163 

Cysts :  alveolar,  974 ;  of  brain,  1365 ; 
gaseous,  966  ;  of  kidney,  1180  ;  of  Hver, 
960 ;  pancreatic,  1059 ;  of  peritoneum, 
888 

Cytodiagnosis,  275 ;  in  acute  meningitis, 
1458 ;  in  cerebral  syphilis,  1395 ;  in 
general  paralysis,  1410 ;  in  pleurisy,  292, 
318  ;  in  syphilitic  myelitis,  1310  ;  in  tabes, 
1255  ;  in  zona,  1551 

Cytosteatonecrosis,  1062,  1069 , 

Cytotoxines,  1832 

D 

Dacryocystitis  in  measles,  1652  ;  in  mumps, 
1760 

Dagger-thrust,  peritoneal,  834 

Dancing  mania,  1523 

Deafness,  after  measles,  1653  ;  in  Meniere's 
disease,  1345 ;  after  mumps,  1760 ;  in 
tabes,  1254  ;  after  typhoid  fever,  1704  ; 
in  typhoid  fever,  1667 

Death,  sudden  :  in  Addison's  disease,  1235 ; 
in  angina  pectoris,  544 ;  in  aortic  lesions, 
443 ;  in  coronaritis,  534 ;  in  diabetes, 
1968  ;  in  embolism,  146  ;  in  hepatic  colic, 
999  ;  in  pleurisy,  259  ;  in  rupture  of  the 
heart,  456  ;  in  typhoid  fever,  1705 

Decapsulation  of  kiclney,  1149 

Dechlorination  (cure),  1141 

Decompression,  1314 

Decubitus,  acute  (bedsore),  1358 

Defervescence  in  tj^^hoid  fever,  1668 

Degeneration  :  amyloid  of  kidney,  1152  ;  of 
liver,  975  ;  fattj^ ,  of  heart,  449  ;  of  liver, 
977  ;   reaction  of,  in  neuritis,  1474 

Delayed  sensation  in  tabes,  1261 

Dehrium  :  ambitious,  1407  ;  epileptic,  1480  ; 
of  grandeur,  1406  ;  hypochondriacal,  1407  ; 


in  lead-poisoning,   2097  ;    of  persecution, 
1407  ;    in  pneumonia,  133  ;    in  rheumatic 
fever,  1921  ;  in  tj^phoid  fever,  1670,  1697  ; 
tremens,  2087  ,-  in  typhus,  1731  ;   ursemic, 
1127 
Deltoid,  paralysis  of,  1593 
Delusions  of  grandeur,  1406 
Dementia    in    syphilis,     1403 ;      paralytica 

(general  paralysis),  1404 
Dengue,  1662 
Dentition  in  rickets,  1964 
Dercum's  disease,  2003 
Dermatitis,  exfoliative,  1641 
Desquamation,  in  measles,  1647  ;  in  rubella, 

1659  ;   in  scarlet  fever,  1629 
Desiccation  in  variola,  1611 
Deviation,  conjugate,  of  head  and  eyes,  1355 
Diabetes  and  traumatism,  1984,  1990 
insipidus,  1982 

mellitus,  1948  ;   aetiology,  1952  ;  ascites, 
1976 ;     coma,    1968 ;     complications, 
1959 ;    description,   1954 ;    diagnosis, 
1978 ;     glycosuria,    1956 ;     liver    in, 
1971 ;   nervous  troubles,  1967  ;   para- 
lysis,    ocular,     1961  ;      pathogenesis, 
1942  ;   pulmonary  tuberculosis,  1964  ; 
treatment,     1979 ;      varieties,     1970 ; 
phosphatic,  1983  ; 
azoturic,  1982 
Diaphragmatic  pleurisy,  353 
Diarrhoea :     in   children,    752 ;     in   cholera, 
1768  ;  of  Cochin-China,  851  ;  in  dysentery, 
849  ;    irritative,  750,  753  ;    lienteric,  799  ; 
nervous,  741,  750 ;    pancreatic,  1058  ;    in 
peritonitis,    874,    885 ;    in   phthisis,    181  ; 
sudoral,  750 ;    summer,  752  ;    in  typhoid 
fever,  1667  ;   ursemic,  1129 
Diathesis,  gouty,  1192,  1945  ;  tubercular,  188 
Dicrotism  of  pulse  in  t%-phoid  fever,  1668 
Diet  :  in  chronic  dyspepsia,  671  ;  in  diabetes, 
1979  ;  in  gout,  1948  ;  in  infantile  enteritis, 
755  ;    in  obesity,  1997  ;    in  scurvy,  1914  ; 
in   tuberculosis,    191  ;    in   t%-phoid   fever, 
1724 
Digestive  system,  diseases  of,  552 
Dilatation  of  bronchi :    aetiology,  96  ;    com- 
pHcations,  98  ;   diagnosis,  98  ;   patho- 
logical anatomv,  94  :  svmptoms,  97 
of  heart,  458  ;    of  stomach.   702,   738  ; 
bile-ducts,  1004;    gall-bladder,  1004 
Diphtheria  :    bacillus,  588  ;    of  bronchi,  51  ; 
buccal,  555  ;    of  larynx,  47  ;    of  nose,  4  ; 
oculo-palpebral,  4 
Diphtheritic  paralysis,  625 
Diplegia,  spasmodic,  1381 
Diplococcus  of  Weichselbaum,  1459 

pneumonia,    123 ;     in    empyema,    127 ; 
in  peritonitis,  872 
Diplopia,  1576 ;    hysterical,  1512 ;    tabetic, 

1245 
Displacement  of  heart  in  pleurisy,  252 
Dittrich's  plugs,  153 
Diuretics,  433 
Diver's  palsy,  1314 


INDEX 


2141 


Boipt  on  radis,  2055 

Dotliirnciiti'Tif.  Hi05 

l)r()|)sy.     See  Aiiii.siirca 

Pracuiu'iilosis,  '20\i 

lini^  rashi-a,  H')'>r> 

Ductus  artcriosis,  ])t>rsistpnt,  44X 

Dulliu'ss,  lluiil,  251  ;  poricardial,  -104 

Duoilonal  ulcer.  S32 

Duuilciiitis,  751 

Dura  mater,  disease  of,  145t> ;  hiPitiatoina  of, 
14{;3 

Dwarfs  (cretins).  2006 

Dyschromatopsy.  1290,  1502 

Dysentery'  :  setiology,  845 ;  bacteriology, 
848 ;  complications,  851  ;  pathological 
anatomy,  84(5 ;  symptoms,  849 ;  treat- 
ment, 851 

Dyspepsia,  667 

Dyspepsia,  of  nurslings,  753 

Dysphagia  :  in  cancer  of  oesophagus,  650 ; 
in  hydrophobia,  1836  ;  in  pericardial  effu- 
sion, 404  ;  in  thoracic  aneurysm,  512  ;  in 
tubercular  laryngitis,  43  ;  in  tumours  of 
the  mediastinum,  391 

Dyspnoea  :  in  acute  tuberculosis,  205 ;  in 
aneurysm,  511  ;  in  angina  pectoris,  543  ; 
in  broncho-pneumonia,  86  ;  cardiac,  428  ; 
in  croup,  49  ;  in  cancerous  pleurisy,  290  ; 
in  diabetic  coma,  1968  ;  in  emphj'sema, 
160;  in  hysteria,  1501;  in  mediastinal 
tumour,  391  ;  in  mitral  disease,  428  ;  in 
myocarditis,  453  ;  in  oedema  of  lung,  164  ; 
in  paralysis  of  larynx,  71  ;  in  pericarditis, 
404 ;  in  pneumonia,  125 ;  in  pneumo- 
thorax, 385  ;  in  stridulous  laryngitis,  44  ; 
uraemic,  1129 

Dystrophies,  progressive  muscular,  2037 


E 


Ecchjiuoses,  spontaneous,  1522  ;  tabetic,  1251 

Echinococcus,  961 

Ecthyma  in  diabetes,  1959 

Eczema,  in  diabetes,  1959 ;  in  gout,  1940  ; 
of  tongue,  565 

Effusion,  chyliforra,  895 ;  pleural,  251  ; 
serous,  in  Bright's  disease,  1115 

Ehrlich's  606,  2119 

Elastic  fibres  in  sputum,  182 

Electrical  reactions  :  in  anterior  polio- 
myelitis, 1295  ;  in  facial  palsy,  1565  ;  in 
multiple  neuritis,  1474 ;  in  Thomsen's 
disease,  2036 

Electro-puncture  in  aneurysm,  520 

Elephantiasis,  2016 

Embolic  abscesses,  417 

Embolism  :  cerebral,  1364  ;  in  chorea,  1527  ; 
pulmonary,  144,  428  ;  in  typhoid  fever, 
1695 

Embryocardia,  451 

Emphysema,  interlobular,  159  ;  intralobular, 
159  ;  mechanism  of,  159  ;  pneumothorax 
in,  160  ;  rupture  of  vesicles,  160  ;  dilata- 
tion of  \entricle,  160;   suffocation  in,  lliO 


Empyernft  :  l)act(M'iulogicul  varieties  of,  311, 
312,  314;  pulHalinK.  327;  Hubi»lin-nic, 
35S,  70 » 

Encephalitis  :  acute,  1376  ;  chronic,  1378  ; 
in  general  puralvsis,  1405;  in  infancy, 
137H 

Enccplialoid  iiiiiicr  of  lung.  214 

Enc(!phal<)palliy,  saturnine,  2097 

Endoarteritis,  505.  507 

ICndocarditiH  :  acute,  409;  acute  Hinii>le, 
410;  biliary,  1010;  in  chorea,  1526; 
chionic,  420  ;  emboligenous,  412  ;  gonor- 
rhoeal,  2058  ;  infective,  412  ;  malignant, 
412  ;  in  pneumonia,  417  ;  in  pregnancy, 
418;  in  rheumatism,  417  ;  in  scarlet  fever. 
1640;  in  tuberculosis,  419;  in  typhoid 
fever,  419  ;   ulcerative,  412 

Engorgement  of  lung,  121 

Enteritis,  750 ;  acute  gastro-enteritis  in 
infants,  752 ;  in  measles,  1652 ;  tuber- 
cular, 812 

Enteroptosis,  748 

Entero-typho-colitis,  787,  798  ;  clinical  cases, 
798  ;  description,  799  ;  diagnosis,  803  ; 
intestinal  lithiasis,  802 ;  relation  to 
appendicitis,  803  ;    treatment,  800 

Eosinophiles,  in  haemothorax,  297 

Eosinophilia  in  hydatid  cyst  of  liver,  970 

Epidemics  of  cholera,  1761  ;  of  malaria, 
1796  ;   of  plague,  1781 

Epididymitis,  gonorrhoeal,  2019 

Epilepsy  :  ffitiology,  1480  ;  description,  1484  ; 
diagnosis,  1481  ;  disguised  form  of,  1481  ; 
essential,  1477  ;  grand  mal,  1477  ;  Jack- 
sonian,  1483  ;  in  lead-poisoning,  2097  ; 
and  mental  alienation,  1479  ;  pathogenic 
diagnosis,  1489  ;  fetit  mal,  1479  ;  secon- 
dary forms  of,  1482  ;  and  sjT)hilis,  14S2  ; 
traiimatic,  1490  ;  treatment,  1481  ;  topo- 
graphical diagnosis,  1485 

Epileptic  fit,  stages  of,  1478 

Epileptiform  conditions,  1482  ;  in  infantile 
hemiplegia,  1383  ;  reflex,  1482  ;  in  syphilis, 
1400  ;   in  ureemia,  1127 

Epistaxis,  18;  a  tamjyonnement  in  Bright's 
disease,  1121;  rheumatic,  1919;  in 
typhoid  fever,  1620 

Epithelioma  of  liver,  948  ;   of  tongue,  568 

Erb's  syphilitic  spinal  paralysis,  1309 

Erethism,  mercurial,  2092 

Erosions  of  stomach,  674 

Eructations  in  hysteria,  1501 

Erysipelas,  facial,  1748  ;  bacteriology,  1748  ; 
description,  1748;    serotherapy,  1755 

Erythema,  infectious  scarletiniform,  1640 ; 
laryngeal,  31;  in  pellagra,  2114;  of 
throat,  638 

Eschars.  1304,  1698 

Esquinancia,  580 

Exanthematic  purpura.  1908 

Exfoliative  dermatitis,  1641 

Exophthalmic  goitre.  470  ;  cardiac  troubles 
in,  470;  ocular  troubles  in.  471  ;  men- 
struation,   475;    mental    condition.    470; 


2142 


TEXT-BOOK  OF  MEDICINE 


paralysis  in,  473  ;   sensory  troubles,  475  ; 
thyroid  gland,  472  ;    tremors,  472  ;    treat- 
ment, 481 ;   surgical,  484 
Exophthalmos,  471 
Expectoration,  albuminous,  161,  265 
Exploratory  punctures  (lung),  154 
Extract,  hepatic,  in  diabetes,  1981 
Exulceratio  simplex  :    cases,  684  ;    descrip- 
tion,  691 ;    diagnosis,   692  ;    pathological 
anatomy,    689 ;     prognosis,    695 ;     treat- 
ment, 695 

F 

Facial  hemiatrophy,  1601 

paralysis :    of  bulbar  origin,   1567 ;    of 
cerebral     origin,     1567 ;      of     intra- 
temporal  origin,  1567  ;    of  peripheral 
origin,  1563  ;   syphilitic,  early,  1571  ; 
late,  1576 
Facies  :   in  acromegaly,  2023  ;   in  consump- 
tion, 181  ;  Hutchinson's,  1328  ;  in  leprosy, 
1828  ;   in  myxcedema,  2006  ;   in  paralysis 
agitans,  1522 
Fsecal    accumulation,     840 ;     fistulse,    868 ; 

vomiting,  841 
Fseces  in  jaundice,  1031 
False  appendicitis,  806 
False  croup,  56  ;  tuberculosis,  207 
Famine  disease,  1734 
Farcy,  1842 

Fat  necrosis  of  pancreas,  1069 
Fatty  degeneration,  of  heart,  433  ;   of  liver, 
975 
stools,  1067 
Fehhng's  test  for  sugar,  1957 
Fetid  pleurisy,  367 
Fever : 

aphthous,  561  ;  bilioseptic,  1006  ;  bilious 
typhoid,  1736  ;  cerebro -spinal,  1444  ; 
famine,  1734  ;  Gambia,  1822  ;  gastric, 
663  ;  hsematuric,  1810  ;  hsemoglobin- 
uric,  1810;  hay,  115;  hysterical, 
1507;  pernicious,  1811;  in  pneu- 
monia, 136 ;  in  pulmonary  tuber- 
culosis, 183  ;  quartan,  1805  ;  relap- 
sing, 1733 ;  scarlatina,  1627 ;  in 
smallpox,  1608,  1610 ;  syphilitic, 
1707;  tertian,  1805;  tonsillar,  580; 
trypanosome,  1822  ;  typhoid,  1663  ; 
typho-malarial,  1808 ;  in  typhus, 
1732 ;  yeUow,  1777 ;  yeUow  fever 
nostras,  1044 ;  zoster,  1550 
intermittent,  in  malaria,  1803 ;  in 
chronic  obstruction  of  bile-ducts  by 
gaU-stones,  1019  ;  in  secondary  syphi- 
lis, 1707 
Fibrinous  bronchitis,  101 
Fibrosis  :   of  heart,  449,  452  ;   of  lung,  139  ; 

of  kidney,  1210  ;   of  pancreas,  1061 
Fifth  nerve,  neuralgia  of,  1540  ;  paralysis  of, 

1595 
Filaria  sanguinis,  2014 
FQariasis,  2014 


Filum  terminale,  1311 

Fingers  dead,  1 1 12 

Fistula  :    anal,   831  ;    biliary,   1012 ;    renal, 

1210 ;  umbihcal,  722 
Flatulent  dyspepsia,  670 
Floating  kidney,  1229 
Fluid,  cerebro-spinal,  1458 
Foetus,  endocarditis  in,  447  ;  tuberculosis  in, 

187  ;  white  pneumonia  in,  244 
Folie  Brightique,  1127 
FoUicle,  tubercular,  172 
Follicular  tonsiUitis,  579 
Fourth  nerve,  paralysis  of,  1583 
Fractures  in  tabes,  1252 
Fremissement  cataire,  1896 
Fremitus,  vocal,  126,  252  ;  hydatid,  965 
Friedreich's  disease,  1266 
Frontal  convolutions,  lesions  of,  1429,  1433, 

1435 
Fungus  of  dura  mater,  1426 
Furuncles    in    diabetes,    1959 ;     in   typhoid 

fever,  1698 

G 

Gait :  ataxic,  1248 ;  cerebeUo-spasmodic, 
1289;  with  dragging  of  feet,  1296;  in 
paralysis  agitans,  1522  ;  in  pseudo-hyper- 
trophic  paralysis,  2041 ;  in  spastic  para- 
plegia, 1285  ;   steppage,  1473,  1829,  2089 

GaU-bladder,  anatomy  of,  995  ;  atrophy  of, 
1007  ;   cancer  of,  954  ;   dilatation  of,  1004 

Gallop  rhythm  in  myocarditis,  450 

GaU-stones,  990 ;  aetiology,  992 ;  angio- 
chohtis,  1006  ;  bihary  fistulse,  1012  ;  chole- 
cystitis, 1007  ;  diagnosis,  1000 ;  hepatic 
cohc,  995 ;  iniection  of  bile-ducts,  1005 ; 
obstruction  of  bile-ducts,  1003  ;  of  bowel, 
1001  ;  of  pylorus,  1002 ;  peritonitis,  1011 ; 
pregnancy,  993 ;  pylephlebitis,  1010  ;  treat- 
ment, 1001 

Ganglia,  semilunar,  in  Addison's  disease, 
1238 

Gangrene  :  diabetic,  1950  ;  gaseous,  2083  ; 
of  the  lung,  149  ;  of  the  mouth,  562  ;  of 
the  penis,  2076  ;  of  the  pharynx,  635 ; 
pleuritic,  343 ;  symmetrical,  1604 ;  sy- 
philitic, 504  ;   treatment  of,  2125 

Gasserian  ganglion,  removal  in  tic  dou- 
loureux, 1545 

Gastralgia,  672 

Gastric  juice,  hyperacidity  of,  731 ;    hypo- 
acidity of,  731 
ulcer,  698 

Gastritis  :  acute,  662  ;  chronic,  665  ;  poly- 
pous, 723  ;  pneumococcal,  676  ;  ulcerative, 
674 

Gastro-enteritis,  752 

Gastroptosis,  748 

Gastrorrhagia,  746 

Gastroxda,  670 

Grelo-diagnosis  in  typhoid  fever,  1713 

General  paralysis,  1404  ;  diagnosis  of,  1408  ; 
influence  of  syphilis  in,  1409 


INDEX 


2143 


Gwipraphiciil  tongui',  .^GS 

GigaiitiHOi,  2U2U 

Gland,  pituitary,  2U25 

Glandcra,  1842 

Gl^oard's  disease,  748 

Glioma  of  brain,  1.384  ;  of  spinal  cord,  1273 

(Globus  hysteiiius,  14'J3 

Glouieruliis.  1078 

Glosaiua  palpalis,  1822 

Glossitis  :    oxfoliativo,  565  ;    sclerotic,  6R7  ; 

in  araokors,  5G7 
Glosao-labiu-laryugeal  paralysis,  1322 
Glossy  skin,  1598 
Glottis,  oedema  of,  58  ;    in  Bright's  disease, 

GO  ;   in  smallpox,  1613  ;  in  typhoid  fever, 

IGiK) 
(Jlucose,  1949 
Glycsemirt.  1949 
Glycogen,  899,  1949 
Glycosxiria,  1956 
Gmelin's  test,  1031 

Goitre,  exophthalmic,  470  ;    setiology,  480  ; 
clinical  features.  470  ;  psychoses,  476  ; 
treatment,  481 
in  cretins,  2007 
Gonococcus,  2045 
Gonococeal  arthritis,  2129 
Gonorrhoea,     2045 ;      baeteriology,     2045 ; 

complications,   2048  ;     description,   2047  ; 

diagnosis,  2060  ;  rheumatism,  1933,  2052  ; 

treatment,  2061 
Gout :    setiology,   1945  ;    alcohol  in,   1945  ; 

articular,  1937  ;    chronic,  1939  ;    heredity 

in,    1945 ;     influence    of   food   in,    1948 ; 

irregular,   1940 ;    and  the  kidney,    1941  ; 

saturnine,  2098 
Graefe's  sign,  471 

Grain,  poisoning  by,  in  pellagra,  2114 
Grandeur,  deliritun  of,  1406 
Orand  mal,  1477 

Granulation,  tubercidar  of  lung,  172,  176 
Gravel,  1191 
Grave's  disease,  470 
Gumma  :   of  aorta,  531  ;   of  brain,  1389  ;   of 

heart,  457  ;    of  larynx,  33  ;    of  lips,  564  ; 

of  lujig,  232  ;  of  tongue,  565 
Gums,  blue  line  in  lead-poisoning,  2094 ;  in 

scurvy,  1913  ;  in  stomatitis,  652,  555 


Haematemesis,  726  ;  aetiology,  746  ;  diagnosis 

747 ;  symptoms,  746 
Hsematoblasts,  1878 
Haematochyluria,  2017 
Hsematoma  :    of  dura  mater,  1463  ;   of  ear, 

1407 ;    pleural,    29 ;     in    typhoid   fever, 

1700 
Hsematomyelia,  1314 
Hsematozoon  (Laveran's),  1797 
Hsematuria,  1199  ;  in  Bright's  disease,  1119  ; 

in  calculus  of  kidney.  1198  ;    in  cancer  of 

kidney,    1189;     chylous,    1221;    in   colic 


(renal),     1194;     t-ndemit,     1220;     gouty 
1944;    in  hydatid  cyst  ol   kidney,   1186: 
in  hy-'ti-ria,    1507  ;    in   polycystic  kidney. 
1182';  rh.uinatic,  1922  ;  Bcarlatinal,  1635  ; 
secondary,  1220;    tubercular,   1157 
Hsemnturia,  essential,  1222 
HaBmodiagnosis  in  typhoid  fever,  1712 
HaemoglobiniBmia,  1225 
Haemoglobiuuria,    1223;     in    biLary    fever, 
1810  ;   pathogenesis  of,  1225  ;    rheumatic, 
1922 
Haemoglobinuric  fever,  1224 
Hsemolytic  icterus,  1053 
Haemophilia,  155 
Hsemoptyses,  interlobar,  335 
Haemoptysis,    154 ;     aetiology   of,    155 ;     in 
cancer  of  larynx,  46  ;  in  heart  lesions,  428  ; 
in    aneurysm    of    aorta,    519;     bronchial 
haemorrhage,   155;    diagnosis,   157;    pul- 
monary   haemorrhage,    155;     symptoms. 
156;   treatment,  158 
Haemorrhage :     in    acute    yellow    atrophy, 
1042  ;  bronchial  and  pulmonary,  155  ; 
in  cancer  of  kidney,  1189 
cerebral,    1349;     aetiology,    1353;     de- 
scription, 1355 ;    topography,  1350 
in  gastric  ulcer,  703  ;    gastro-intestinal, 

in  cirrhosis,  915  ;  in  hysteria,  1507 
intestinal,  in  duodenal  ulcer,  832  ;    in 

typhoid  fever,  1672 
in  invagination,  841  ;   meningeal,  1467  ; 
in  nephrohthiasis,  1198  ;  of  pancreas, 
1061, 1071  ;  peritoneal,  in  cancer,  887  ; 
in  purpura,  1907  ;    retinal,  1815 ;    in 
scurvy,  1913  ;   in  smallpox,  1612  ;   in 
typhoid  fever,  1672  ;   in  yellow  fever, 
1779 
Haemorrhagic  :    scarlet  fever,  1629 ;    small- 
pox, 1612 
Haemothorax,    traumatic,    297 ;     comphca- 
tions,    303 ;     cytology,    299 ;     pathology, 
298 ;   symptoms,  301  ;   treatment,  305 
Hallucinations  in  hysteria,  1500 
Hay-asthma,  115 
Haj'^-fever,  115 

Headache,   in   cerebral   syphilis,    1393 ;     in 
cerebral  tumour,  1385 ;    in  gastric  ulcer, 
702  ;   in  typhoid  fever,  1666  ;   in  uraemia, 
1119 
Heart : 

aneurysm,  454  ;  bovine,  441  ;  congenital 
affections  of,  446 ;    dilatation,   458  ; 
displacement  in  pleural  effusion,  252. 
290  ;   fatty,  451  ;    fatty  degeneration 
of,  449  ;    fibrous,  452  ;    hypertrophy, 
458  ;    muscle  in  typhoid  fever,  1720  ; 
neuroses  of,  463  ;    palpitation,   463  ; 
renal,  1106 ;    nipture,  45G ;    sounds, 
423  ;  syphilis,  457  ;  tubercle  of,  458 
valves,  lesions  of,  421 ;  rupture  of,  454 
Hectic  fever,  183 
Hectine,  2119 

Hemianaesthesia,    1357 ;     hysterical,    1496 ; 
in  lesions  of  internal  capsule,  1431 


2144 


TEXT-BOOK   OF   MEDICINE 


Hemianopia  :    homonymous,   1387  ;    lateral 
homonymous,   1368 ;    nasal,   1387 ;    tem- 
poral, 1387 
Hemiathetosis,  infantile,  1381 
Hemiatrophy  of  face,  1601  ;   of  tongue,  1253 
Hemichorea,  post-hemiplegic,  1359 
Hemicrania,  1538 

Hemiplegia,     1356 ;      arthropathies,     1361  ; 
exaggeration    of    reflexes,    1358 ;     hemi- 
antesthesia,  1357  ;    infantile,  1381  ;    post- 
hemiplegic movements,   1359  ;    secondary 
contractures,   1358  ;    syphilitic,   1393 ;    in 
typhoid  fever,  1697 
Hepatalgia,  1000 
Hepatic  abscess,  977  ;  colic,  995 
Hepatism,  749,  911 

Hepatitis  :  acute,  977  ;  in  appendicitis,  981  ; 
in  malignant  jaundice,    1038 ;    calculous, 
1006  ;    chronic,   904  ;    in  malaria,    1818  ; 
nodular,  945  ;  in  syphilis,  956  ;  in  heredi- 
tary syphilis,  959 
Hepatization,  121 
Hepatomegalia  in  diabetes,  1972 
Hepatoptosis,  748 
Hereditary  cerebral  syphilis,  1404 
Heredity  :  arthritic,  1953  ;  in  diabetes,  1952  ; 
in  diabetes  insipidus,  1984  ;  in  Friedreich's 
ataxy, 1267  ;  gouty,  1937  ;  nervous,  1953 ; 
in  rheumatic  fever,  1917 ;  in  tuberculosis,  188 
Heredo-ataxy,  cerebellar,  1266 
Herpes :     angina,    630 ;     in    cerebro-spinal 
meningitis,     1444 ;      chancriform,     2068 ; 
genital,   2067 ;    in  malaria,    1804 ;    para- 
syphilitic,    637 ;     of    pharynx,    602  j     in 
pneumonia,  136 
Hiatus,  costolumbar,  1213 
Hiccough,  1460 
High-tension  pulse,  549 
Hippocratic  succussion,  385 
His's  bundle,  468 
Hodgkin's  disease,  1890 
Horse-pox,  1616 

Hour-glass  stomach  {en  bissac),  739 
Hyahne  casts  in  urine,  1118 
Hydatid  cysts  : 

of  the  kidney,  1184;    diagnosis,  1186; 
pathogenesis,  1184  ;  symptoms,  1185  ; 
treatment,  1186 
of  the  liver,  960  ;    alveolar,  974  ;    ana- 
tomy, 960  ;    course,  965  ;    diagnosis, 
969  ;  life  history  of  the  hydatid,  960  ; 
rupture,  967  ;  symptoms,  963  ;  treat- 
ment, 970 
of  the  lung,  219  ;  diagnosis,  224  ;  evolu- 
tion, 223  ;    rupture,  225  ;    symptoms, 
219  ;   treatment,  230  ;   vomica,  227 
of  the  peritoneum,  888 
of    the    spleen :     clinical    case,     1858 ; 
diagnosis,  1872  ;    hsematology,  1865  ; 
pathological  anatomy,  1864  ;  varieties 
of  cysts,  ascending,  1869  ;  descending, 
1872  ;  external  intrasplenic  and  juxta- 
splenic  cysts,  1864 
Hydatid  thriU,  965 


Hydrargyrism,  2090 

Hydrocele,  chylous,  2016 

Hydrocephalus,  1469  ;  acquired,  1470  ;  con- 
genital, 1470 

Hydromeha,  1273 

Hydronephrosis,  1219  ;  in  movable  kidney, 
1230 

Hydropericardium,  408 

Hydro-pneumo-pericardium,  408 

Hydrophobia,  1836 

Hydro-pneumo-thorax,  383 

Hydrothorax,  382 

Hypera3sthesia  :  in  ataxia,  1261 ;  in  hysteria, 
1497 

Hyperchlorhj^dria,  707 

Hypercrinia,  1932 

Hyperhepatia,  1952 

Hjrperpyrexia,  hysterical,  1507 ;  in  rheu- 
matic fever,  1921  ;  in  scarlet  fever,  1628  ; 
in  tetanus,  1790 

Hypertension,  arterial,  548 

Hyperthyroidization,  484 

Hypertrophic,  tuberculoma  of  the  csecum, 
816  ;   cirrhosis,  922,  930 

Hypertrophy,  compensatory  :  of  kidney  in 
Bright's  disease,  1105 ;  in  cancer, 
1187  ;  in  hydatid  cyst,  1184  ;  in  poly- 
cystic disease,  1182;  in  tuberculosis, 
1163 
of  heart,  458 

of  liver  in  alcoholic  cirrhosis,  923 
of  tonsils,  585 

Hypnotism,  1509 

Hypo-azoturia,  orthostatic,  1151 

Hypophysis,  enlargement  of,  2025 

Hypostatic  congestion  of  lungs  in  typhoid 
fever,  1667 

Hypotension,  arterial,  548 

Hypothermia  in  typhoid  fever,  1676 

Hypotonia,  1253 

Hysteria,  1492  ;  setiology,  1508  ;  blindness, 
1504 ;  clavus  hystericus,  1497 ;  convul- 
sive form,  1492 ;  non-convulsive  form, 
1494  ;  diagnosis,  1507  ;  hemiplegia,  1495  ; 
organs  of  the  senses,  1502  ;   tremors,  1496 

Hysterical  angina  pectoris,  547 ;  chorea, 
1528 

Hystero-epilepsy,  1493 

Hysterogenic  zones,  1497 


Ichthyosis,  1252 

Icterus,  1030 ;  benign^  955 ;  simple  infec- 
tious, 1047 ;  catarrhal,  1047 ;  pro- 
longed catarrhal,  1050 ;  cholsemia, 
1036;  chronic,  844,  933,  1052;  de- 
scription, 1030 ;  diagnosis,  1044 ; 
effects,  1031  ;  gastro-intestinal  trou- 
bles, 1031  ;  Gmehn's  reaction,  1031 ; 
hsemolytic,  1053 ;  pathogenesis,  1033, 
1047  ;  symptoms,  1041  ;  treatment, 
1053 
gravis,  1037 ;  ajtiology,  1044 ;  course, 
1043  ;   diagnosis,  1044  ;  pathogenesis. 


INDEX 


'ill; 


1037  ;     palluilngicttl   Hnatoiny.    104U  ; 
piuTporiil    HtuU',     1045 ;     syniplom«, 
1041 
Itliwy,  i;{H2  ;    myxa?dcmatoii8,  200ii 
Idioputhio  niiu'inia,  1882 
Ilcu-fiifal  rc^'ion  :    in  appcndicitie,  709  ;    in 

typhoid  fcvor, IlltiT 
llous.  8;{S 

Immunization,  21.'i0 
ImpotcMu-e.  in  tliabctcs,  1955 ;   in  locomotor 

ataxy, 1247 
Impulses  in  epilopsy,  1480 
Index,  colour,  1877 
Indigestion,  785 
Indol  reaction,  1703 
Inequality  of  the  pupils  :   in  aneurysm,  513  ; 

in  general  paraljsis,  1407 
Inexhaustible  pleuritic  effusion,  319 
Infantile  gastro-enteritis,  752 

paralysis,  1294  ;  scurvy,  1914 
Infarcts  :    of  brain.  1305  ;    ha?moptoic,  145  ; 

150  ;  haemorrhagie.  428  ;  of  kidney,  1191  ; 

of  myocartlium,  455  ;   of  placenta,  1904 
Infiltration,   tubercular,   of  lar3'nx-,   37 ;     of 

lung,  177 
Inflammation  of  the  chest,  119 
Influenza,  1771;    bacteriology,   1770;    cere- 
bral, 1772  ;    complications,  1772  ;   gastro- 
intestinal, 1774  ;    thoracic,  1773 
Injections   of    mercurj',    2117 ;     of   tetanus 

antitoxine,  1795 
Inoculation    preventive,    against    smallpox, 

1016  ;    in  hydrophobia,  1834  ;    in  plague, 

1787  ;  in  typhoid  fever,  1728 
Insane,  general  paralysis  of,  1404 
Insomnia  in  typhoid  fever,  1660 
InsuflSciency,     aortic,     441  ;      mitral,     420 ; 

renal,  1133;    suprarenal,  1241;   tricusijid, 

443 
Insular  sclerosis,  1287 
Intention  tremor,  1289 
Intercostal  neuralgia,  1549 
Intermittent  fever,  1804 
Internal  capsule,  1350 
Intestinal,  cancer,  837  ;  coils,  tumour  formed 

bv,   841;    lithiasis,   798,   802;    occlusion, 

838  ;  sand,  801  ;   worms,  852 
Intestines  : 

diseases  of,  750  ;   occlusion,  838  ;   stran- 

gidation,  838  ;   tuberculosis  of,  812 
haemorrhage  from,   in   dysenter}%   849 ; 
in  invagination,  841  ;   in  tuberculosis, 
815  ;  in  typhoid  fever,  1072 
Intoxications,  2080 
Intubation  of  Iar\-nx,  55 
Intussusception,  839 
Invagination  of  the  gut,  839 
Ipecacuanha  :    in  exophthalmic  goitre,  483  ; 

in  haemoptysis,  158 
Irido-choroiditis  in  relapsing  fever,  1730 
Iritis,  rheumatic,  19.32 
Ischajmia  of  the  heart,  544 
Ischuria,  paradoxical,  1312 
Island  of  Roil,  1350 


Itchini'iii  HrijilitKdiHcaHf,  1113  ;  in  <liiilM>teH, 
Mt.W;     in    jaundice,     1032;    in    ura>mia, 

iii;i 


.lacksonian  (  pilr-pKy,  1388,  1400,  1483 
Jaundice,  1030,  1037 

Joints  in  locomotor  ataxy,  1252  ;  in  syringo- 
myelia, 1274 

K 

Kerato-conjunctivitis  in  measles,  1052 

Kernig's  sign,  1453 

Kidney  :  acute  nephritis,  1082 ;  amyloid, 
1152;  anatomy,  1077;  appendicular, 
1090 ;  in  Bright's  disease,  1098  ;  cancer, 
1180;  cardiac,  1081;  in  diabetes,  1909; 
gouty,  1941  ;  hydatid  cyst  of,  1184;  large 
white,  1100;  movable,  1228  ;  pneumonic, 
129;  polycystic,  1180;  small  red,  1102; 
strangulation  of,  1230;  syphilis,  1105 1 
tuberculosis,  1153 

Klebs-Loffler  bacillus,  588 

Knee-jerks,  loss  of,  in  ataxia,  1244 ;  in 
diphtheritic  paralysis,  620 

Koch's  bacillus,  170;  tuberculin,  193 

Koplik's  sign,  1054 

Korsakoff's  syndrome,  1475 

ICrishaber's  disease,  1520 


Labyrinthine  syndrome,  1345 

Laced  liver,  950 

Lacunae  of  brain,  1309 

LarJ^Jgeal  crises,  1247 

Laryngitis :  acute  catarrhal,  27 ;  chronic 
catarrhal,  29  ;  erysipelatous,  1750  ;  glan- 
dular, 29  ;  gouty,  29  ;  hypertrophic,  30  ; 
in  measles,  1048  ;  cedematous,  57  ;  pseudo- 
membranous, 47  ;  stridulous,  50  ;  tuber- 
cular, 40 

Laryngopathy  :  cancerous,  38 ;  syphilitic, 
31  ;  tubercular,  40 

Laryugotyphus,  1090 

Larynx,  oedema  of  :  in  Bright's  disease,  60  ; 
in  mumps,  1700 ;  in  syphilis,  35, 
57  ;  tubercular,  44  ;  in  typhoid  fever, 
1690 
paralj'sis  of,  71,  1324 
ulceration  of,  31.  41  ;  in  tvphoid  fever, 
1690 

Lateral  sclerosis,  primary,  1283 ;  amyo- 
trophic, 1285 

Lavage,  672 

Lead-colic,  2094 

Lcad-line,  2094 

Ijead- poisoning,  2094 

Leprosy,  1826  ;  a?tiology,  1826  ;  anaesthetic 
form',  1828;  Hansen's  bacillus.  1829; 
pathological  anatomy.  1830;  sero-therapy, 
1831  ;  treatment,  1831 ;  tubercular  form, 
1827 


2146 


TEXT-BOOK    OP  MEDICINE 


Lesions,  valvular  of  heart,  42]  ;   aortic,  44]  ; 
mitral,  426 ;  pulmonary,  445 ;  tricuspid,  443 
Lethargy,  1509 

Leucocythaemia,     1885 ;      aetiology,     1886 ; 
pathological  anatomy,  1886 ;    symptoms, 
1890 
Leucocytosis,  1880  ;   in  erysipelas,  1752  ;   in 
leucocythsemia,  1886  ;  in  pneumonia,  125  ; 
in  pleurisy,  277 
Leucomyelitis,  1291 
Leucopenia,  1880 
Leucoplasia,  567 
Leyden's  crystals,  110 
Lienteria,  799 
Lightning  pains,  1243 
Lips,  paralysis  of,  1323  ;   syphilis  of,  563 
Lipoma,  lingual,  568 
Lipomatosis,     diffuse     symmetrical,     1998 ; 

perinephritic,  1208 
Lithiasis,    broncho-pulmonary,    216 ;     intes- 
tinal, 803  ;   pancreatic,  1061  ;    renal,  1191 
Little's  disease,  1378 

Liver  :    abscess,  977  ;    amyloid,  976 ;    ana- 
tomy, 896  ;    appendicular,  981 ;    atrophic 
cirrhosis,    907 ;      biliary    cirrhosis,     933 ; 
hypertrophic     alcohohc     cirrhosis,    922 ; 
congestion,  900  ;  disease  of,  896  ;  cirrhosis, 
904  ;   fatty,  975  ;   hob-nail,  907  ;   hydatid 
cyst,  960  ;  movable,  748  ;  regeneration  of, 
922 ;    rusty,  931 ;    syphihs,  955 ;    tuber- 
culosis, 943  ;   acute  yellow  atrophy,  1038 
Lobar  pneumonia,  121 
Lobe  abnormal,  of  liver,  1030 
Lobule  :    biliary,  898  ;   hepatic,  896  ;    para- 
central, 1486 
Localization  cerebral,  1427  ;    errors  in  diag- 
nosis, 1431 ;  radicular,  1592 
Locomotor  ataxy,  1243 
Locomotor  system,  diseases  affecting,  2018 
Lumbar  neuralgia,  1552  ;   puncture,  1454 
Lung,  actinomycosis  of,  1848  ;   anatomy  of, 
117 ;    aspergillosis  of,   207 ;    cancer, 
213  ;  congestion,  118  ;  disease  of,  117  ; 
emphysema,      159 ;       fibrous,      130 ; 
hsemorrhagic,   154 ;    hepatization  of, 
82  ;    hydatid  cyst,  219 ;    infarcts  in, 
145 ;     oedema,    161  ;     pseudo-tuber- 
culosis,   207  ;     splenization    of,    82  ; 
syphihs,  231  ;  tuberculosis,  176 
gangrene   of,    149 ;     bacteriology,    152 ; 
forms    of,    150,    151 ;     pathogenesis, 
151 ;  symptoms,  153 
Lupus,  15  ;  of  anus,  830 
Lymphadeiua,  1885 
Lymphadenoma,  1894 
Lymphatism,  2008 
Lymph-glands,  tuberculosis  of,  2010 
Lymphocytes,  1872 
Lymphocytosis  of  cerebral-spinal  fluid,  1255, 

1410 
Lymph,  scrotum  in  filariasis,  2016 

vaccine,  1617 
Lysis,  1668 
Lyssse,  1836 


M 

Maculae,  leprous,  1827 

Main :  en  griffe,  1278 ;  en  pince,  1275 ;  en  singe 

(monkey's  hand),  1278  ;  en  trident,  1600 
Maize,  poisoning  by,  2114 
Malaria,    1796 ;     aetiology,    1800 ;     chronic 

form,  1815  ;    haematozoon,  1797  ;    haemo- 

globinuric  fever,  1810  ;  intermittent  fever, 

1804 ;     larval    form,     1816 ;     pernicious 

fever,  1811 ;  pathological  anatomy,  1817  ; 

remittent  fever,  1807  ;   treatment,  1819 
Malarial  cachexia,  1815  ;   nephritis,  1816 
Mallein,  1843 
Mania,  acute,  1402 
Marriage  in  tuberculosis,  189 
Marrow-bone  :    in  leukaemia,  1889 ;    in  per- 
nicious anaemia,  1883  ;   in  malaria,  1817 
Masked  tuberculosis  of  tonsils,  645 
Mastication,  muscles  of,  paralysis  of,  1597 
Mastodynia,  1507 
MastzeUen,  1880 
Measles,  1645  ;     broncho -pneumonia,    1650  ; 

diagnosis,    1654 ;     noma,     1652 ;     ocular 

compHcations,    1652 ;     symptoms,    1646 ; 

treatment,  1657 ;   tubercolosis,  1651 
Measly  pork,  2012 
Meckel's  diverticulum,  839 
Mediastinal  pleurisy,  347,  357  ;    syndrome, 

347,  389  ;  syphHoma,  392 
Mediastinum,  affections   of,    387 ;    tumours, 

of,  387 
Medulla,  nuclei  in,  1337 
Meloena  :  in  cancer  of  bowel,  837  ;  in  cancer 

of  stomach,  726  ;   in  duodenal  ulcer,  832 ; 

in  exulceration,  692  ;  in  Tilcer,  702 
Melan^mia,  1817 
Melanodermia,  1234,  1237 
Membrane,  germinative,  of  hydatid  cyst,  961 
Membranous  entero-typhlo-cohtis,  798 
Meniere's  vertigo,  1345 
Meningeal  haemorrhage,  1467  ;  permeability, 

1458 
Meningitis  : 

acute,  non-tubercular,  1441 ;  chronic, 
1463  ;  cerebro-spinal,  1444 ;  aetiology, 
1451  ;  bacteriology,  1459  ;  description, 
1452 ;  diagnosis,  1459 

spinal,  1318  ;  syphilitic,  1397 

tubercular,     1437 ;    aetiology,    1437 ;    de- 
scription, 1438 ;  diagnosis  by  laboratory 
methods,  1456 
Meningococcus,  1459 
Meningo-encephalitis,  chronic,  1404 
Meningo-myelitis,  diffuse,  1301 
Meralgia,  1560  ;   paraesthetic,  1660 
Mercurial  poisoning,  2090 
Mercurial  stomatatis,  553 
Mercury,  treatment  by,  2116 
Mesenteric    glands,    tuberculosis   of,     867 ; 

in  typhoid  fever,  1720 
Metallic  tinkling,  385 
Metalloscopy,  1497 
MetaUotherapy,  1497 


INDEX 


2147 


M^taniorism.  I  Ml 

Mtleorirtin   in    inti-stinul  ocfltision,   841  ;    in 

fHritonitiB.  8G1  ;   in  typhoiti  (over.  Kit}? 
Mrthi.d  :       lirnnd'8     (cold      baths),      1722; 

Friu'nkol'8    (in    tabos),    \2{\r> ;     HiilTkim-V 

(.•itti'iiuiitiou     of     roiniua    bmiJliiw),   1704; 

Zifhl's  (stainiiif;  tiilxTile  bacilli),  J70 
Miorolipomatosis,  1853 
•*  Miiiosfupio  appindii  itis,"  808 
Miliary   absoesst-s   in    typhoid    fever,    1R96 ; 

aneurysms,   1392;   tubercles,  1.16;    tubti- 

oulosis,  acutf.  2u;{ 
Miliary  fever,  1  ().'>'.( 
Milk,  in  Bright's  disease,  1J:<!>;    in  typhoid 

fever,  172-t ;   tubercular  infection  from,  189 
Miner's  anspraia,  1883  ;   luiit;,  142 
MitralinsulKcieiKy,43l ;  orifice, disease  of, 426 
Mononuclear  cells,  1879 
Monoplegias  (localization),  1429;  in  hysteria, 

1494 
Morbilli,  1G45 

Morbus,  coeruleus,  446, 1910;  coxae  senilis,  1929 
Morphinism,  107 

Mortality  :  in  appendicitis,  792  ;  in  cerebro- 
spinal meningitis,  1469  ;  in  typhoid  fever, 

1705  ;   in  yellow  fever,  1779 
Morvan's  disease,  1275 
Mosquitoes;    in  filaria^is,  2015;   in  malaria, 

1800  ;   in  yellow  fever,  1777 
Mouth,  diseases  of,  52 
Mouth -breathing,  586 
Mouth,  tuberculosis  of,  574 
Movable  kidney,  1228 
Movements  in  chorea,  1530  ;    choreiform,  in 

Basedow's  disease,  474 
Mucous  entero-typhlo-colitis,  798 
Mumps,  1766;  complications,  1759  ;  orchitis, 

1757 
Murmurs,  cardiac  : 

in  aortic  disease,  425  ;  in  mitral  disease, 
424 ;    in  pulmonary  valves,  446  ;    in 
tricuspid  insufSciency,   444 ;    in  tri- 
cuspid stenosis,  445 
crural  (double),  442  ;   extra-cardiac,  432 
Muscles,  diseases  of,  1599  ;    degeneration  of 
in  typhoid,   1700 
of  larynx,  71  :    paralysis  of,  71  ;   physi- 
ology of,  23 
Muscular   atrophy,    forms    of,    1599 ;     pro- 
gressive, 1276 
contractures,  in  hemiplegia,  1355,  1358  ; 
in  hysteria,  1495 
Muscular   dystrophies,    2037 ;     rheumatism, 

1931  ;   sense,  1249 
Musculo -spiral  nerve,  paralysis  of,  1588 
Mutism,  hysterical,  149S 
Myelitis  :    acute,  1291  ;    acute-difluse,  1302  ; 

chronic,  1305  ;  compression,  1317  j  syphi- 

btic,  1307 
Myelocytes,  1880 
Myelocythsemia,  1887 
Myocarditis  :    acute,  449 ;    experimental,  in 

typhoid  fever,  1692  ;    fatty  degeneration, 

451  ;    interstitial,  452 


Myociinlium  disenst^n  f»f.  440  ;    tub«rouloiiii 

of,  458 
Myopathies  primary.  2042 
Myopathy,  prognttsivo  atrophic,  2042 
Myosis  in  talie.s,  1246;   Hpecial,  1246 
Myotonic  reaction,  Krb'M,  2036 
MyxcBdema,  20<i4  ;    idiocy,  2006 
Mythomania,  1615 

N 

Naeri,  915 
Nails  in  tabes,  1251 

Nasal  diphtheria,  4  ;  fossae,  diseases  of,  1 
Neck,  adenophlegmon  of,  1638 
Necrosis  of  bone  in  ty])hoid  fever,  1703 
phosphorus,  of  jaw,  2103 
syphilitic,    of    skull  :     anatomy,    1411  ; 
diagnosis,   1423;    of  external  syphi- 
loma,     1418 ;       endocranial,      1419 ; 
evolution,    1422 ;     hydatid    cyst    of 
cranial    bones,    1425 ;     osteotubercu- 
loma,  1424  ;   symptoms,  1418  ;  treat- 
ment, 1426 
Nematodes,  852 
Nephrectomy,  1165 
Nephritis  : 

acute,  1050  ;  aetiology,  1085  ;  diagnosis, 
1089 ;    prognosis,    1089 ;    symptoms, 
1088;  treatment,  1089. 
chronic,  1098  ;    parenchymatous,  1099  ; 
interstitial,      1102;      mixed,     1105; 
siippurative,  1212;   uraemia,  1124 
syphilitic,     early,     1165 ;      description, 
1170 ;     diagnosis,    1171 ;     symptoms, 
1169;   treatment,  1172 
syphilitic,  late,  1173  ;  description,  1175  ; 

treatment,  1179 
unilateral,  1144;    causes,  1165;    Luy's 

segregator,  1166  ;   treatment,  1169 
paratubercular,  1161 
tubercular,  1161 
Nephropexy,  1232 
Nephroptosis,  1229 
Nephrotomy,  1165 
Nerve  fibres,  lesion  of,  in  tuberculosis,  1472  ; 

roots  posterior  in  ataxia,  12t;l 
Nerves :     cranial,    1322 ;     common    oculo- 
motor,   1328,     1578  ;   fourth,    1583 ;     re- 
current, 516  ;  sixth,  1583  ;  trifacial,  1595 
Nervous    diarrhoea,    750 ;     dyspepsia    (gaa- 

troxia),  670  ;  system,  diseases  of,  1243 
Neuralgia,  153S  : 

cervico-brachial,  1547 ;  cervico-ocoi- 
pital,  1547  ;  cordis,  541 ;  in  dia- 
phragmatic pleurisy,  354 ;  epilepti- 
form, 1542  ;  in  hysteria,  1497  ; 
intercostal,  1549  ;  lumbar,  1552  ;  in 
malaria,  1644  ;  phrenic,  1548  ;  of  the 
trifacial  nerve,  1540  ;  aetiology,  1643  ; 
tic  douloureux,  1642 ;  treatment, 
1544 ;  syphiUtic,  1545 
Neurasthenia,  1616  ;  diagnosis,  1517  ;  symp- 
toms, 1516;  treatment,  1517;  varieties,  1517 


2148 


TEXT-BOOK    OF  MEDICINE 


Neuritis :  in  cerebral  tumours,  1386 ;  in 
diphtheria,  629  ;  of  the  femoro-cutaneous 
nerve,  1560  ;  infective,  1472  ;  oedematous 
in  tuljercular  meningitis,  1440  ;  optic  in 
tabes,  1246 ;  peripheral,  1471;  toxic, 
1472  ;   in  tuberculosis,  186 

Neuro-fibromatosis,   1600 

Neuropathy,  cerebro-cardiac,  1520 

Neuroses,  1477 

of  the  heart,  463  ;   occupation,  1537 

Neutrophiles,  1879 

Nicotine,  2109 

Night-blindness,  2088 

Ninth  nerve,  paralysis  of,  1566 

Nodes  :    Bouchard's,  739  ;   Heberdec's,  1930 

Nodules  in  leprosy,  1827 

Noma,  562 

Normoblasts,  854 

Nose,  bleeding  from,  18 

Nuclei  of  the  cranial  nerves,  1322 

Nucleus  :  caudate,  1350  ;  Dieter's,  1338 ; 
lenticular,  1350 

Nutmeg  liver,  903 

Nyctalopia,  2088 

Nystagmus  in  Friedreich's  disease,  1267 ; 
in  insular  sclerosis,  1289 ;  in  syringo- 
myelia, 1274 

O 

Obesity,  1995 

Obliterating  endarteritis,  1391  ^ 

Obliteration    of    common    bile   duct,    1013 ;  ■• 
diagnosis,  1021  ;    symptoms,  1020  ;   treat- 
ment, 1022 

Obstruction  by  gall-stones  :  of  the  intestine, 
1001  ;   of  the  pylorus,  1002 

Occlusion  :  intestinal,  838,  868  ;  aetiology, 
839 ;  diagnosis,  841  ;  prognosis,  842 ; 
s\'mptoms,  840  ;   treatment,  843 

Oculomotor  nerve,  paralysis  of,  1578 

Occupation  neuroses,  1537 

(Edema:  in  Bright's  disease,  1115;  in 
cardiac  disease,  429  ;  of  the  larynx,  57  ; 
of  the  lung,  161  ;  of  the  lung  after  thora- 
centesis, 265  ;  malignant,  1839  ;  in  acute 
nephritis,  1088 

Oesophageal  varices,  915 

CEsophagism,  655 

ffisophagitis,  654 

(Esophagus :  cancer,  656 ;  spasm,  625 ; 
stenosis,  655  ;    syphihs,  654  ;    ulcer,  659 

Oidium  albicans,  557 

Oliguria,  1143 
orthostatic,  1151 

Omentum,  cysts  of,  in  cancer  of  peritoneum, 
886  ;  fixation  of,  in  cirrhosis,  922  ; 
tumour  of,  in  tubercular  peritonitis,  866 

Ophthalmia,  gonorrhoeal,  2059 

Ophthalmoplegia,  external,  1586 ;  internal, 
1586  ;   progressive  nuclear,  1327 

Opium  poisoning,  2106 

Opotherapv  :  in  diabetes,  1981  ;  suprarenal, 
1240  ;   thjTToid,  2008 


Opsonic  method,  Wright's,  2130 
Optic    nerve,    atrophy    of,    primary,    1387 ; 
secondary,  1387  ;  in  tabes,  1246 
neuritis  :  in  brain  tumour,  1387  ;  in  syph- 
ilis 1399  ;  in  tubercular  meningitis,  1440 
Orchitis  :     gonorrhoeal,    2049 ;     in    mumps, 
1757  ;  scrofulous,  2011  ;  in  tonsilhtis,  581  ; 
in  typhoid  fever,  1696 
Osteitis  deformans,  2027 
Osteo-arthropathy,  hypertrophic  pidmonary, 

2020 
Osteomalacia,  2021 
OsteomyeHtis,  1701 
Osteoph^-tes,  1930 
Osteoporosis  in  tabes,  1252 
Otitis  : 

complications :    abscess  of    cerebellum, 

1339  ;   and  of  cerebrum,  1377 
influenzal,  1775  ;    in  measles,  1652  ;    in 
meningitis,  1442, 1448  ;  pneumococcal, 
130 ;    scarlatinal,   1639  ;    tubercular, 
187 
Oxalate  calculi,  1193 
Oxide  of  carbon,  poisoning  by,  2110 
Oxyuris  vermicularis,  852 
Oysters  and  typhoid  fever,  1715 
Ozsena  :    in  chronic  coryza,  3  ;    in  syphilitic 

rhinitis,  11  ;  tracheal,  18;   true,  17 
Ozsenous  pleurisies,  367 


Pachymeningitis,  1463  ;   cervical,  1320 

Pachy-pleuritis,  319 

Paget's  disease,  2027 

Pain  :  in  appendicitis,  767 ;  in  cancer  of 
stomach,  725  ;  in  pleurisy,  250  ;  in  pneu- 
monia, 125  ;   in  ulcer  of  stomach,  701 

Pains,  hghtning,  1243 

Palate,  paralysis  of,  in  diphtheria,  25 ;  per- 
foration of,  10,  569 

Palate,  tubercle  of,  576 

Palpitation  of  heart,  463 

Paludism  (Malaria),  1796 

Pancreas  :  calculi  of,  1061  ;  cancer  of, 
1059  ;  cancer  of  head  of,  1017  ;  cysts  of, 
1059 ;  diseases  of,  1058 ;  in  diabetes, 
1958  ;   haemorrhage  into,  1060 

Pancreatic  drama,  1069  ;   lithiasis,  1074 

Pancreatico  bdiary  syndrome,  1065 

Pancreatitis  and  its  relations  to  gall-stones, 
1062  ;  cytosteatonecrosis,  1069  ;  haemor- 
rhage, 1071  ;  exuberans,  1065 ;  stenosans, 
1065 

Paracentesis  :     abdominis,    921 ;    pericardii, 

406 
Paracholecystitis,  1024 

Paralyses  (localization),  1429 ;  alcoholic, 
2088 ;  alternate,  1329 ;  diabetic,  1961  ; 
diphtheritic,  625  ;  hysterical,  1494  ;  Jack- 
sonian  epilepsy.  1436  ;  leprous,  1776  ;  of 
the  nerves,  1563;  radicular,  1592;  satur- 
nine, 2095 ;  typhoid,  1698 ;  uremic, 
1128 


INDEX 


2149 


ParalvHis,    ncuto     asci-nilin?,     1298  ;     nculo 

"  .spinal,    in     adults,     1298  ;     agitans, 

1521 ;  MslluMiic  bulbar,  1H2I) ;  iif  cranial 

nerves,  i:i86 

faiiul,     ir>li3;     syphilitic,  early,    1571; 

late,  ITui) ; 
general.  MOl  ;    juvenile  general  ;    1408  ; 
anterior  spinal  nenoral,  1290;  pseudo- 
aleolinlic,     2087  ;      saturnine,     2095  ; 
sypliilitie,  1403;    in  taheties,  1251 
infantile,    1294;    labio-glossu-laryngcal. 
1322;    of  laryngeal    muscles,   71;    of 
motor  nerves  of  eye,  1578,  1583 
museulo-spiral,    1588;     diagnosiB    from 

lead  palsy,  2095 
Ocular  :  of  associated  movements,  1584  ; 
of   convergence,    1585 ;    in   diabetes, 
witli   pain,    19til  ;     in   sclero-gumma- 
tous     syphilis    of     brain,     1398 ;     in 
tabes,    1245 ;    in    tumours    of    brain, 
1387 
pseudobulbar,      1325;      pseudo-hyper- 
trophic  muscular,  2039 
radicular,    1592  ;     inferior   type,    1594 ; 

superior  type,  1593 
syphilitic  spinal   (Erb's)   1309  ;    c-f  tri- 
facial nerve,  1595  ;    of   velum  palati, 
625 
Paramyoclonus  multiplex,  1519 
I'araphasia,  1371 

i'araplegia  :    ataxo-spasmodic,   1271  ;    from 
compression    of    cord,     1317  ;      diabetic, 
1967  ;   diphtheritic,  626  ;   epidemic,  1305  ; 
spasmodic  family,  1266  ;  in  hsematomyelia, 
1315  ;  hysterical,  1494  ;  in  acute  myelitis, 
1303  ;  in  tabes,  1251 
Parasitic  infection,  2012 
Paratyphoid  appendicitis,  1682 
Parenchymatous  nephritis,  1099 
Parkinson's  disease,  1521 
Parotiditis,     1756 ;      in     pneumonia,     130 ; 

saturnine,  2101  ;  typhoid,  1698 
Paroxysmal  haemoglobinuria,  1223 
Paroxy'smal  tachycardia,  465 
Pasteur's  original  ideas,  2130 
Patches  :   erysipelatous,  1748  ;   mucus,  567  ; 

white,  in  smokers,  565 
Patellar  reflex,  1244 
Pathomimia,  1513 
Pectoriloquy,  aphonic,  252 
Pediculi,  1238 
Peliosis  rheumatica,  1908 
PeUagra,  2113 

Pelviperitonitis,  gonorrhoea!,  2051 
Penis,  fulminant  gangrene  of,  2076 
Perforating  ulcer :     buccal,    573 ;     diabetic, 

1960  ;  palmar,  1598  ;  plantar,  1252 
Perforation  :  of  appendix  in  typhoid  fever, 
1682  ;  in  duodenal  ulcer,  833  ;  of  intes- 
tine in  appendicitis,  755  ;  of  nasal  sep- 
tum, 9  ;  in  typhoid  fever,  1673  ;  of  ulcer 
of  stomach,  709  ;  of  vaidt  of  palate,  569  ; 
of  velum  palati,  10 
Periangiocholitis,  981 

II. 


I'.-riarfcritiR,  501 
Pericardidl  ml),  403 

PoricarditiH,    acute,    401;     diannofiiH,    405; 
Hyni|)toms,  402  ;    treatment  405  ;   chronic, 
407  ;    dynphagia  in,  404  ;    in  rh<  iirnatiHTii, 
1920  ;    ])uisuM  paradoxus  in,  404  ;    tuber- 
cuhjus,  405  ; 
Pericardium,  adherent,  407 
Pericholecystitis,  1010 
Perichondritis  in  typhoid  fever,  f690 
Perigastritis,  suppurative,  in  cancer,  722 
Perihepatitis,  8(54 
Perimeningitis,  acute  spinal,  1319 
Perinephritis,  1207;    calculous  1207;    fibro- 

fatty,  1208  ;   supjjurative,  1209 
Periostitis  in  gonorrhoea,  2058 
Peripheral  neuritis,  1471 ;  tubercular,  186 
Perisplenitis,  1865 

Peritoneum  :    anatomy  of,  860  ;    cancer  of, 
880 ;    diseases  of,   859 ;    tuberculosis  of, 
863,  865  ;   hydatid  cysts  of,  888 
Peritonitis,    859 ;     appendicular,    860 ;     in 
gall-stones,     1011  ;      in     gonorrhoea, 
2050  ;   partial,  862 
from  perforation,  860  ;    in  appendicitis, 
771;      in     cholecystitis,     1689;      in 
enteritis,  863;    in  gall-stones,   1011; 
in  typhoid  fever,   1673  ;    in  ulcer  of 
duodenum,    833 ;     in    ulcer    of    the 
stomach,  703,  709 
pneumococcal,  872  ;   streptococcal,  880  ; 
tubercular,  863 
Peritonsillitis,  579 
Peritj'philitis,  fibro-adipose,  817 
Pcrles  (Liiennec's),  110 
Permeability :     meningeal,     1458 ;     pleural, 

250  ;  renal,  1134 
Pernicious  anremia,  1882  ;   malaria,  1811 
Petechias :     in   plague,    1784 ;     in    relapsing 
fever,  1735  ;   in  scurvy,  1913  ;   in  typhus, 
1732 
Petit  mal,  1479 
Peyer's  patches,  1718 
Phagedsena,  2066  ;   of  velum  palati,  640 
Pharyngitis,  acute,  577  ;  chronic,  585 
Pharynx,  diseases  of,  577 
Phimosis  in  diabetes,  1955 
Phlebitis,    488  ;     of    sinuses    in    cerebellar 
abscess,     1342 ;     syphilitic,    493 ;     rheu- 
matic, 1920 
Phlegmasia  alba  dolens,  488 
Phosphatic  calculi,  1192 
Phosphorus  poisoning,  2102 
Phototherapy  :    in  lupus,   17  ;    in   measles, 

1658  ;  in  variola,  1615 
Phrenic  nerve,  neuralgia  of,  1548 
Phthisis  : 

fibroid,  195 ;  larval,  190  ;  laryngeal, 
40  ;  chronic  pulmonarj',  176  ;  pneu- 
monic, 198  ;  subacute,  198 
pulmonary :  granulations,  176 ;  infil- 
trations, 177  ;  cavities,  178  ;  aneurys- 
mal dilatation,  179 ;  calcification, 
179  ;   fibrosis,  179  ;   pleurisy  in,  179  ; 

136 


2150 


TEXT-BOOK   OF  MEDICINE 


bacteriology  of,  180  ;  sputum  in,  182  : 
fever  in,  183  ;  pulse  in,  183  ;  haemop- 
tysis in,  184 ;  genital  functions  in, 
185 ;  contagion  in,  188  ;  lesions  of 
other  organs,  186 ;  course,  187 ; 
treatment,  191 ;  tuberculin  (Koch's) 
in,  193 

Physiological  albuminuria,  1150 

Pigment,  biliary,  1034 

Pigmentation  of  skin  :  in  Addison's  disease, 
1234  ;  from  arsenic,  2106  ;  in  Base- 
dow's disease,  475  ;  in  cirrhosis,  930  ; 
in  solerodermia,  1603  ;  in  vagabond's 
itch,  1238 
of  viscera  in  pellagra,  2115 

Pituitary  body  in  acromegaly,  2025 

Placenta  truffg,  1904 

Plague,  1781 

Plasmodium  malarise,  1798 

Pleura,  diseases  of,  248 

Pleural  effusion :  Bacelh's  sign  in,  252 ; 
displacement  of  heart  in,  252  ;  sudden 
death  in,  259 ;  thoracentesis,  262, 
291 ;  inexhaustible,  319  ;  hsematoma, 
294 

Pleurisy,  acute  sero-fibrinous,  248  ;  aerolar, 
354 ;  bacteriology,  249 ;  clinical 
forms,  257 ;  course  and  duration, 
254  ;  cyto-diagnosis,  275  ;  diagnosis 
as  to  its  tubercular  nature,  268 ; 
gangrenous,  375 ;  loculated,  354 ; 
polymorphous,  354  prognosis,  255 ; 
putrid,  367,  370 ;  sero-diagnosis, 
274  ;  symptoms,  250  ;  thoracentesis, 
258 
varieties  :  appendicular,  358 ;  biliary, 
1012;  in  Bright's  disease,  1123; 
diaphragmatic,  353  ;  foetid  and  gan- 
grenous, 343,  367 ;  hsemorrhagic, 
284 ;  interlobar,  335 ;  mediastinal, 
347;  with  puriform  effusion,  316; 
purulent,  307 ;  pulsating  empyema, 
327  ;  rheumatic,  257  ;  syphilitic,  356  ; 
tubercxdar  purulent,  314 

Pleuroperitoneal  tuberculosis,  864 

Plexus,   brachial,  anatomy  of,  1592 ;    solar, 
in  Addison's  disease,  1238 

Pneumococcal  pleurisy,  purulent,  312 

Pneumococcia  of  the  stomach,  676 

Pneumococcus,  123 

Pneumokoniosis,  142 

Pneumonia  : 

in  the  aged,  132  ;  agglutinative  reaction 
in,  124 ;  alba,  244 ;  apical,  131  ; 
arthritis,  129 ;  central,  131  ;  in  chil- 
dren, 132 ;  chronic,  139 ;  chnical 
varieties,  132  ;  double,  131  ;  endocar- 
ditis, 127 ;  engorgement,  121 ;  he- 
patization, 122  ;  lymphangitis,  123  ; 
meningitis,  129  ;  nephritis,  129  ;  occu- 
pation, 142  ;  otitis,  130  ;  pericarditis, 
128 ;  peritonitis,  129 ;  pleurisy, 
127 
acute  lobar  :    bacteriology,   123  ;    clini- 


cal signs,  125  ;  diagnosis,  136  ;  patho- 
logical anatomy,  121  ;  treatment,  138  ; 
varieties,  131 

Pneumonic  plague,  1784 

Pneumopathy,  syphilitic,  242 

Pneumorrhagia,  154 

Pneumothorax,  383 ;  partial,  383 ;  from 
putrefaction,  386 

Pneumotomy,  154 

Podagra,  1938 

Poikilocytes,  1883 

Point:  Erb's,  1592  j  McBurney's,  769; 
spinal  (Trousseau's),  1549 

Poisoning  by:  arsenic,  2104;  grain,  2113; 
lead,  2094  ;  mercury,  2090  ;  oxide  of  cau- 
bon,  2110 

Polio-encephalitis,  1321 ;  acute  and  subacute, 
1335 ;  chronic  inferior,  1322 ;  superior, 
1327;   syphilitic,  1330 

Poliomyehtis,  acute  :  in  adults,  1248  ;  infan- 
tile, 1294 

Pollakiuria,  1111 

Polyadenoma,  gastric,  723 

Polyarthritis,  deformans,  1926 

Polydipsia,  1927,  1957 

Polyneuritis,  1283,  1471 

Polynuclear  cells,  1879 

Polyphagia  in  diabetes,  1958,  1989 

Polypi :  gastric,  723  ;  laryngeal,  39 

Polysarcia,  1995 

Polyuria:  in  Bright's  disease,  1112;  dia- 
betic, 1957;   hysterical,  1502 

Pons,  disease  of,  1321 

Porencephalia,  1378 

Portal  vein,  lesions  of,  in  cirrhoses,  909 

Post-operative,  streptococci  a,  1744 

Postparalytic  hemichorea,  1360 

Potassisemia,  1125 

Potassium  iodide,  2il8 

Pott's  disease,  1450 

Pregnancy  :  appendicitis,  781  ;  hydatid  cyst 
of  peritoneum,  869 ;  gall-stones,  993 ; 
nephritis,  1087 ;   pneumonia,  134 

Pre- oedema,  1116 

Presystolic  murmur,  425 

Professional  spasms,  1537 

Prognathism,  2023 

Progressive  atrophic  myopathy,  2042  ;  mus- 
cular atrophy,  1276 ;  muscular  dystro- 
phies, 2037  ;  osteitis  deformans,  2027  ; 
pernicious  ansemia,  1822 

Prophylaxis  against :  cholera,  1770  ;  plague, 
1787 ;  scurvy,  1914 ;  smallpox,  1615 ; 
yellow  fever,  1729 

Pruritis  in  diabetes,  1955  ;  in  jaundice,  1032  ; 
in  uraemia,  1125 

Pseudo-actinomycosis,  1850 

Pseudo-bulbar  paralysis,  1325 

Pseudo-coUc  :   hepatic,  1000  ;   renal,  1196 

Pseudo-diphtheria,  620 

Pseudo-gonococcus,  2046 

Pseudo-hypertrophic   muscular   paralysis, 
2039 

Pscudo-Iipoma,  1932 


INDEX 


2151 


Pseudoparalysis  :  sypliilitio  genoral,  1402  ; 
Bypbilitic  Iiibro-j^ldssu-luryiigeal,  1401 

Pscudo-phthibis,  J'JU 

P8eudo-j>orcncephaly,  1379 

PseDdo-rheumatisin,  ii)33 

Pseudo-stranguhitiun  of  gut,  840 

Pseudo-tabes,  1255  ;  alcoholic,  2088  ;  neurae- 
tlienic,  1515 

Psittacosis,  1853 

PsortMitoria  iu  cholera,  1767 

Psoriasis,  lingual,  565 

Psychoses :  in  Basedow's  disease,  476 ; 
choreic,  1630  ;  polyneuritic,  1475 

Ptomaines,  1049 

Ptoses  :  visceral,  748  ;  ptosis,  1245,  1581  ; 
pseudo-paral.vtic,  ^504  ;  in  tubercular 
meningitis,  1440 

Ptyalism  (in  Bright's),  1123 

Pterygoid  muscles  :  paralysis  of,  1324 

Puerperal  state  and  diabetes,  1970 ;  gall- 
stones, 993  ;  icterus,  1045  ;  renal-calculi, 
1193;  peritoneal  infection,  85'J;  strepto- 
coccia,  1744 

PiUmonary  apoplexy,  154,  428  ;  artery,  em- 
bolism of,  144  ;  hfemorrhage,  155  ;  oritice, 
lesions  of,  445  ;  osteo-arthropathy,  2026 

Pulsating  abscesses,  334 

Pulsating  empyema,  327 

Pulse  :  capillary,  441  ;  Corrigan's,  441  ;  pul- 
sus paradoxus,  388 ;  permanently  slow, 
466  ;  in  typhoid  fever  (dicrotic),  1668 

Puncture,  lumbar,  1454 

Pupil,  Argyll-Robertson,  1246 

Pupils  unequal  in  general  paralysis,  1507  ; 
in  aneurysm,  513 

Purpura,  1907  ;  in  Basedow's  disease,  475  ; 
exanthematic,  1908  j  haemorrhagica,  1907  ; 
rheumatoid,  1908  ;   simplex,  1907 

Pustule:  malignant,  1840;  vaccinal,  1618; 
in  variola,  1610 

Putrid  pleurisy,  370 

Pysemic  abscess  of  liver,  977 

Pyelitis,  1205,  1212 

I^elonephritis,  1205 

Pylephlebitis,  928  ;   calculous,  1010 

Pylorus,  constriction  of,  740  ;  spasm  of,  669  ; 
stenosis,  1002 

Pyopneumothorax,  subphrenic,  774 ;  ap- 
pendicular, 358  ;  in  ulcer  of  the  stomach, 
704 

Pyopneumohydatid,  966 

Pyramidal  tract,  anatomy  of,  1351 

Pyramid  :  of  Ferrein,  1079  j  of  Malpighi, 
1077 

Pyrosis,  2087 

Pyuria,  tubercular,  1158 

Q 

Quarantine,    in    cholera,    1770;     in    yellow 

fever,  1780 
Quartan  fever,  1805 
Quincke's  lumbar  puncture,  1454 
Quinine  in  malaria,  1819 


Quinsy.  580 
Quotidian  fovor,  1805 

R 

Rabies,  1834 

Radial  (musculo-spiral)  paralysis,  1688 

Radicular  paralysis,  1592 

Ra<iio8Copy  :  in  calculous  cholecystitis,  1009  ; 
in  renal  calculi,  1200;  in  interlobar 
pleuri.?y,  346  ;  in  gangrene  of  lung,  164 

Radiography,  in  gangrene  of  lung,  154 

Radiculitis,  1561 

Rale,  crepitant,  126 

Rashes,  drug,  1655;  in  glanders,  1843;  in 
measles,  1647  ;  in  rubella,  1659  ;  in  scarlet 
fever,  1625;  in  smallpox,  1609;  in 
syphilis,  1054;  in  typhoid  fever,  1667; 
in  typhus,  1732;  in  vaccination,  1619; 
in  varicella,  1622 

Ray  fungus,  1792 

Raynaud's  disease,  1604 

Reaction  :  of  degeneration,  1474  ;  mvotonic 
(Erb's),  2036 

Recklinghausen's  disease,  1853 

Recrudescence  of  fever  during  convalescence 
in  typhoid  fever,  1730 

Rectal  crises  in  tabes,  1254 

Rectum,  cancer  of,  838 

Recurrent  larjTigeal  nerve  and  aneurysm, 
528 

Red  softening  of  brain,  1364 

Reduplication  of  heart-sounds,  423,  425 

Re-education  of  movements,  1265 

Reflex :  exaggeration  of,  1358 ;  patellar, 
1244  ;  plantar  cutaneous,  1363  ;  of  tendo- 
Achillis,  1245 

Reflexes  :  in  amyotrophic  lateral  sclerosis, 
1286 ;  in  combined  spasmodic  sclerosis, 
1270;  in  Friedreich's  ataxy,  1267;  in 
hereditary  cerebeDar  ataxy,  1268 ;  in 
poliomyelitis,  1295  ;  in  polyneuritis,  1474  ; 
in  secondary  descending  lateral  sclerosis, 
1286  ;   in  tabes,  1244. 

Relapse  in  typhoid  fever,  1704 

Relapsing  fever,  1733 

Remittent  fever,  1807 

Renal  calculi,  1191;  colic,  1193;  sand,  1191; 
syphUis,  1165 

Renal  fistulse,  1210 ;  ectopia,  1229 ;  in- 
sufficiency, 1133;  permeability,  1134 

Resolution  in  pneumonia,  122 

Resonance,  skodaic,  261 

Respiration  :  amphoric,  182,  385 ;  puerile, 
252  ;   savring,  49 

Respiratory  system,  diseases  of,  1 ;  paralvsis, 
1324 

Retention  of  chlorides,  1116 

of  urine  :  in  compression  of  the  spinal 
cord,  1317  ;  in  gonorrhoea,  2047  ;  in 
tabes,  1264 

Retinal  hsemorrhage  in  malaria,  1816 

Retinitis  :    diabetic,  1961  ;   leuksemic,  1891 

Retraction  of  head  in  meningitis,  1542  ;  of 
palmar  fascia,  1959 

186—2 


2152 


TEXT-BOOK   OF  MEDICINE 


Retropharyngeal  abscess,  584 

Retropulsion,  1522 

Reves  d'accAs  in  epilepsy,  1479 

Rheumatism :  abarticular,  1930 ;  acute 
articular,  1916  ;  atrophic  deltoid,  1931  ; 
cerebral  form,  1921  ;  chronic,  1925  ;  endo- 
carditis, 1920  ;  gonorrhoeal,  2054  ;  fibrous 
chronic,  1930 ;  infective,  1933  ;  nodular, 
1926  ;  partial,  1929  ;  relation  with  chorea, 
1526  ;    symptoms,  1917  ;    treatment,  1925 

Rhinitis,  3  ;   fibrinous,  5  ;  syphilitic,  9 

Rhino-bronchitis,  spasmodic,  115 

Ribs,  resection  of,  in  empyema,  334 

Rickets,  2018 

Rigors,  in  malaria,  1804 ;  in  pneumonia, 
125 ;  in  pyelitis,  1206 ;  in  tuberculosis, 
183 

Risus  sardonicus,  1790 

Rosary,  rachitic,  2020 

Roseola  :  from  drugs,  1655  ;  ros4ole  saison- 
niire,  1659  ;  syphihtic,  1654 

Rose  spots  in  typhoid  fever,  1667 

Round  worms,  852 

Rubella,  1658 

Rupture  :  of  aorta,  508  ;  of  chordae  tendinese 
427  ;  of  gaU-bladder,  999,  1011  ;  of  heart, 
454  ;  of  muscles  in  typhoid  fever,  1700  ; 
of  spleen,  1736 

S 

Sabulous  entero-typhlocohtis,  798 

Saccharomyces  albicans,  557 

Sahne  injections,  2123 

Salivation  :  mercurial,  554 ;  in  variola, 
1610 

Salpingitis,  2050 

Sand  :  intestinal,  801  ;  renal,  1191 

Sarcinae,  739 

Sarcoma  :  of  brp,in,  1384  ;  of  heart,  458  ;  of 
of  liver,  949  ;  of  nasal  fossae,  6  ;  of  tongue, 
668 

Saturnine  aneemia,  2094 ;  asthma,  2101  ; 
encephalopathy,  2097  ;    nephritis,  2099 

Saturnism,  cerebro-spinal,  2097 

Scarlatina,  1624  ;  angina,  1626,  1630  ;  anuria, 
1636  ;  complications,  1630  ;  defaced,  1629; 
desquamation,  1627  ;  dropsy,  1637  ;  erup- 
tions, 1625  ;  hsematuria,  1635  ;  invasion, 
1625  ;  maUgnant,  1628  ;  nephritis,  1633  ; 
otitis,  1639  ;  pseudo-rheumatism,  1637  ; 
puerperal,  1641 

Sciatic  nerve,  anatomy  of,  1552 

Sciatica,  1552  ;   syphilitic,  1555 

Scirrhous  cancer,  of  lung,  214 ;  of  stomach, 
724 

Sclerema,  1603 

Sclerodermia,  1603 

Sclerosis,  amyotrophic  lateral,   1285  ;    com- 
bined   forms,    1269 ;     insular,    1287 ;     of 
lateral  columns,  1284  ;  of  posterior  column, 
1257  ;  of  stomach,  665 
Scolex,  962 
Scoliosis,  1552 


Scorbutus  (scurvy),  1912 

Scrofula,  2008 

Scrofnhte  de  verole,  13 

Scury,  1912  ;  infantile,  1914 

Secondary,  contracture  in  hemiplegia,  1358  ; 

fever  in  smallpox,  1610 
Semilunar  space,  Traube's,  253 
Sense  of  attitudes,  1249 
Sensibihty,  recurrent,  1589 
Septicsemic  plague,  1784 
Sero-diagnosis  :    method,  1708  ;    in  cholera, 
1770 ;     in    psittacosis,    1856 ;     in    tuber- 
culosis, 274 
Serotherapy  :    in  croup,  54  ;  in  diphtheria, 
615 ;    in   dysentery,   852 ;    in   erysipelas, 
1755 ;      in     hBemoglobinuria,     1227 ;      in 
leprosy,     1831.;      in    plague,     1786;      in 
scarlatina,    1645 ;    in  tetanus,    1795 ;    in 
typhoid  fever,  1726 
Serum  :   anti-anthrax,  1842  ;   artifical,  2123  ; 
hsemolytic,  hepatolytic,  and  nephrolytic, 
1831 
Sexes  :   relative  proportion  affected  in  chlo- 
rosis,   1894 ;     in   chorea,    1526 ;     in   exo- 
phthalmic goitre,  480  ;  in  hysteria,  1492  ; 
in  general  paralysis,  1408 
Shocks,   electric,  in  patients  with   Bright's 

disease,  1114 
Sialorrhcea,  ursemic,  1123 
Sickness,  sleeping,  1821 
Siderosis,  143 

Sigmoid  valves,  lesions  of,  441 
Sign  :  AxgyU-Robertson's,  1246  ;  Babinski's, 
1363  ;     Bolognini's,   1654  ;    Kernig's,   1453  ; 
Koplik's    1654 ;     Romberg's  temporal,   in 
Bright's  disease,  114  ;    Trousseau's,  1446  ; 
Westphal's,  1244 
Signe  du  peaiKier,  1363 
Sinus    thrombosis,    in    chlorosis,    1898 ;     in 

otitis  media,  1342 
Sixth  nerve,  paralysis  of,  1583 
Skin,  dystrophies,  1598 
Skodaic  resonance,  251 

SkuU,  hydatid  of,  1425  ;    osteo-tuberculoma 
of,  1424  ;   syphilitic,  necrosis  and  perfora- 
tion of,  1410 
Slackening  of  nutrition,  1953 
Sleep,  nervous,  1509 
Sleeping  sickness,  1821 
vSmallpox.     See  variola 

Softening  :    of  bones  in  osteomalacia,  2021 ; 
cerebral,  causation,  1364 ;    onset,  sudden, 
1367  ;  gradual,  1368  ;  in  tubercular  menin- 
gitis, 1438  ;   of  spinal  cord,  1303 
Somnambulism,  1509 
Sordes,  1667 
Sound,  skodaic,  251 
Space,  Traube's,  253 

Spasms  :  functional,  of  glottis,  69  ;  in  hydro- 
phobia, 1836  ;   in  hysteria,  1495  ;   of  ceso- 
phagus,  655  ;    of  pylorus,  669 ;    reflex  of 
pulmonary  vessels,  443 
Spastic  paraplegia,  1271 
Spectroscope,  use  of,  1035 


INDEX 


2153 


Speech  :     in    biill)ar    paralysis,     1323 ;     in 
goneriil    j)artii_vsis,     1-M)7  ;     in    hereditary 
atuxy,  1-1)7  ;   in  iiisiilar  sclerosiH,  125M) ;  in 
perforation  of  palate,  .')72  ;    in  tonsillitis, 
578 
Sphygmomanometer,  548 
b^pinal :  accessory  nervo,  lesions  of,  71  ;  cord, 
diseases  of,   1243  ;    compression  of,  1317  ; 
mcniniiitis,  13 IH 
Sijirals.  I'virsclininnn's,  HO 
Spiriiliuu  :     of   cholera,    1703  ;     Obermeier's 

1733 
Spleen,  in  cirrhosis  of  liver,  937  ;   leuktemia, 
1873 ;     in    malaria,    1873  ;     movable, 
1815;    in  typhus,   1783;    in  typhoid 
fever,  1720 
tumours    of :     epithelioma,     1875 ;    hy- 
datid    cj'st,    1858 ;     leucocythaemic, 
1873 ;     malaria],     1873  ;     tubercular, 
1874 
Splenectomy,  blood  studies  in,  1866 
Splenic  leukaemia,  1SS7 
Splenization  of  lung.  82 
Splenomegalia  primary,  1874 
Splenoptosis.  748 

Spores  :  anthrax,  1888  ;   tetanus,  1793 
Sporotrichosis,  1850 

Sputum    (albuminous)    after    thoracentesis, 
265  ;  in  anthracosis,  142  ;  in  asthma, 
1 10  ;    in  bronchiectasis,  97  ;    in  acute 
bronchitis,    76 ;     in    chronic,    92  ;    in 
pseudo-membranous  bronchitis,   101  ; 
in  cancer  of  lung,  214  ;   in  gangrene 
of  lung,  151,  153  ;   in  hepatic  abscess, 
981  ;  in  phthisis,  182  ;  in  pneumonia, 
125 
currant  jelly,    214 ;     nummular,    182 ; 
pearls.  111  ;   rusty,  125 
St.  Vitus'  dance,  1523 
Staphylococcal  vaccine,  1755,  2133 
Staphylococci,    in    broncho-pneumonia,    85 ; 
in  diphtheria,  600;    in  endocarditis,  413; 
in  pleurisy,  314  ;  in  tonsillitis,  581 
Status  choreicus,    1535  ;    epiiepticus,   1479  ; 

hystericus,  1494 
Steatosis  of  liver,  976 
Stegomya  fasciata,  1777 

Stenosis  of  orifices  :  aortic,  441  ;  mitral,  426  ; 
pulmonary,  445  ;  pyloric,  1002  ;  tricuspid, 
443 
Steppage-gait,  1473,  1829,  2089 
Stigmata  in  hysteria,  1508  ;  in  neurasthenia, 

1516 
Stokes-Adams  disease,  467 
Stomach  :  cancer  of,  724  ;  chronic  catarrh 
of,  665;  contents,  examination  of,  730; 
dilatation  of,  738  ;  disappearance  of  hy- 
drochloric acid,  731  ;  diseases  of,  662 ; 
exulceration,  684 ;  haematemesis,  726 ; 
haemorrhage  from,  746 ;  hour  glass  (en 
bi^sac),  739  ;  lavage  of,  672  ;  pain,  725  ; 
phlegmasia,  727 ;  polyadenoma,  723 ; 
stenosis,  664 ;  svphilis,  734 ;  ulcer,  674, 
698 :   vomiting,  726 


Stomatitis,  aphthous,  601  ;  erythematous, 
552 ;  in  nieaHles,  1651  ;  morourial, 
563 ;  thruHh,  657  ;  ulceromembranous, 
555 

Stools,  in  dysentery,  849  ;  in  jaundice,  1031  ; 
in  phosphorus  poisoning,  2102  ;  rice  water, 
in  cholera,  1769;  in  typhoid  fever,  1007; 
in  ulcer  of  stomach.  70:i 

Strabismus  :  convergent,  1583  ;  divergent, 
1581 

Strangulation  of  bowel,  839 ;  of  kidney, 
1230 

Strawberry  tongue,  1629 

Streptococci,  in  diphtheria,  599  ;  in  endo- 
carditis, 413  ;  in  peritonitis,  880 ;  in 
pleurisy,  311  ;   in  tonsillitis,  581 

Streptococcal  infection   of    the    blood,   1743 

Streptococcia,  1743;  medical  1745;  post- 
operative, 1744  ;  puerperal,  1744  ;  penis, 
2080 

Streptococcus  erysipelaiis,  1748 

Streptothrix,  Eppinger's,  211 

Stricture,  of  intestine,  839 ;  of  oesophagus, 
656 ;  of  pylorus,  738 ;  of  sigmoid  and 
rectum,  839  ;   of  urethra,  2049 

StjTia,  arsenic  eating  in,  2043 

Subacute  combined  degeneration  of  the 
spinal  cord,  1271 

Subphrenic  abscess,  704  ;   empyema,  358 

Subsultus  tendinum,  1670 

Succussion,  hippocratic,  385  ;  splash  in  dila- 
tation of  stomach,  739 

Sudoral,  form  of  tj-phoid  fever,  1670 

Sugar  in  urine,  1956 

Superacute  peritonitis,  832 

Suppression  of  urine  (anuria),  1201 

Superheated  air,  treatment  with,  2125 

Suprarenals,  disease  of,  1233  ;  insufficiency 
of,  1241  ;  lesions  of,  1238 ;  mediastinal, 
392 

Suppurative  nephritis,  1212 ;  tonsillitis, 
579 

Suspension  in  tabes,  1265 

Sweat,  in  acute  rheumatism,  1919 ;  in 
malaria,  1804 ;  in  phthisis,  183 ;  in 
rickets,  2020  ;  in  typhoid  fever,  1671 

Sweating  sickness,  1659 

Sydenham's  chorea,  1523 

Symmetrical  gangrene,  1604 

Sympathetic  ganglia  in  Addison's  disease, 
■^1238 

Symptomatic  purpura,  1908 

Syncinesia,  1359 

Syncope  :  hysterical,  1494  ;  in  pleural  effu- 
sion, 267  ;  in  tj'phoid  fever,  1706 

Syndrome:  Bonnier's,  1338;  Brown-Se- 
quard's.  1307 ;  cerebellar,  1344 ;  Erb's, 
1336 ;  Korsakoff's,  1475 ;  labyrinthine, 
1345;  Little's,  1378;  mediastinal  347, 
389  ;  pancreaticobiliary,  1065  ;  of  para- 
doxical ischuria,  1312  ;  of  sleeping  sicfaiess, 
1823;  Weber's,  1336 

Syphilides :  of  lips,  564 ;  of  nose,  7 ;  of 
tongue,  565 


2154 


TEXT-BOOK   OF  MEDICINE 


Syphilis : 

chancre,  2067  ;  setiology,  2067  ;  bacteri- 
ology,    2072 ;      conceptional,     2067 ; 
description,    2068  ;     diagnosis,    2069  ; 
treatment,  2116 
of  aorta,   520;    arteritis,   504;     1390; 
of  cerebellum,   1339,   1346 ;    of  cere- 
brum, 1389  ;    gummata,  1397  ;    coro- 
noritis,    534 ;     of   heart,    457 ;     here- 
ditary cerebral,  1404;    kidney,  1165; 
of  larynx,  31  ;    of  lips,  563  ;    of  liver, 
955 ;    of  lung,   231 ;    malignant  hy- 
pertoxic,      1707 ;     of     nose,     5 ;     of 
oesophagus,    655 ;     pleura,    356 ;     of 
skull,    1410;     of    soft    palate,    638; 
spinal  cord,  1307  ;    of  stomach,  734 ; 
of    tongue,    564 ;     tracheo-bronchial, 
102  ;    vaccinal,  treatment  of,  2116 
Syphilitic  membranous  angina,  624 ;  phlebitis, 
493  ;   pharyngitis,  583  ;    pachymeningitis, 
1464 ;     pohoencephalitis,     1330 ;    perfora- 
tion palate,  569  ;  general  pseudo-paralysis, 
1389,  1402  ;   spinal  paralysis,  1309 
Syringomyelia,    1272,    1282 ;    Morvan's   dis- 
ease, 1275 


Tabes,  1243  ;    astiology,  1264 ;    angina  pec- 
toris,    537;      ataxy,     1248;      cyto- 
diagnosis,    1255 ;     description,    1243  ; 
diagnosis,    1254 ;     pathological    ana- 
tomy, 1256 ;  treatment,  1265 
varieties ;     cerebral,    1403 ;     combined, 
1269 ;     defaced,    1253 ;     and   general 
paralysis,  1250  ;    labyrinthine,  1245  ; 
spasmorlic,   1283  ;    mesenterica,   815  ; 
superior,  1247 
Tache  cer^bralc,  1446 
Tachycardia,  465 
Tactile  vocal  fremitus,  in  pneumonia,  126  ; 

in  pleural  eifusion,  251 
Tsenise,  855 
Tape-worms,  855 
Tapping,  in  ascites,  925 ;    in  cirrhosis,  921  ; 

in  pericarditis,  406 
Taste,  loss  of,  1566 
Teeth,  shedding  of,  in   diabetes,    1961 ;    in 

tabes,  1252 
Temperature  sense,  loss   of,   in  alcoholism, 
1276 ;     in    diabetes,    1276 ;     in    Morvan's 
disease,  1276  ;   in  syringomyelia,  1274  ;  in 
tabes,  1261 
Temporal  lobe,  abscess  in,  1377 
Tender  point  (YaUeix's)  in  neuralgia,  1540 
Tendon-reflexes.     See  Reflexes 
Tension,  arterial,  548 
Tertian  fever,  1805 
Test  meals,  731 
Testes  in  mumps,  1757 

Tetanus,  1787  ;   cephalic,  1791  ;   after  injec- 
tion  of   gelatinized   serum,    1791 ;    treat- 
ment, 1795 
Tetany,  1535 


Therapeutics,  appendix  on,  2116 

Thirst  in  diabetes,  1957 

Thomsen's  disease,  1519,  2035 

Thoracentesis,  262,  291 

Thoracic  duct,  cancer  of,  398 

Thorax,  in  emphysema,  160  ;  in  rickets,  2020 

Throat,  disease  of,  577 

Thrombosis :     cerebral,    1364 ;     of    cerebral 

sinuses,  1342,  1898  ;   pidmonary,  144 
Thrombus,  490 
Thrush,  557 

Thymus  in  acromegaly,  2025 
Thvmus.  degeneration  of,  389 
Thyroid  extract,  2008 

gland  in  Basedow's    disease,     483 ;     in 
myxoedema,  2005 
Thyroiodin,  2007 
Tic  douloureux,  1540  ;   removal  of  Gasserian 

gangHon  in,  1545 
Tics,  1529 

Tinkling,  metallic,  385 
Tobacco  poisoning,  2109 
Tongue,  eczema  of,  565  ;  epithelioma  of,  568  ; 

hemiatrophy  of,  1602  ;  paralysis  of,  1323  ; 

syphilis  of,  564  ;   tuberculosis  of,  575 
Tonsillitis :      acute,     578 ;      chronic,     585 ; 

scarlatinal,      1629 ;       suppurative,     579 ; 

ulcero-membranous     (Vincent's     angina), 

583 
Tonsils,  diseases  of,  578  ;    chancre  of,  632 ; 

masked  tuberciilosis  of,  644 
Tophus,  1939 

Torticollis  in  Bright's  disease,  1114 
Toxaemia  in  appendicitis,  797 
Toxicity :     of    serum,    in    Bright's    disease, 

1136  ;    of  urine  in  Bright's  disease,  1133  ; 

in  chlorosis,  1906 
Toxine  :     in    diphtheria,    590 ;     in    tetanus, 

1788  ;   in  typhoid  fever,  1721 
Trachea,  compression  of,  391 
Tracheitis,  102 
Tracheostenosis,  103 
Transfusion  of  blood,  1141 
Traube's  space,  253 
Trauma     and     epilepsy,     1490 ;      diabetes, 

1984  ;    meningitis,  1450 
Tremors  :     in    Basedow's    disease,    472 ;     in 

hemiplegia,   1359 ;    in  hysteria,  1496 ;    in 

insular  sclerosis,  1289  ;    in  lead-poisoning, 

2096 ;      mercurial,     2092 ;      in     paralysis 

agitans,  1521  ;   in  sleeping  sickness,  1823 
Treponema  pallidum,  2072 
Trichinosis,  2012 
Trichocephalus,  853 

Tricuspid  insufficiency  and  stenosis,  443 
Trifacial  neuralgia,  1540 ;   paralysis,  1595 
Trismus,  1790 

Trophic  disorders,  1500,  1598 
Trophcedema,  hereditary  chronic,  1599 
Trophoneurosis,  facial,  1601 
Trypanosomes,  1821 
Trypanosomiasis,  1821 
Tsetse-fly,  1821 
Tubercle  bacillus,  170 


INDEX 


2155 


Tuborclps  of  choroid,  1438 
Tuberculin.  11*3 
Ihiboreulocidin.  195 

TulxTCuJoina,  l>yiK>rtrophic,  of  csDcum,  816 
Tuberculoais,   l<i!»;   setiolopy,   188;    bacillus, 
Kochs,  170;  pill  hulogical  anatomy,  17- 
acute,  of  lung,  1!»H  ;   acute  miliary,  203  ; 
ano-rectal,    830;     of    bladder,    1160; 
and     cerebral     abscess,     1377 ;      and 
cirrhosis,   913 ;    of  choroid   plexuses, 
1438 ;     of    cranial    vault,    1438 ;     of 
intestine,  812;    of  kidney,   1153;    of 
larynx,   40;    of  liver.   943;    of  lung 
(fibroid  phthisis),   195;    of  meninges, 
1437  ;   of  mouth,  574  ;   of  nasal  fossae, 
14  ;  of  peritoneum,  863  ;   of  pharynx, 
643;    of   pleura,   248,   268,   273;    of 
stomach,    674 ;     of    tonsils    (masked 
form),  644 
chtonic  pulmonary,  176  ;    bacteriology, 
180 ;     description,     180 ;     diagnosis, 
190 ;     hjemoptysis,    184 ;     lesions   in 
other  organs,  186,   195;    pathological 
anatomy,  176;  prognosis,  187;  treat- 
ment, 191 
Tubercular  rheumatism,  1933 
Tumour :    cerebral,  1384 ;    dorsal,  of  wrist, 
2096  ;    of  heart,  458  ;    of  right  iliac  fossa, 

816  ;   lachrymal,  10  ;   mediastinal,  387 
Tw-ists  and  kinks  in  bowel,  839 
Typhlitis,  757 

Typhoid  fever,  1665  ;   abscess  of  liver,  1689  ; 
aetiology,  1713  ;   aphasia,  1697  ;   appendi- 
citis,   paratyphoid,     1682 ;     bacteriology, 
1715  ;   cholecystitis,  1688  ;   clinical  forms, 
1669 ;      complications,     1671  ;      delirium, 
1697  ;  diagnosis,  1706  ;  haematoma.  1700  ; 
haemorrhage,    intestinal,     1672 ;     orchitis, 
1696;    osteomyelitis,   1702;    pathological 
anatomy,  1718  ;   perforation  and  peritoni- 
tis,   1673;     phlebitis,    1694;     pulmonary 
congestion,  1091  ;  symptoms,  1665  ;  treat- 
ment, 1722 
Typho-lumbricosis,  1706 
Typho-malaria,  1810 
Typhosis,  syphilitic,  1707 
Typho-toxine,  1713 
Typhus,  1730 
Tyrosia,  1041,  1043 

U 

Ulcer : 

of  the  duodenum,  832  ;  perforation,  of 
stomach  and  duodenum  in  appendi- 
citis, 713 

of  the  stomach,  674  ;  latent  form,  705  ; 
perforation,  709 

perforating,  in  diabetes,  1960  ;  in  tabes, 
1252 
Ulceration,     intestinal :      dysenteric,     846 ; 
tubercular,  813  ;    in  anorectal  tuber- 
culosis, 830;   in  typhoid  fever,  1719 

of  the  lacyni,  33,  41  ;  in  typhoid  fever, 
1690 


of  the  stomach  :  general  conKideratioiui, 

«J74 
of  vault  of  palate,  tubercular,  576 
Ulcers  :      in     follicular    cnteritiB,     751  ;      Id 

glanders,  1844  ;   of  nasal  septum,  9 
Ulnar  nerve,  uUcctions  of,  1594 
Unemia,    1124;     acute,    1088;     Brightism, 
minor  symptoms  of,  1111,  1 125  ;  calculous, 
1201;    in   chlorosis,    1906;    in    polycyntic 
kidney,  1182;   prognosis,  1137;   in  scarlet 
fever,  1636;   treatment,  1139 
Urate  of  soda  in  gout,  1946 
Urea  in  the  sweat,  1123 
Ureter,    blocking    by   calculi,    12(>f) ;     com- 
pression of,  1219 
Ureteritis,  tubercular,  1155 
Urethritis :      diabetic,     1955 ;      gonorrhoeal, 
2046 ;      non-gonorrhoeal,     2046 ;      gouty, 
2046 
Uricaemia  in  gout,  1946 
Uric   acid   calculi,    1192;     in    gout,    1945; 
(gouty)  diathesis,  1945 ;    theory  of  gout, 
1945 
Urine  : 

in  acute  nephritis,  1088  ;  in  acute  yellow 
atrophy,  1043  ;  in  chlorosis,  1896  ;  in 
chronic  nephritis,  1117;  in  diabetes 
insipidus,  1982  ;  in  diabetes  meUitus, 
1957 ;  in  gout,  1941  et  aeq.  ;  in 
jaundice,  1034  ;  in  malaria,  1810  ;  in 
typhoid  fever,  1668 
cryscopy  of,  1136;  normal  composition 
of,  1080 ;  passage  of  methvlene  blue, 
1134;  leucin,  1043;  pus  in,  1158 
Urobilin,  1034 

Urticaria  :  after  aspiration,  972  ;  in  a^hma, 
112;  in  hydatid  cyst  of  liver,  964;  in 
hydatid  cyst  of  the  lung,  227  ;  in  jaundice, 
1032 
Uvula,  swelling  of,  in  diphtheria,  693 ; 
membrane  on,  593 


Vaccination  lymph,  1617 ;  antiseptic  pre- 
cautions, 1617  ;   Jenner's  method,  1617 

Vaccine  lymph,  1617 

Vaccines,  2130 

Vaccinia,  1615 ;  vaccinal  syphilis,  1619 ; 
vaccination,  1617 

Vagabond's  itch,  1238 

Vaginismus,  hysterical,  1507 

Valleix's  points,  1540 

Valves  of  the  heart,  lesions  of,  421 

Varicella,  1621 

Varices,  lymphatic,  2016 

Varices,  oesophageal,  915 

Varicocele  in  cancer  of  kidney,  11 90 

Variola,  1607 ;  complications,  1613 ;  con- 
fluent, 1611;  coherent-confluent,  1607; 
discrete,  1607 ;  eruption,  1609 ;  haemor- 
rhagic,  1612;  invasion,  1608;  photo- 
therapy in,  1615  ;   prophylaxis,  1615 

Varioloid,  1611 


2156 


TEXT-BOOK    OF  MEDICINE 


Vas  deferens,  tuberculosis  of,  1156 

Vasomotor  troubles,  1598 

Vater's  ampulla,  cancer  of,  843 

Vegetations,  adenoid,  586 

Vein,  portal,  871  ;   accessory,  914 

Velum  palati :  diphtheritic  paralysis  of,  626  ; 
erythema,  638  ;  gumma,  639  ;  paralysis 
of,  1323  ;  phagedsena  of,  640  ;  syphilis  of 
638  ;  zona,  639 

Vena  cava,  compresssion  of,  390 

Venereal  diseases,  2045 

Ventricular  hydrocephalus,  1469 

Verlhoff's  disease,  1910 

Vertigo  :  in  Bright's  disease,  1113  ;  epileptic, 
1479;   Meniere's,  1345 

Vesiculse  seminales,  tuberculosis  of,  1156 

Vestibular  nerve,  1345 

Vincent's  angina,  583 

Vision,  disorders  of,  1386 

Visual  field,  narrowing  of,  1502 

Vitihgo,  1599 

Vocal  fremitus,  126,  385 

Voice,  physiology  of,  26 

Volitional  tremor,  1289 

Volvulus,  838 

Vomicse,  340,  377 

Vomiting :  in  Addison's  disease,  1234 ;  in 
cerebral  abscess,  1378  ;  in  cerebral  tumour, 
1385  ;  fsecal,  840  ;  in  gastric  cancer,  726  ; 
in  gastric  ulcer,  701  ;  in  hepatic  colic,  996  ; 
in  intestinal  occlusion,  839 ;  in  migraine, 
1538 ;  pancreatic,  1060 ;  porraceous,  in 
peritonitis,  861 ;  in  tubercular  meningitis, 
1439  ;  in  typhoid  fever,  1672 ;  ursemic, 
1129 

Vomito  negro  (appendicular),  679 


W 

Warnings  (prodromata)  in  cerebral  haemor- 
rhage, 1355 

Warty  tuberculosis  of  the  anus,  830 

Wassermann's  reaction,  2121 

Water  infection  by,  in  cholera,  1762 ;  in 
typhoid,  1716 

Weber's  syndrome,  1336 

Weil's  disease,  1051 

Weinberg's  reaction,  225 

White  softening  of  brain,  1365 

Whitlow,  painless,  1275 

Whooping-cough,  104 

Widal's  reaction  in  typhoid  fever,  1708 

Wine,  Trousseau's  diuretic,  435 

Word-bHndness,  1371 

Word-deafness,  1371 

Worms,  intestinal,  852 

Wright's  opsonic  method,  2130 

Wrist  drop,  1474 

Writer's  cramp,  1537 


Xanthelasma,  1032 
Xanthin,  1043 


Yellow  fever,  1777  ;  nostras,  1044 
softening,  1365 

Z 

Zona,  1549  ;   palato-pharyngea,  639 

Zoster,  1549 

Zone,  motor,  1429,  1486 


THE   END 


BaUliire,  Tindall  <&  Cox,  8,  Henrietta  Street,  Covent  Oarden. 


Extracts    from    Rcxicws 

of     the      P^.no:lish      Translation      of 

Dieulafoy's    Medicine. 


The  Lancet. — "  A  text-book  on  medicine  by  so  distinguished  a  clinician  as 
Professor  Dieulafoy  should  be  of  special  interest  and  value,  not  only  as  representa- 
tive of  French  teaching  on  medicine  but  as  the  work  of  a  physician  of  wide 
experience.  .  .  .  At  the  outset,  we  may  affirm  that  this  book  is  a  tnost  useful  one,  and 
the  translators  have  performed  a  notable  service  in  rejidering  it  available  in  readable 
English.  The  tendency  in  modem  text-books  of  medicine  is  to  describe  in  detail 
the  general  characters  of  diseases  in  systematic  or  categorical  arrangement,  whereas 
the  older  text-books,  such  as  those  of  Trousseau  and  Watson,  were  written  in  descrip- 
tive style,  and  were  truly  works  on  clinical  medicine,  since  the  character  of  the 
diseases  were  illustrated  by  special  cases  rather  than  by  collected  summaries  of  many 
cases  elevated  into  an  abstraction.  Professor  Dieulafoy's  method  combines  both  of 
these  methods,  since,  although  the  systematic  method  is  adopted  as  a  general  basis, 
the  symptoms  are  often  brought  out  descriptively  by  means  of  real  or  hypothetical 
cases.  This  gives  a  somewhat  original  and  at  the  same  time  an  attractive  character 
to  the  book,  rendering  it  easy  to  read.  .  .  .  Professor  Dieulafoy's  book  affords  an 
interesting  presentation  of  French  practice  in  medicine  and  is  well  worth  study.  We 
have  read  it  with  great  interest,  as  it  is  both  original  and  suggestive,  and  it  must  be 
helpful  to  the  practitioner  since  it  is  especially  calculated  to  afford  light  in  regard 
to  obscure  and  rare  cases." 

British  Medical  Journal. — "It  is  an  excellent  book,  clearly  written  and 
illustrated  with  admirable  diagrams,  drawings,  and  photomicrographs,  while  the 
translators  deserve  praise  for  their  work.  .  .  There  is  a  well  arranged  index.  .  .  . 
The  book  is  one  which  all  who  value  the  perspicuousness  of  French  teaching  will 
appreciate." 

Medical  Press  and  Circular. — "  The  translation  has  been  excellently  accomplished 
by  Drs.  Collins  and  Liebmann.  .  .  .  Professor  Dieulafoy  treats  all  subjects  with  the 
same  independent  judgment  and  wide  experience.  His  literary  gifts  render  the 
volumes — like  most  of  French  origin — easy  and  pleasant  to  read.  For  the  English 
edition  we  have  little  but  praise." 

Gay's  Hospital  Gazette. — "The  English  translation  of  Professor  Dieulafoy's  well- 
known  book,  which  has  reached  its  15th  edition,  will  no  doubt  appeal  strongly  to 
many  post  graduates  whose  knowledge  of  French  is  weak.  The  authors  are  to  be 
congratulated  upon  the  results  of  their  labours,  which  must  have  been  immense.  We 
have  had  abutidant  proof  in  our  review  of  the  care  which  they  have  taken  to  insure  that 
the  book  should  lose  nothing  of  accurcuy  or  of  graphic  description  by  their  translation. 
The  work  has  been  thorough,  and  it  is  characterized  by  an  exhaustive  attention  to 
detail  in  production." 


Australasian  Medical  Gazette. — "  Dr.  Dieulafoy,  one  of  the  great  masters  of 
medicine,  and  once  assistant  of  Trousseau,  has  attempted,  and  with  great  success,  to 
preserve  the  best  of  the  old  work  which,  although  of  great  value,  was  sometimes 
neglected,  and  to  incorporate  with  it  the  most  recent  advances.  Some  sections  of 
the  book  are  unusually  extensive.  .  .  .  The  chapters  on  hydatid  diseases  of  the  lung, 
liver,  spleen,  etc.,  are  better  than  those  in  the  ordinary  English  books  on  medicine, 
and  will  appeal  specially  to  Australian  physicians.  .  .  .  Throughout  the  book  one 
comes  across  particularly  interesting  philosophical  dissertations.  .  .  .  Such  discus- 
sions are  of  great  interest.  .  .  The  translators  are  to  be  congratulated  upon  their 
successful  attempt  to  make  available  in  English  the  vast  experience  oj  the  author" 

South  African  Medical  Record. — "This  is  the  first  translation  into  English  of 
Dieulafoy's  well-known  work  which  a  good  many  of  us  have  read  in  the  original 
with  pleasure  and  profit.  It  is  of  such  exceptional  merit  that  we  make  little  doubt 
about  its  becoming,  now  that  it  is  accessible  to  English  readers  in  general,  the 
standard  text-book  of  medicine  for  years  to  come.  In  France,  it  has  held  that 
position  for  a  considerable  time.  We  confess  to  a  weakness  for  Gallic  books  on 
medicine  and  surgery.  In  our  humble  opinion,  no  people  write  so  clearly,  so 
incisively,  so  tersely,  none  succeed  so  well  in  the  task  of  presenting  their  facts  in  a 
form  to  be  remembered.  But  they  have  to  be  well  translated,  or  the  tours  deforce 
of  the  language  are  lost.     In  this  case  the  translation  has  been  excellently  done." 

New  York  Medical  Record. — "A  pupil  of  Trousseau,  Dieulafoy  was  his  worthy 
successor — a  keen  observer,  possessed  of  the  discriminating  judgment  necessary 
for  the  diagnostician,  the  reasoning  faith  that  makes  the  successful  therapeutist,  and 
the  facile  pen  of  a  ready  writer.  All  these  qualities  are  in  evidence  in  his  treatise, 
which  is  the  work  of  a  master.  The  translation  is  well  done,  the  illustrations  are  few 
but  good,  and  the  topography,  paper,  and  binding  are  all  that  could  be  desired." 

Canadian  Practitioner, — "  Professor  Dieulafoy's  work  has  been  a  standard  in  his 
native  land  for  many  years,  and  the  translators  have  successfully  rendered  his  thoughts 
ifi  bright,  crisp  English  that  reads  like  a  novel.  In  fact  the  book  is  so  fascinating 
that  one  hates  to  lay  it  down  .  .  .  Taken  as  a  whole,  these  two  volumes  are  filled 
with  new  and  practical  thoughts,  in  most  readable  English,  and  fully  equal  to  any- 
thing that  has  appeared  in  Canada  during  this  century." 

Allegemeine  Wiener  Medizienische  Zeitung. — "It  would  be  a  mistake  if,  in  this 
short  critique,  the  translation,  as  such,  from  the  French  into  English,  were  not 
referred  to.  It  must  be  called  an  excellent  one,  because  it  is  not  merely  a  simple 
literal  rendering  into  English,  but  does  justice  to  all  the  linguistic  idiosyncrasies  of 
the  scientific  subject.  This  is  only  possible  when  the  translator  knows  his  work 
thoroughly,  and  such  must  be  the  case  with  Drs.  Collins  and  Liebmann  in  a  very 
marked  degree  indeed." 

Indian  Medical  Gazette. — "We  have  been  much  impressed  with  our  perusal  of 
these  handsome  volumes.  It  is  very  refreshing  to  find  subjects  handled  in  a  wa)' 
different  to  what  we  have  been  accustomed  to,  and  new  lights  are  constantly  thrown 
on  old  subjects.   ..." 


There  are  many  other  criticisms  equally  as  good  but  too  numerous 
to  be  included  here. 


COLUMBIA  UNIVERSITY 

This  book  is  due  on  the  date  indicated  below,  or  at  the 
expiration  of  a  definite  period  after  the  date  of  borrowing, 
as  provided  by  the  rules  of  the  Library  or  by  special  ar- 
rangement with  the  Librarian  in  charge. 

DATE  BORROWED 

DATE  DUE 

DATE  BORROWED 

DATE  DUE 

C28(63B)MS0 

